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Journal of Medicine and Pharmacy","Tạp chí Y Dược học Cần Thơ",{"EN":487,"VI":488},"\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">04\u002F10\u002F2015 Ministry of Information and Communications allowed Can Tho journal of medicine and pharmacy to operate (102 \u002FGP-BTTTT)\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">07\u002F16\u002F2015 Can Tho journal of medicine and pharmacy is internationally recognized: ISSN 2354-1210\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">In 2016, The journal has been included in the list of medical science journals by The State Council for professorship which is awarded a work score of 0-0.5 points for a published article.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Can Tho Journal of Medicine and Pharmacy welcome original works that haven’t been submitted or published in other medical journals. Posts must contain content related to one of the journal’s categories.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The content published\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The journal is divided into 3 categories:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Scientific research article: are valuable scientific works, which have been researched and accepted.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Overview of medicine, biology and pharmacy: serving the objective of continuing training in the fields of medicine, biology and pharmacy; to systematize classical and modern knowledge.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Update information on new knowledge about medicine, biology, pharmacy in the country and in the world.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Scope\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Publication and introduction of scientific research in the fields:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Medicine (internal medicine, surgery, pediatrics, obstetrics and gynecology, odonto-stomatology, laboratory, oncology, traditional medicine, nursing).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Biology (genetics, biotechnology).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Pharmacology (pharmaceutics, drug quality analysis-control, synthetic pharmaceutical chemistry, biochemistry, pharmacognosy, botany, clinical pharmacy).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- To enhance the quality of undergraduate, postgraduate education, scientifically researching and meet the necessary treatment in hospital.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Introducing the updated domestic and oversea information about science technology to promote scientific research and exchanging technology in local, other universities.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Exchanging pharmaceutical and medical information for social health developing in the Mekong Delta and Vietnam.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The object\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Postgraduate students, student of Can Tho University of Medicine and Pharmacy, scientists from schools, research institutes, hospitals, health centers, pharmaceutical companies of the Mekong Delta; other provinces and regions in Vietnam and other country.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Address\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Headquarters of Can Tho Journal of Medicine and Pharmacy, located Scientific Research and International Cooperation Office: 179 Nguyen Van Cu Street, An Khanh Ward, Ninh Kieu District, Can Tho City, Vietnam.\u003C\u002Fspan>\u003C\u002Fp>","\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Ngày 16\u002F7\u002F2015, Tạp chí Y Dược học Cần Thơ được cấp chỉ số quốc tế: ISSN 2354-1210.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Từ tháng 4\u002F2016, Tạp chí đã được Hội đồng Giáo sư ngành Y đưa vào danh sách các tạp chí khoa học Y học được tính điểm công trình 0-0,5 điểm cho một bài báo đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Năm 2020 Tạp chí Y Dược học Cần Thơ đã được phê duyệt vào danh mục của các Hội đồng Giáo sư ngành Dược học được tính điểm công trình 0-0,5 điểm cho một bài báo đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ ra 12 số\u002Fnăm, 180-200 trang\u002Fsố.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Từ tháng 12\u002F2022 Tạp chí Y Dược học Cần Thơ là thành viên của hệ thống Crossref và từ tháng 01\u002F2023 tạp chí thực hiện bình duyệt online kín 2 chiều nhằm tăng tính minh bạch, tin cậy của các công trình nghiên cứu khoa học và đảm bảo tốt nhất chất lượng khoa học của bài viết.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tôn chỉ, mục đích và phạm vi của tạp chí\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tôn chỉ và mục đích hoạt động của tạp chí: xuất bản nhằm mục đích phổ biến kết quả từ các đề tài nghiên cứu khoa học; giao lưu trao đổi khoa học, chia sẻ kinh nghiệm, học tập, đồng thời cập nhật thông tin khoa học mới trong các lĩnh vực y, sinh, dược học trong và ngoài nước.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Phạm vi của tạp chí: Tạp chí xuất bản được chia thành 3 chuyên mục: (i) Bài báo nghiên cứu khoa học là kết quả công trình nghiên cứu khoa học có giá trị đã được triển khai nghiên cứu, (ii) Bài tổng quan y, sinh, dược học: phục vụ mục tiêu đào tạo liên tục trong lĩnh vực y, sinh, dược học; nhằm hệ thống hóa những kiến thức kinh điển và hiện đại; (iii) Thông tin cập nhật kiến thức mới về y, sinh, dược học trong nước và trên thế giới.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Chính sách truy cập mở\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ áp dụng chính sách truy cập mở đối với các bài báo đã xuất bản đến với độc giả, nhằm mở rộng cơ hội tiếp cận các kết quả nghiên cứu chất lượng cao và tăng cường trao đổi kiến thức. Tạp chí đăng tải trực tuyến (miễn phí) toàn văn các bài báo được công bố trên website của Tạp chí (https:\u002F\u002Ftapchi.ctump.edu.vn).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đạo đức xuất bản\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ cam kết tuân thủ đạo đức xuất bản phù hợp với các hướng dẫn và tiêu chuẩn của the Committee on Publication Ethics (COPE), tuân thủ các nguyên tắc của COPE’s Core Practices, Best Practices Guidelines for Journal Editors và Guidelines on Good Publication Practices.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Bản thảo bài báo chỉ được chấp nhận khi được tác giả chịu trách nhiệm chính cam kết các nội dung sau: Các nội dung của bản thảo chưa được đăng tải toàn bộ hoặc một phần ở các tạp chí khác; Tất cả các tác giả đều có đóng góp một cách đáng kể vào quá trình nghiên cứu hoặc chuẩn bị bản thảo và cùng chịu trách nhiệm về các nội dung của bản thảo; Tuân thủ các biện pháp đảm bảo đạo đức nghiên cứu (ví dụ thỏa thuận đồng ý tham gia nghiên cứu).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Cam kết bảo mật\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí cam kết thực hiện và tuân thủ các quy định của luật và các văn bản hướng dẫn liên quan đến bảo mật thông tin cá nhân trên không gian mạng. Các thông tin mà người dùng (tác giả, độc giả, biên tập viên, người phản biện) nhập vào các biểu mẫu trên Hệ thống Quản lý xuất bản trực tuyến của tạp chí chỉ được sử dụng vào các mục đích đã được tuyên bố rõ ràng và sẽ không được cung cấp cho bất kỳ bên thứ ba nào khác, hay dùng vào bất kỳ mục đích nào khác.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Phí gửi bài\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Lệ phí gửi đăng bài: 1.000.000đ\u002Fbài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Lệ phí gửi đăng nhanh: 1.500.000đ\u002Fbài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đối với tác giả là cán bộ viên chức thuộc Trường Đại học Y Dược Cần Thơ thì được hỗ trợ 50% lệ phí gửi đăng bài.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đối với sinh viên thực hiện đề tài nghiên cứu khoa học cấp trường được hỗ trợ 100% lệ phí đăng bài ( Tác giả gửi đính kèm “ Quyết định về việc giao tổ chức thực hiện đề tài nghiên cứu khoa học cấp Trường của sinh viên”).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Hình thức nộp lệ phí:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Tiền mặt:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Nộp trực tiếp tại Phòng Tài chính - Kế toán, Trường Đại học Y Dược Cần Thơ, số 179 Nguyễn Văn Cừ, P. An Khánh, Q. Ninh Kiều, thành phố Cần Thơ.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Chuyển khoản:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tên Tài khoản: Trường ĐHYD Cần Thơ, Số TK: 0111000115668, tại ngân hàng Vietcombank chi nhánh Cần Thơ.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Thời gian: Áp dụng từ ngày 01\u002F02\u002F2023.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">* Phí gửi bài không được hoàn trả khi bài viết bị từ chối hoặc tác giả xin rút bài viết.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Quy trình phản biện bài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ thực hiện quy trình phản biện kín hai chiều nghiêm ngặt. Danh tính của những người phản biện không được tiết lộ cho các tác giả và ngược lại. Quy trình thẩm định bài báo đăng gồm các bước sau:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tiếp nhận bản thảo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tác giả liên hệ gửi bản thảo đến Tạp chí qua hệ thống trực tuyến tại website: https:\u002F\u002Ftapchi.ctump.edu.vn. Hướng dẫn về cách đăng ký, gửi bài và chuẩn bị bản thảo được cung cấp trên website của Tạp chí.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Sàng lọc sơ bộ\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Sau khi Tòa soạn nhận được bài báo của tác giả, Ban Thư ký sẽ tiến hành kiểm tra sơ bộ bài báo (các yêu cầu về nội dung và hình thức). Những bài báo không đúng quy cách hoặc có nội dung không phù hợp hoặc vi phạm bản quyền sẽ bị từ chối (Ban Thư ký thông báo phản hồi đến tác giả trong vòng 1 tuần). Những bài báo đủ điều kiện, được Ban Thư ký tòa soạn chuyển đến Ban Biên tập có cùng chuyên môn với nội dung bài báo để đề xuất người phản biện. Thời gian kể từ khi Ban Biên tập nhận bài báo đến khi đề xuất người phản biện bài báo chậm nhất là 5 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Vòng phản biện\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Ban Thư ký gửi bài và yêu cầu phản biện đến 02 phản biện độc lập.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Các phản biện gởi nhận xét cho Ban Thư ký. Thời gian từ khi gửi bài cho phản biện đến khi nhận ý kiến của phản biện tối đa là 20 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Xử ký kết quả phản biện\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Nếu ý kiến đồng ý cho đăng và không cần chỉnh sửa, Ban Thư ký tiếp tục đăng bài theo qui trình.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Nếu ý kiến đồng ý đăng và cần chỉnh sửa, Ban Thư ký sẽ thông tin đến tác giả chỉnh sửa theo yêu cầu của người phản biện. Thời gian chỉnh sửa và gửi lại kéo dài không quá 2 tuần, từ khi tác giả bài báo nhận được thông tin (Quá trình này có thể lặp lại tối đa 2 lần\u002F1 bài báo). Khi có sự thống nhất, đồng ý của người phản biện; bài báo được tiếp tục đăng theo qui trình.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">3. Những bài báo có chất lượng không đạt yêu cầu, cả 2 phản biện không đồng ý cho đăng sẽ bị Tòa soạn từ chối đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Xuất bản\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Ban Thư ký tổng hợp các bản thảo đã được tác giả hoàn thiện sau thẩm định trình Ban Biên tập xem xét, Tổng Biên tập phê duyệt, quyết định bài đăng theo các tiêu chí: sự phù hợp nội dung với tôn chỉ và mục đích, thể loại bài viết (ưu tiên các bài có bài có nghiên cứu chuyên sâu, hàm lượng khoa học cao), đóng góp mới bài báo, bài báo được ưu tiên đăng trong số gần nhất của Tạp chí theo thứ tự: tính thời sự, chất lượng bài báo và thời gian gửi bài.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Ban Biên tập và Ban Thư ký biên tập bản thảo, chế bản, đọc rà soát lỗi. Thời gian hoàn thành từ 10-15 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">3. Ban Thư ký có trách nhiệm thông báo cho tác giả bài báo (bằng e-mail) về tình hình phê duyệt bài báo, thời gian, số kỳ, tập xuất bản bài báo theo qui định.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">4. Danh sách bài báo theo số Tạp chí được in ấn và phát hành trong năm định kỳ được công bố chính thức trên website: https:\u002F\u002Ftapchi.ctump.edu.vn\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>",{"VOID":490},"wcQ1uqwAAAAJ","2023-05-30T08:17:21.868+00:00",[],[494],{"id":495,"createTime":28,"updateTime":28,"relativeEntities":496,"slug":28,"properties":497,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":507,"parentIds":508,"statistic":28},"6413896b-eca9-442b-a73f-182a58a0ce40",[],{"title":498,"address":501,"country":504,"abbreviation":505},{"EN":499,"VI":500},"Can Tho University of Medicine and Pharmacy","Trường Đại học Y Dược Cần Thơ",{"EN":502,"VI":503},"No 179, Nguyen Van Cu street, An Khanh ward, Ninh Kieu district, Can Tho city, Vietnam","Số 179, đường Nguyễn Văn Cừ, phường An Khánh, quận Ninh Kiều, thành phố Cần Thơ, Việt Nam",{"VOID":15},{"VOID":506},"ctump","http:\u002F\u002Fwww.ctump.edu.vn\u002F",[],[],"https:\u002F\u002Ftapchi.ctump.edu.vn\u002Findex.php\u002Fctump",{"impactFactor":32,"impactFactorByYear":512,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":514,"totalPublicationByYear":515,"totalCitation":520,"totalCitationByYear":521,"totalCitationPerPublication":108,"totalCitationPerPublicationByYear":523,"hindexLast5Year":45,"hindex":45},{"2022":513,"2023":111,"2024":106},0.01,1556,{"2020":47,"2021":516,"2022":517,"2023":518,"2024":519,"2025":122},57,306,801,358,161,{"2021":146,"2022":280,"2023":522},99,{"2021":524,"2022":318,"2023":104},0.23,{"impactFactor":28,"impactFactorByYear":28,"i10Index":123,"i10IndexLast5Year":123,"totalPublication":526,"totalPublicationByYear":527,"totalCitation":526,"totalCitationByYear":528,"totalCitationPerPublication":40,"totalCitationPerPublicationByYear":531,"hindexLast5Year":49,"hindex":49},476,{"0":205,"2019":123,"2021":139,"2022":459,"2023":451,"2024":357,"2025":49,"2026":48},{"2021":42,"2022":123,"2023":161,"2024":529,"2025":360,"2026":530},136,83,{"2021":105,"2022":513,"2023":532,"2024":127,"2025":533,"2026":534},0.62,25.43,13.83,{"id":536,"createTime":537,"updateTime":382,"relativeEntities":538,"slug":539,"properties":540,"entityType":25,"verifyStatus":26,"verifyTime":28,"verifyNote":28,"languages":552,"translateLanguages":28,"viewCount":133,"subjectFields":553,"manageAffiliations":554,"indexDatabases":555,"url":556,"thumbnailPath":557,"statistic":558,"gsStatistic":594,"type":55,"analyzePriority":28},"6984a56a-db70-403b-9cc4-4013e1ceaffa","2023-05-09T06:47:40.346+00:00",[],"T%E1%BA%A1p%20ch%C3%AD%20Nghi%C3%AAn%20c%E1%BB%A9u%20n%C6%B0%E1%BB%9Bc%20ngo%C3%A0i",{"country":541,"issn":542,"title":544,"introduce":547,"gsId":550},{"VOID":15},{"VOID":543},"25252445",{"EN":545,"VI":546},"VNU Journal of Foreign Studies","Tạp chí Nghiên cứu nước ngoài",{"EN":548,"VI":549},"{\"ops\":[{\"insert\":\"\\n\\nThe \\n\"},{\"attributes\":{\"italic\":true},\"insert\":\"VNU Journal of Science\"},{\"insert\":\"\\n was established in 1985 for the publication of national and international research papers in all fields of natural sciences and technology, social sciences and humanities. 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issues in industrialized nations play an important role in the lives of most citizens. The acts of flying and driving, especially in the United States, intersect with many peoples’ lives on almost a daily basis. Although some larger cities have modern and efficient public transportation systems, many do not, thus placing considerable responsibility on the individual to manage their own transportation needs. A person with epilepsy faces considerable challenges when it comes to transportation. Defining these challenges and understanding how to deal with the person with epilepsy and transportation issues is the focus of this article.",{"EN":1004},"Driving and flying with epilepsy",{"VOID":1006},"Bureau of Transportation Statistics: State Transportation Statistics. http:\u002F\u002Fwww.bts.gov. Accessed April 15, 2007.\nNational Transportation Safety Board: http:\u002F\u002Fwww.NTSB.gov. Accessed April 15, 2007.\nSirven JI, Claypool DW, Sahs KL, et al.: Is there a Neurologist on this flight? Neurology 2002, 58:1739–1744.\nGilliam F, Kuzniecky R, Faught E, et al.: Patient-validated content of epilepsy-specific quality-of-life measurement. Epilepsia 1997, 38:233–236\nFisher RS, Parsonage M, Beaussart M, et al.: Epilepsy and Driving: an international perspective. Joint commission on Drivers’ Licensing of the International Bureau for Epilepsy and the International league Against Epilepsy. Epliepsia 1994, 35:675–684.\nKrauss GL, Ampaw L, Krumholz A: Individual state driving restrictions for people with epilepsy in the US. Neurology 2001, 57:1780–1785.\nEpilepsy and Driving in Europe. A report of the Second European Working Group on Epilepsy and Driving. http:\u002F\u002Fec.europa.eu\u002Ftransport\u002Froadsafety. Accessed April 15, 2007.\nFederal Motor Carrier Safety Administration: http:\u002F\u002Fwww.fmcsa.dot.gov\u002Fespanol\u002Fenglish\u002F. Accessed March 27, 2007.\nThalwitzer F: Epileptiker als Autofahrer. Munch Med Wochenschr 1906, 37:1818.\nDrazkowski JF, Fisher RS, Sirven JI, et al.: Seizure-related motor vehicle crashes in Arizona before and after reducing the driving restriction from 12 to 3 months. Mayo Clin Proc 2003, 78:819–825.\nSheth SG, Krauss G, Krumholz A, Li G: Mortality in epilepsy: driving fatalities vs other causes of death in patients with epilepsy. Neurology 2004, 63:1002–1007.\nKrauss G, Krumholtz A, Carter RC, et al.: Risk factors for seizure-related motor vehicle crashes in patients with epilepsy. Neurology 1999, 52:1324–1329.\nSalinsky M, Wegner K, Sinnema F: Epilepsy, driving laws and patient disclosure to physicians. Epilepsia 1992, 33:469–472.\nEpilepsy Foundation: http:\u002F\u002Fwww.epilepsyfoundation.org. Accessed March 27, 2007\nVilla J: Burned police officer takes stand in cabby’s trial. The Arizona Republic. February 22, 2002; Sect.A:1.\nSpano J: A driver’s swath of death. Los Angeles Times. September 13, 2006; Sect.A:1.\nDrazkowski JF: Management of the social consequences of seizures. Mayo Clin Proc 2003, 78:641–649.\nSirven JI, Fife TD, Wingerchuk DM, Drazkowski JF: Second-generation antiepileptic drugs’ impact on balance: a meta analysis. Mayo Clin Proc 2007, 82:40–47.\nNational Transportation Safety Board: http:\u002F\u002Fwww.ntsb.gov\u002FEvents\u002F2004\u002FSR_A-95-51\u002FSR_A-95-51_board_meeting. ppt. Accessed March 27, 2007.\nFederal Aviation Administration: Licenses and certificates. http:\u002F\u002Fwww.faa.gov\u002Flicenses_certificates. Accessed March 27, 2007.",{"VOID":1008},"10.1007\u002Fs11910-007-0050-2","PUBLICATION","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11910-007-0050-2",[1012],{"id":1013,"sortIndex":32,"researcher":28,"roles":1014,"affiliations":1016,"properties":1025,"displayName":1027,"givenName":28,"familyName":28},"ffa4745e-7880-459c-9dc6-a8b1aa2acd32",[1015],"AUTHOR",[1017],{"id":1018,"sortIndex":32,"affiliation":1019,"properties":28},"bce406f2-4074-4d0f-ae92-86374fb2aa44",{"id":1018,"createTime":28,"updateTime":28,"relativeEntities":1020,"slug":28,"properties":1021,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1024,"statistic":28},[],{"title":1022},{"VI":1023},"Department of Neurology Comprehensive Epilepsy Program, Mayo Clinic, Scottsdale, USA",[],{"title":1026},{"VI":1027},"Joseph F. 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provides important information about the identity of the objects we encounter. After early processing stages in the retinal cones, thalamus, and occipital cortex, retinal signals reach the ventral temporal cortex for high-level color and object processing, which links color perception with top-down expectations and knowledge. In the language-dominant hemisphere, some of these regions communicate with the language systems; by assigning verbal labels to percepts, these circuits speed up stimulus categorization, and permit fast and accurate inter-individual communication. This paper provides a review of color processing deficits, from dysfunction of wavelength discrimination in the retinal photoreceptors to deficits of high-level processing in the ventral temporal cortex. Neuroimaging evidence defined the existence and localization of color-preferring domains in the ventral occipito-temporal cortex. Evidence from the performance of a brain-damaged patient with color anomia but preserved color categorization demonstrated the independence of color categorization from color naming in the adult brain. Evidence from patients with brain damage suggests that high-level color processing may be divided into at least three functional domains: perceptual color experience, color naming, and color knowledge.",{"EN":1162},"Color Vision Deficits",{"VOID":1164},"Conway BR. Color vision, cones, and color-coding in the cortex. Neuroscientist. 2009;15(3):274–90.\nSiuda-Krzywicka K, Boros M, Bartolomeo P, Witzel C. The biological bases of colour categorisation: from goldfish to the human brain. Cortex. 2019;118:82–106. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.cortex.2019.04.010.\nNothdurft HC. The role of features in preattentive vision: comparison of orientation, motion and color cues. Vision Res. 1993;33(14):1937–58. https:\u002F\u002Fdoi.org\u002F10.1016\u002F0042-6989(93)90020-w.\nMishkin M, Ungerleider LG, Macko KA. Object vision and spatial vision: two cortical pathways. Trends Neurosci. 1983;6:414–7.\nCatani M, Howard RJ, Pajevic S, Jones DK. Virtual in vivo interactive dissection of white matter fasciculi in the human brain. Neuroimage. 2002;17(1):77–94.\nMilner AD, Goodale MA. The visual brain in action. Oxford: Oxford University Press; 1995.\nGrill-Spector K, Weiner KS. The functional architecture of the ventral temporal cortex and its role in categorization. Nat Rev Neurosci. 2014;15:536. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fnrn3747.\nBartolomeo P. Visual objects and their colors. In: Miceli G, Bartolomeo P, Navarro V, editors. Handbook of clinical neurology: the temporal lobe. Elsevier; in press.\nBartolomeo P, Vuilleumier P, Behrmann M. The whole is greater than the sum of the parts: distributed circuits in visual cognition. Cortex. 2015;72:1–4. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.cortex.2015.09.001.\nMahon BZ, Caramazza A. What drives the organization of object knowledge in the brain? Trends Cogn Sci. 2011;15(3):97–103. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.tics.2011.01.004.\nBartolomeo P. The quest for the ‘critical lesion site’ in cognitive deficits: problems and perspectives. Cortex. 2011;47(8):1010–2. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.cortex.2010.11.007.\n•• Lafer-Sousa R, Conway BR, Kanwisher NG. Color-biased regions of the ventral visual pathway lie between face- and place-selective regions in humans, as in macaques. J Neurosci. 2016;36(5):1682–97. https:\u002F\u002Fdoi.org\u002F10.1523\u002FJNEUROSCI.3164-15.2016. Functional MRI evidence for the color-preferring regions in the ventral occipito-temporal cortex.\nSiuda-Krzywicka K, Bartolomeo P. What cognitive neurology teaches us about our experience of color. Neuroscientist. 2020;26(3):252–65. https:\u002F\u002Fdoi.org\u002F10.1177\u002F1073858419882621.\nWade AR, Brewer AA, Rieger JW, Wandell BA. Functional measurements of human ventral occipital cortex: retinotopy and colour. Philos Trans R Soc Lond B Biol Sci. 2002;357(1424):963–73. https:\u002F\u002Fdoi.org\u002F10.1098\u002Frstb.2002.1108.\nBrewer AA, Liu J, Wade AR, Wandell BA. Visual field maps and stimulus selectivity in human ventral occipital cortex. Nat Neurosci. 2005;8(8):1102–9. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fnn1507.\n• Conway BR. The organization and operation of inferior temporal cortex. Annu Rev Vis Sci. 2018;4:381–402. https:\u002F\u002Fdoi.org\u002F10.1146\u002Fannurev-vision-091517-034202. A model of caudo-rostral organization of ventral temporal cortex, ranging from more perceptual to more cognitive stages of processing.\nSiuda-Krzywicka K, Witzel C, Bartolomeo P, Cohen L. Color naming and categorization depend on distinct functional brain networks. Cereb Cortex. 2020;31(2):1106–15. https:\u002F\u002Fdoi.org\u002F10.1093\u002Fcercor\u002Fbhaa278.\nWitzel C, Gegenfurtner KR. Color perception: objects, constancy, and categories. Annual Review of Vision Science. 2018;4(1):475–99. https:\u002F\u002Fdoi.org\u002F10.1146\u002Fannurev-vision-091517-034231.\nShort RA, Graff-Radford NR. Localization of hemiachromatopsia. Neurocase. 2001;7(4):331–7. https:\u002F\u002Fdoi.org\u002F10.1093\u002Fneucas\u002F7.4.331.\nBouvier SE, Engel SA. Behavioral deficits and cortical damage loci in cerebral achromatopsia. Cereb Cortex. 2006;16(2):183–91.\nBartolomeo P, Bachoud-Levi AC, Thiebaut de Schotten M. The anatomy of cerebral achromatopsia: a reappraisal and comparison of two case reports. Cortex. 2014;56:138–44. doi: https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.cortex.2013.01.013.\nBartolomeo P, Bachoud-Lévi AC, Denes G. Preserved imagery for colours in a patient with cerebral achromatopsia. 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The authors concluded that color names may be important for the last, relatively abstract task; instead, colored objects may be processed in a holistic way, perhaps by right hemisphere circuits in this patient.\n•• Siuda-Krzywicka K, Witzel C, Chabani E, Taga M, Coste C, Cools N, et al. Color categorization independent of color naming. Cell Reports. 2019;28(10):2471–9 e5. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.celrep.2019.08.003. The demonstration that colors can be grouped into categories without relying on their names.\nDavidoff J. Language and perceptual categorisation. Trends Cogn Sci. 2001;5(9):382–7.\nMiceli G, Fouch E, Capasso R, Shelton JR, Tomaiuolo F, Caramazza A. The dissociation of color from form and function knowledge. Nat Neurosci. 2001;4(6):662–7.\nStasenko A, Garcea FE, Dombovy M, Mahon BZ. When concepts lose their color: a case of object-color knowledge impairment. Cortex. 2014;58:217–38. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.cortex.2014.05.013.\nBeauvois MF, Saillant B. Optic aphasia for colours and colour agnosia: a distinction between visual and visuo-verbal impairments in the processing of colours. Cogn Neuropsychol. 1985;2(1):1–48.\nDe Renzi E, Saetti MC. Associative agnosia and optic aphasia: qualitative or quantitative difference? Cortex. 1997;33(1):115–30. https:\u002F\u002Fdoi.org\u002F10.1016\u002FS0010-9452(97)80008-1.\nLuzzatti C, Davidoff J. Impaired retrieval of object-colour knowledge with preserved colour naming. Neuropsychologia. 1994;32(8):933–50.",{"VOID":1166},"10.1007\u002Fs11910-021-01137-8","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11910-021-01137-8",[1169],{"id":1170,"sortIndex":32,"researcher":28,"roles":1171,"affiliations":1172,"properties":1181,"displayName":1183,"givenName":28,"familyName":28},"c30e4b5a-b0e7-433a-b780-228434b5da3c",[1015],[1173],{"id":1174,"sortIndex":32,"affiliation":1175,"properties":28},"d2f652dd-6c2a-4c50-be69-582d319083c8",{"id":1174,"createTime":28,"updateTime":28,"relativeEntities":1176,"slug":28,"properties":1177,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1180,"statistic":28},[],{"title":1178},{"VI":1179},"Sorbonne Université, Institut du Cerveau \u002F Paris Brain Institute - ICM, Inserm, CNRS, AP-HP, Hôpital de la Pitié-Salpêtrière, Paris, France",[],{"title":1182},{"VI":1183},"Paolo Bartolomeo",{"url":1167,"publisher":1185,"properties":1231},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1186,"slug":872,"properties":1187,"entityType":25,"verifyStatus":882,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1191,"manageAffiliations":1200,"indexDatabases":1211,"url":28,"thumbnailPath":28,"statistic":1226,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1188,"title":1189,"eissn":1190},{"VOID":877},{"EN":879},{"VOID":875},[1192,1196],{"id":885,"createTime":28,"updateTime":28,"relativeEntities":1193,"label":1194,"description":1195,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":888},{},{"id":891,"createTime":28,"updateTime":28,"relativeEntities":1197,"label":1198,"description":1199,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":894},{},[1201,1206],{"id":898,"createTime":28,"updateTime":28,"relativeEntities":1202,"slug":28,"properties":1203,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1205,"statistic":28},[],{"title":1204},{"EN":902},[],{"id":905,"createTime":28,"updateTime":28,"relativeEntities":1207,"slug":28,"properties":1208,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1210,"statistic":28},[],{"title":1209},{"EN":909},[],[1212,1219],{"id":913,"indexDatabase":1213,"url":925,"indexYears":28,"academicFieldIds":1218,"indexDatabaseRanking":28},{"id":915,"createTime":28,"updateTime":28,"relativeEntities":1214,"label":1215,"description":1216,"key":922,"publicationTags":1217,"standard":28},[],{"EN":918,"VI":918},{"EN":920,"VI":921},[924,813],[927,928],{"id":930,"indexDatabase":1220,"url":936,"indexYears":937,"academicFieldIds":1225,"indexDatabaseRanking":941},{"id":786,"createTime":28,"updateTime":28,"relativeEntities":1221,"label":1222,"description":1223,"key":792,"publicationTags":1224,"standard":28},[],{"EN":789,"VI":789},{"EN":789,"VI":791},[794],[939,940],{"impactFactor":32,"impactFactorByYear":1227,"i10Index":954,"i10IndexLast5Year":136,"totalPublication":955,"totalPublicationByYear":1228,"totalCitation":957,"totalCitationByYear":1229,"totalCitationPerPublication":973,"totalCitationPerPublicationByYear":1230,"hindexLast5Year":689,"hindex":689},{"2012":944,"2013":339,"2014":174,"2015":945,"2016":946,"2017":947,"2018":948,"2019":949,"2020":950,"2021":951,"2022":952,"2023":953},{"2001":157,"2002":328,"2003":688,"2004":151,"2005":281,"2006":50,"2007":152,"2008":161,"2009":139,"2010":50,"2011":328,"2012":160,"2013":560,"2014":161,"2015":281,"2016":611,"2017":161,"2018":600,"2019":611,"2020":152,"2021":279,"2022":280,"2023":50,"2024":45},{"2001":959,"2002":607,"2003":607,"2004":960,"2005":961,"2006":962,"2007":520,"2008":963,"2009":359,"2010":617,"2011":964,"2012":965,"2013":966,"2014":967,"2015":968,"2016":969,"2017":970,"2018":526,"2019":834,"2020":971,"2021":972,"2022":151,"2023":199,"2024":40},{"2001":975,"2002":976,"2003":633,"2004":977,"2005":978,"2006":979,"2007":980,"2008":632,"2009":981,"2010":982,"2011":983,"2012":583,"2013":984,"2014":985,"2015":973,"2016":986,"2017":987,"2018":988,"2019":989,"2020":990,"2021":991,"2022":589,"2023":316,"2024":168},{"pages":1232,"volume":1234},{"VOID":1233},"1-7",{"VOID":1235},"21","2021-10-04",2021,[941,924],{"id":1240,"createTime":1241,"updateTime":1241,"relativeEntities":1242,"slug":28,"properties":1243,"entityType":1009,"verifyStatus":882,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1252,"fullTextUrl":28,"authors":1253,"publicationType":1028,"publisherRelationship":1282,"citationCount":28,"citationInfo":28,"publishDate":1334,"publishYear":1335,"citationAnalyzeStatus":882,"lastCitationAnalyze":28,"indexDatabases":1336,"openAccess":28,"references":28,"isForceReanalyzing":1084},"01152ad0-9250-4ad3-b792-f137fc84204a","2024-02-22T05:06:56.753+00:00",[],{"abstract":1244,"title":1246,"references":1248,"doi":1250},{"EN":1245},"Given the potential for exogenous hormones to influence risk and course of MS, this narrative review aims to summarize current knowledge from observational and interventional studies of exogenous hormones in humans with MS. Large randomized clinical trials for combined oral contraceptives and estriol both show modest effect on inflammatory activity, with the latter showing potential neuroprotective effect. After fertility treatment, large actively treated cohorts have not confirmed any elevated risk of relapse. Preclinical data suggest that androgens, selective estrogen receptor modulators (SERMs), and selective androgen receptor modulators (SARMs) may be neuroprotective but clinical data are lacking. Gender affirming treatment, particularly estrogen in trans-women, could possibly be associated with elevated risk of inflammation. For women with MS entering menopause, hormone therapy appears safe during the appropriate menopausal window, but its long-term effects on neuroprotection are unknown. Exogenous hormones, used in varied doses and for diverse indications, have variable effects on MS risk, inflammatory activity, and neuroprotection. Large randomized trials are needed before it is possible to determine the true effect of exogenous hormones in a condition as complex as MS.",{"EN":1247},"Hormonal Therapies in Multiple Sclerosis: a Review of Clinical Data",{"VOID":1249},"Ysrraelit MC, Correale J. Impact of sex hormones on immune function and multiple sclerosis development. Immunology. 2019;156(1):9–22. https:\u002F\u002Fdoi.org\u002F10.1111\u002Fimm.13004.\nColquitt CW, Martin TS. Contraceptive methods. J Pharm Pract. 2017;30(1):130–5. https:\u002F\u002Fdoi.org\u002F10.1177\u002F0897190015585751.\nHuck LC, Truhn D, Wilpert C, Zanderigo E, Raaff V, Dethlefsen E, et al. Background parenchymal enhancement in contrast-enhanced MR imaging suggests systemic effects of intrauterine contraceptive devices. Eur Radiol. 2022;32(11):7430–8. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs00330-022-08809-0.\nDepypere HT, Stanczyk FZ, Croubels S, Blondeel PN, Roche NA, Depypere BP, et al. Breast levonorgestrel concentrations in women using a levonorgestrel-releasing intrauterine system. Contraception. 2019;100(4):299–301. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.contraception.2019.07.002.\nBove R, Rankin K, Chua AS, Saraceno T, Sattarnezhad N, Greeke E, et al. Oral contraceptives and MS disease activity in a contemporary real-world cohort. Mult Scler. 2018;24(2):227–30. https:\u002F\u002Fdoi.org\u002F10.1177\u002F1352458517692420.\n• Otero-Romero S, Carbonell-Mirabent P, Midaglia L, Zuluaga M, Galán I, Cobo-Calvo A, et al. Oral contraceptives do not modify the risk of a second attack and disability accrual in a prospective cohort of women with a clinically isolated syndrome and early multiple sclerosis. Mult Scler. 2022;28(6):950–7. https:\u002F\u002Fdoi.org\u002F10.1177\u002F13524585211053001. 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Mult Scler Relat Disord. 2016;9:56–9. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.msard.2016.06.015.\nZeydan B, Atkinson EJ, Weis DM, Smith CY, Gazzuola Rocca L, Rocca WA, et al. Reproductive history and progressive multiple sclerosis risk in women. Brain Commun. 2020;2(2):fcaa185. https:\u002F\u002Fdoi.org\u002F10.1093\u002Fbraincomms\u002Ffcaa185.\nHarlow SD, Gass M, Hall JE, Lobo R, Maki P, Rebar RW, et al. Executive summary of the Stages of Reproductive Aging Workshop + 10: addressing the unfinished agenda of staging reproductive aging. J Clin Endocrinol Metab. 2012;97(4):1159–68. https:\u002F\u002Fdoi.org\u002F10.1210\u002Fjc.2011-3362.\nThe 2022 hormone therapy position statement of The North American Menopause Society. Menopause (New York, NY). 2022;29(7):767–94. https:\u002F\u002Fdoi.org\u002F10.1097\u002Fgme.0000000000002028.\nMorales-Rodriguez D, Anderson A, Nylander A, Hsu S, Singh J, Rowles W, et al. 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(This study found higher tau deposition in cognitively unimpaired females compared to age-matched cognitively unimpaired males, and more specifically, found that earlier age at menopause and later initiation of hormone therapy increased tau levels.)\nLord C, Buss C, Lupien SJ, Pruessner JC. Hippocampal volumes are larger in postmenopausal women using estrogen therapy compared to past users, never users and men: a possible window of opportunity effect. Neurobiol Aging. 2008;29(1):95–101. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.neurobiolaging.2006.09.001.\nShumaker SA, Legault C, Kuller L, Rapp SR, Thal L, Lane DS, et al. Conjugated equine estrogens and incidence of probable dementia and mild cognitive impairment in postmenopausal women: Women’s Health Initiative Memory Study. JAMA. 2004;291(24):2947–58. https:\u002F\u002Fdoi.org\u002F10.1001\u002Fjama.291.24.2947.\nEspeland MA, Shumaker SA, Leng I, Manson JE, Brown CM, LeBlanc ES, et al. 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Hormone therapy use and physical quality of life in postmenopausal women with multiple sclerosis. Neurology. 2016;87(14):1457–63. https:\u002F\u002Fdoi.org\u002F10.1212\u002FWNL.0000000000003176. (This observational study found that systemic hormone therapy use was associated with better physical quality of life in postmenopausal women with MS.)\nFoster SC, Daniels C, Bourdette DN, Bebo BF Jr. Dysregulation of the hypothalamic-pituitary-gonadal axis in experimental autoimmune encephalomyelitis and multiple sclerosis. J Neuroimmunol. 2003;140(1–2):78–87. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fs0165-5728(03)00177-2.\nTomassini V, Onesti E, Mainero C, Giugni E, Paolillo A, Salvetti M, et al. Sex hormones modulate brain damage in multiple sclerosis: MRI evidence. J Neurol Neurosurg Psychiatry. 2005;76(2):272–5. https:\u002F\u002Fdoi.org\u002F10.1136\u002Fjnnp.2003.033324.\nBove R, Musallam A, Healy BC, Raghavan K, Glanz BI, Bakshi R, et al. Low testosterone is associated with disability in men with multiple sclerosis. Mult Scler. 2014;20(12):1584–92. https:\u002F\u002Fdoi.org\u002F10.1177\u002F1352458514527864.\nWhitacre CC, Reingold SC, O’Looney PA. A gender gap in autoimmunity. Science. 1999;283(5406):1277–8. https:\u002F\u002Fdoi.org\u002F10.1126\u002Fscience.283.5406.1277.\nGold SM, Voskuhl RR. Estrogen and testosterone therapies in multiple sclerosis. Prog Brain Res. 2009;175:239–51. https:\u002F\u002Fdoi.org\u002F10.1016\u002FS0079-6123(09)17516-7.\nGubbels Bupp MR, Jorgensen TN. Androgen-induced Immunosuppression. Front Immunol. 2018;9:794. https:\u002F\u002Fdoi.org\u002F10.3389\u002Ffimmu.2018.00794.\nSicotte NL, Giesser BS, Tandon V, Klutch R, Steiner B, Drain AE, et al. Testosterone treatment in multiple sclerosis: a pilot study. Arch Neurol. 2007;64(5):683–8. https:\u002F\u002Fdoi.org\u002F10.1001\u002Farchneur.64.5.683.\nKurth F, Luders E, Sicotte NL, Gaser C, Giesser BS, Swerdloff RS, et al. Neuroprotective effects of testosterone treatment in men with multiple sclerosis. NeuroImage Clinical. 2014;4:454–60. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.nicl.2014.03.001.\nBhasin S, Brito JP, Cunningham GR, Hayes FJ, Hodis HN, Matsumoto AM, et al. Testosterone therapy in men with hypogonadism: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2018;103(5):1715–44. https:\u002F\u002Fdoi.org\u002F10.1210\u002Fjc.2018-00229.\nAn KC. Selective estrogen receptor modulators. Asian Spine J. 2016;10(4):787–91. https:\u002F\u002Fdoi.org\u002F10.4184\u002Fasj.2016.10.4.787.\nSolomon ZJ, Mirabal JR, Mazur DJ, Kohn TP, Lipshultz LI, Pastuszak AW. Selective androgen receptor modulators: current knowledge and clinical applications. Sex Med Rev. 2019;7(1):84–94. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.sxmr.2018.09.006.\nPerez EA. Safety profiles of tamoxifen and the aromatase inhibitors in adjuvant therapy of hormone-responsive early breast cancer. Ann Oncol. 2007;18(Suppl 8):viii26-35. https:\u002F\u002Fdoi.org\u002F10.1093\u002Fannonc\u002Fmdm263.\n• Rankin KA, Mei F, Kim K, Shen YA, Mayoral SR, Desponts C, et al. Selective estrogen receptor modulators enhance CNS remyelination independent of estrogen receptors. J Neurosci. 2019;39(12):2184–94. https:\u002F\u002Fdoi.org\u002F10.1523\u002Fjneurosci.1530-18.2019. (The authors validated the SERM bazedoxifene as a potent agent of OPC differentiation and remyelination.)\nGonzalez GA, Hofer MP, Syed YA, Amaral AI, Rundle J, Rahman S, et al. Tamoxifen accelerates the repair of demyelinated lesions in the central nervous system. Sci Rep. 2016;6:31599. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fsrep31599.\nKorade Z, Kim HY, Tallman KA, Liu W, Koczok K, Balogh I, et al. the effect of small molecules on sterol homeostasis: measuring 7-dehydrocholesterol in Dhcr7-deficient Neuro2a cells and human fibroblasts. J Med Chem. 2016;59(3):1102–15. https:\u002F\u002Fdoi.org\u002F10.1021\u002Facs.jmedchem.5b01696.\nMoebius FF, Reiter RJ, Bermoser K, Glossmann H, Cho SY, Paik YK. Pharmacological analysis of sterol delta8-delta7 isomerase proteins with [3H]ifenprodil. Mol Pharmacol. 1998;54(3):591–8. https:\u002F\u002Fdoi.org\u002F10.1124\u002Fmol.54.3.591.\nGylling H, Pyrhonen S, Mantyla E, Maenpaa H, Kangas L, Miettinen TA. Tamoxifen and toremifene lower serum cholesterol by inhibition of delta 8-cholesterol conversion to lathosterol in women with breast cancer. J Clin Oncol. 1995;13(12):2900–5. https:\u002F\u002Fdoi.org\u002F10.1200\u002FJCO.1995.13.12.2900.\n• Kara F, Lohse CM, Castillo AM, Tosakulwong N, Lesnick TG, Jack CR Jr, et al. Association of raloxifene and tamoxifen therapy with cognitive performance, odds of mild cognitive impairment, and brain MRI markers of neurodegeneration. Cancer Med. 2023;12(3):2805–17. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fcam4.5175. (In this cross-sectional study, the authors found that use of tamoxifen or raloxifen was not associated with cognition in postmenopausal women.)\nUnderwood EA, Rochon PA, Moineddin R, Lee PE, Wu W, Pritchard KI, et al. Cognitive sequelae of endocrine therapy in women treated for breast cancer: a meta-analysis. Breast Cancer Res Treat. 2018;168(2):299–310. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs10549-017-4627-4.\nLiao KF, Lin CL, Lai SW. Nationwide case-control study examining the association between tamoxifen use and Alzheimer’s disease in aged women with breast cancer in Taiwan. Front Pharmacol. 2017;8:612. https:\u002F\u002Fdoi.org\u002F10.3389\u002Ffphar.2017.00612.\nBranigan GL, Soto M, Neumayer L, Rodgers K, Brinton RD. association between hormone-modulating breast cancer therapies and incidence of neurodegenerative outcomes for women with breast cancer. JAMA Netw Open. 2020;3(3): e201541. https:\u002F\u002Fdoi.org\u002F10.1001\u002Fjamanetworkopen.2020.1541.\nMirkin S, Komm BS. Tissue-selective estrogen complexes for postmenopausal women. Maturitas. 2013;76(3):213–20. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.maturitas.2013.06.003.\nNylander A, Anderson A, Rowles W, Hsu S, Lazar AA, Mayoral SR, et al. Re-WRAP (Remyelination for women at risk of axonal loss and progression): a phase II randomized placebo-controlled delayed-start trial of Bazedoxifene for myelin repair in multiple sclerosis. Contemp Clin Trials. 2023;134: 107333. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.cct.2023.107333.\nAkita K, Harada K, Ichihara J, Takata N, Takahashi Y, Saito K. A novel selective androgen receptor modulator, NEP28, is efficacious in muscle and brain without serious side effects on prostate. Eur J Pharmacol. 2013;720(1–3):107–14. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.ejphar.2013.10.042.\n• Graham EL, Bakkensen JB, Anderson A, Lancki N, Davidson A, Perez Giraldo G, et al. Inflammatory activity after diverse fertility treatments: a multicenter analysis in the modern multiple sclerosis treatment era. Neurology(R) neuroimmunology & neuroinflammation. 2023;10(3). doi: https:\u002F\u002Fdoi.org\u002F10.1212\u002Fnxi.0000000000200106. (In this multicenter observational study of patients with MS undergoing fertility treatments (FT), no elevated relapse risk after FT was observed.)\nBove R, Rankin K, Lin C, Zhao C, Correale J, Hellwig K, et al. Effect of assisted reproductive technology on multiple sclerosis relapses: case series and meta-analysis. Mult Scler. 2020;26(11):1410–9. https:\u002F\u002Fdoi.org\u002F10.1177\u002F1352458519865118.\nMainguy M, Tillaut H, Degremont A, Le Page E, Mainguy C, Duros S, et al. Assessing the risk of relapse requiring corticosteroids after in vitro fertilization in women with multiple sclerosis. Neurology. 2022. https:\u002F\u002Fdoi.org\u002F10.1212\u002Fwnl.0000000000201027.\nRosendale N, Ostendorf T, Evans DA, Weathers A, Sico JJ, Randall J, et al. American Academy of Neurology members’ preparedness to treat sexual and gender minorities. Neurology. 2019;93(4):159–66. https:\u002F\u002Fdoi.org\u002F10.1212\u002Fwnl.0000000000007829.\nRosendale N, Wong JO, Flatt JD, Whitaker E. Sexual and gender minority health in neurology: a scoping review. JAMA Neurol. 2021;78(6):747–54. https:\u002F\u002Fdoi.org\u002F10.1001\u002Fjamaneurol.2020.5536.\nAnderson A, Dierkhising J, Rush G, Carleton M, Rosendale N, Bove R. Experiences of sexual and gender minority people living with multiple sclerosis in Northern California: an exploratory study. Multiple sclerosis and related disorders. 2021;55: 103214. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.msard.2021.103214.\nKhayambashi S, Salter A, Tyry T, Cutter GR, Fox RJ, Marrie RA. Gender identity and sexual orientation affect health care satisfaction, but not utilization, in persons with multiple sclerosis. Multiple sclerosis and related disorders. 2020;37: 101440. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.msard.2019.101440.\nLavorgna L, Moccia M, Russo A, Palladino R, Riccio L, Lanzillo R, et al. Health-care disparities stemming from sexual orientation of Italian patients with multiple sclerosis: a cross-sectional web-based study. Multiple Sclerosis Relat Disorders. 2017;13:28–32. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.msard.2017.02.001.\nSullivan A, Kane A, Valentic G, Rensel M. Recommendations to address the unique clinical and psychological needs of transgender persons living with multiple sclerosis. Int J MS Care. 2022;24(1):35–40. https:\u002F\u002Fdoi.org\u002F10.7224\u002F1537-2073.2021-066.\nPakpoor J, Wotton CJ, Schmierer K, Giovannoni G, Goldacre MJ. Gender identity disorders and multiple sclerosis risk: a national record-linkage study. Mult Scler. 2016;22(13):1759–62. https:\u002F\u002Fdoi.org\u002F10.1177\u002F1352458515627205.\nCampochiaro C, Host LV, Ong VH, Denton CP. Development of systemic sclerosis in transgender females: a case series and review of the literature. Clin Exp Rheumatol. 2018;36 Suppl 113(4):50–2.\nHill BG, Hodge B, Misischia R. Lupus nephritis in a transgender woman on cross-sex hormone therapy: a case for the role of oestrogen in systemic lupus erythematosus. Lupus. 2020;29(13):1807–10. https:\u002F\u002Fdoi.org\u002F10.1177\u002F0961203320946372.\nPontes LT, Camilo DT, De Bortoli MR, Santos RSS, Luchi WM. New-onset lupus nephritis after male-to-female sex reassignment surgery. Lupus. 2018;27(13):2166–9. https:\u002F\u002Fdoi.org\u002F10.1177\u002F0961203318800571.\nSalgado E, Romera-Baurés M, Beltran-Catalan E, Naredo E, Carreira PE, Garcia-Vivar M, et al. Inmune-mediated inflammatory rheumatic diseases in transgender people: a scoping review. Semin Arthritis Rheum. 2022;52: 151920. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.semarthrit.2021.10.004.\nSantos-Ocampo AS. New onset systemic lupus erythematosus in a transgender man: possible role of feminizing sex hormones. J Clin Rheumatol. 2007;13(1):29–30. https:\u002F\u002Fdoi.org\u002F10.1097\u002F01.rhu.0000256169.05087.ad.\nConnelly PJ, Marie Freel E, Perry C, Ewan J, Touyz RM, Currie G, et al. Gender-affirming hormone therapy, vascular health and cardiovascular disease in transgender adults. Hypertension. 2019;74(6):1266–74. https:\u002F\u002Fdoi.org\u002F10.1161\u002Fhypertensionaha.119.13080.\nLaHue SC, Torres D, Rosendale N, Singh V. Stroke characteristics, risk factors, and outcomes in transgender adults: a case series. Neurologist. 2019;24(2):66–70. https:\u002F\u002Fdoi.org\u002F10.1097\u002Fnrl.0000000000000226.\nPatel KT, Adeel S, Rodrigues Miragaya J, Tangpricha V. progestogen use in gender-affirming hormone therapy: a systematic review. Endocr Pract. 2022;28(12):1244–52. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.eprac.2022.08.012.",{"VOID":1251},"10.1007\u002Fs11910-023-01326-7","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11910-023-01326-7",[1254,1269],{"id":1255,"sortIndex":32,"researcher":28,"roles":1256,"affiliations":1257,"properties":1266,"displayName":1268,"givenName":28,"familyName":28},"405f8084-2bb9-4278-85e5-8587126a486f",[1015],[1258],{"id":1259,"sortIndex":32,"affiliation":1260,"properties":28},"0b53aa0a-6680-4aca-b0f8-b6cbfe5262f8",{"id":1259,"createTime":28,"updateTime":28,"relativeEntities":1261,"slug":28,"properties":1262,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1265,"statistic":28},[],{"title":1263},{"VI":1264},"UCSF Weill Institute for Neuroscience, Division of Neuroimmunology and Glial Biology, Department of Neurology, University of California San Francisco, San Francisco, USA",[],{"title":1267},{"VI":1268},"Stephanie Hsu",{"id":1270,"sortIndex":40,"researcher":28,"roles":1271,"affiliations":1272,"properties":1279,"displayName":1281,"givenName":28,"familyName":28},"4ad9de17-e872-409e-9e79-0eb068c8f666",[1015],[1273],{"id":1259,"sortIndex":32,"affiliation":1274,"properties":28},{"id":1259,"createTime":28,"updateTime":28,"relativeEntities":1275,"slug":28,"properties":1276,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1278,"statistic":28},[],{"title":1277},{"VI":1264},[],{"title":1280},{"VI":1281},"Riley 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aim of this review is to summarize the current evidence on the relationship between sleep and cognition and present available data reporting the impact that sleep alterations may have on cognitive functions. Research findings support the idea that sleep is involved in cognitive processes and that altered sleep homeostasis or circadian rhythms may lead to clinical and biochemical changes associated with cognitive impairment. Evidence is particularly solid for the association between specific sleep architecture and circadian alterations and Alzheimer’s disease. Sleep changes, as early manifestations or possible risk factors for neurodegeneration and cognitive decline, may be appropriate targets for interventions aiming to reduce the likelihood of dementia.",{"EN":1347},"Sleep-Related Changes Prior to Cognitive Dysfunction",{"VOID":1349},"Ramar K, Malhotra RK, Carden KA, Martin JL, Abbasi-Feinberg F, Aurora RN, et al. Sleep is essential to health: an American Academy of Sleep Medicine position statement. J Clin Sleep Med. 2021;17(10):2115–9.\nWang C, Holtzman DM. Bidirectional relationship between sleep and Alzheimer’s disease: role of amyloid, tau, and other factors. Neuropsychopharmacol. 2020;45(1):104–20.\nDuncan MJ, Veasey SC, Zee P. Editorial: Roles of sleep disruption and circadian rhythm alterations on neurodegeneration and Alzheimer’s disease. Front Neurosci. 2021;6(15):737895.\nBorbély AA. A two process model of sleep regulation. Hum Neurobiol. 1982;1(3):195–204.\nBorbély A. The two-process model of sleep regulation: beginnings and outlook. J Sleep Res. 2022;3:e13598.\nMusiek ES, Holtzman DM. Mechanisms linking circadian clocks, sleep, and neurodegeneration. Science. 2016;354(6315):1004–8.\nJu YES, Lucey BP, Holtzman DM. Sleep and Alzheimer disease pathology—a bidirectional relationship. Nat Rev Neurol. 2014;10(2):115–9.\nDijk DJ, Czeisler CA. Contribution of the circadian pacemaker and the sleep homeostat to sleep propensity, sleep structure, electroencephalographic slow waves, and sleep spindle activity in humans. J Neurosci. 1995;15(5 Pt 1):3526–38.\nBódizs R. Theories on the functions of sleep. In: Bassetti C, McNicholas W, Paunio T, Peigneux P, editors. Sleep medicine textbook. 2nd ed. Regensburg: European Sleep Research Society (ESRS); 2021. p. 41–55.\nIliff JJ, Wang M, Liao Y, Plogg BA, Peng W, Gundersen GA, et al. A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid β. Sci Transl Med. 2012;4(147):147ra111.\nXie L, Kang H, Xu Q, Chen MJ, Liao Y, Thiyagarajan M, et al. Sleep drives metabolite clearance from the adult brain. Science. 2013;342(6156):373–7.\n•• Mander BA. Local sleep and Alzheimer’s disease pathophysiology. Front Neurosci. 2020;23(14):525970. Excellent review that presents available evidence on the relationship between alterations in the oscillatory functions of sleep and Alzheimer’s disease pathophysiology.\nSteriade M. Grouping of brain rhythms in corticothalamic systems. Neuroscience. 2006;137(4):1087–106.\nFerini-Strambi L, Galbiati A, Marelli S. Sleep microstructure and memory function. Front Neurol. 2013;11(4):159.\nLafortune M, Gagnon JF, Martin N, Latreille V, Dubé J, Bouchard M, et al. Sleep spindles and rapid eye movement sleep as predictors of next morning cognitive performance in healthy middle-aged and older participants. J Sleep Res. 2014;23(2):159–67.\n• Guadagni V, Byles H, Tyndall AV, Parboosingh J, Longman RS, Hogan DB, et al. Association of sleep spindle characteristics with executive functioning in healthy sedentary middle-aged and older adults. J Sleep Res. 2021;30(2):e13037. Cross-sectional study that investigates the association between sleep spindle characteristics and neurocognitive outcomes in healthy adults.\nTononi G, Cirelli C. Sleep and the price of plasticity: from synaptic and cellular homeostasis to memory consolidation and integration. Neuron. 2014;81(1):12–34.\nHu X, Cheng LY, Chiu MH, Paller KA. Promoting memory consolidation during sleep: a meta-analysis of targeted memory reactivation. Psychol Bull. 2020;146(3):218–44.\nSmith C. Sleep states and memory processes in humans: procedural versus declarative memory systems. Sleep Med Rev. 2001;5(6):491–506.\nDiekelmann S, Born J. The memory function of sleep. Nat Rev Neurosci. 2010;11(2):114–26.\nSimor P, van der Wijk G, Nobili L, Peigneux P. The microstructure of REM sleep: Why phasic and tonic? Sleep Med Rev. 2020;52:101305.\nZüst MA, Ruch S, Wiest R, Henke K. Implicit vocabulary learning during sleep is bound to slow-wave peaks. Curr Biol. 2019;29(4):541-553.e7.\nMa N, Dinges DF, Basner M, Rao H. How acute total sleep loss affects the attending brain: a meta-analysis of neuroimaging studies. Sleep. 2015;38(2):233–40.\nKrause AJ, Simon EB, Mander BA, Greer SM, Saletin JM, Goldstein-Piekarski AN, et al. The sleep-deprived human brain. Nat Rev Neurosci. 2017;18(7):404–18.\nSlama H, Chylinski DO, Deliens G, Leproult R, Schmitz R, Peigneux P. Sleep deprivation triggers cognitive control impairments in task-goal switching. Sleep. 2018;41(2):zsx200.\nSmarr BL, Jennings KJ, Driscoll JR, Kriegsfeld LJ. A time to remember: the role of circadian clocks in learning and memory. Behav Neurosci. 2014;128(3):283–303.\nValdez P. Circadian rhythms in attention. Yale J Biol Med. 2019;92(1):81–92.\nJilg A, Lesny S, Peruzki N, Schwegler H, Selbach O, Dehghani F, et al. Temporal dynamics of mouse hippocampal clock gene expression support memory processing. Hippocampus. 2010;20(3):377–88.\nKillgore WDS, Kent HC, Knight SA, Alkozei A. Changes in morning salivary melatonin correlate with prefrontal responses during working memory performance. NeuroReport. 2018;29(6):488–94.\nLucey BP. It’s complicated: the relationship between sleep and Alzheimer’s disease in humans. Neurobiol Dis. 2020;144:105031.\nOhayon MM, Carskadon MA, Guilleminault C, Vitiello MV. Meta-analysis of quantitative sleep parameters from childhood to old age in healthy individuals: developing normative sleep values across the human lifespan. Sleep. 2004;27(7):1255–73.\nMander BA, Winer JR, Walker MP. Sleep and human aging. Neuron. 2017;94(1):19–36.\nAlfini AJ, Tzuang M, Owusu JT, Spira AP. Later-life sleep, cognition, and neuroimaging research: an update for 2020. Curr Opin Behav Sci. 2020;33:72–7.\nMa Y, Liang L, Zheng F, Shi L, Zhong B, Xie W. Association between sleep duration and cognitive decline. JAMA Netw Open. 2020;3(9):e2013573.\nJohar H, Kawan R, Thwing RE, Karl-Heinz L. Impaired sleep predicts cognitive decline in old people: findings from the prospective KORA age study. Sleep. 2016;39(1):217–26.\n• Xu W, Tan CC, Zou JJ, Cao XP, Tan L. Sleep problems and risk of all-cause cognitive decline or dementia: an updated systematic review and meta-analysis. J Neurol Neurosurg Psychiatry. 2020;91(3):236–44. This comprehensive systematic review and meta-analysis includes longitudinal studies and assesses the associations between sleep disturbances and cognitive disorders.\nCox SR, Ritchie SJ, Allerhand M, Hagenaars SP, Radakovic R, Breen DP, et al. Sleep and cognitive aging in the eighth decade of life. Sleep. 2019;42(4):zsz019.\nJaussent I, Bouyer J, Ancelin ML, Berr C, Foubert-Samier A, Ritchie K, et al. Excessive sleepiness is predictive of cognitive decline in the elderly. Sleep. 2012;35(9):1201–7.\nKeage HAD, Banks S, Yang KL, Morgan K, Brayne C, Matthews FE. What sleep characteristics predict cognitive decline in the elderly? Sleep Med. 2012;13(7):886–92.\nKitamura K, Watanabe Y, Nakamura K, Takano C, Hayashi N, Sato H, et al. Short daytime napping reduces the risk of cognitive decline in community-dwelling older adults: a 5-year longitudinal study. BMC Geriatr. 2021;21(1):474.\n•• Eide PK, Vinje V, Pripp AH, Mardal KA, Ringstad G. Sleep deprivation impairs molecular clearance from the human brain. Brain. 2021;144(3):863–74. Extremely relevant study that demonstrates in vivo the consequences of sleep deprivation on the glymphatic system of the human brain.\nMcSorley VE, Bin YS, Lauderdale DS. Associations of sleep characteristics with cognitive function and decline among older adults. Am J Epidemiol. 2019;188(6):1066–75.\nTaillard J, Sagaspe P, Berthomier C, Brandewinder M, Amieva H, Dartigues JF, et al. Non-REM sleep characteristics predict early cognitive impairment in an aging population. Front Neurol. 2019;13(10):197.\nMander BA, Rao V, Lu B, Saletin JM, Lindquist JR, Ancoli-Israel S, et al. Prefrontal atrophy, disrupted NREM slow waves and impaired hippocampal-dependent memory in aging. Nat Neurosci. 2013;16(3):357–64.\nJu YES, McLeland JS, Toedebusch CD, Xiong C, Fagan AM, Duntley SP, et al. Sleep quality and preclinical Alzheimer disease. JAMA Neurol. 2013;70(5):587.\nVarga AW, Wohlleber ME, Giménez S, Romero S, Alonso JF, Ducca EL, et al. Reduced slow-wave sleep is associated with high cerebrospinal fluid Aβ42 levels in cognitively normal elderly. Sleep. 2016;39(11):2041–8.\nJu YES, Ooms SJ, Sutphen C, Macauley SL, Zangrilli MA, Jerome G, et al. Slow wave sleep disruption increases cerebrospinal fluid amyloid-β levels. Brain. 2017;140(8):2104–11.\nMander BA, Marks SM, Vogel JW, Rao V, Lu B, Saletin JM, et al. β-amyloid disrupts human NREM slow waves and related hippocampus-dependent memory consolidation. Nat Neurosci. 2015;18(7):1051–7.\nHelfrich RF, Mander BA, Jagust WJ, Knight RT, Walker MP. Old brains come uncoupled in sleep: slow wave-spindle synchrony, brain atrophy, and forgetting. Neuron. 2018;97(1):221-230.e4.\nPase MP, Himali JJ, Grima NA, Beiser AS, Satizabal CL, Aparicio HJ, et al. Sleep architecture and the risk of incident dementia in the community. Neurology. 2017;89(12):1244–50.\nSchreiner SJ, Imbach LL, Valko PO, Maric A, Maqkaj R, Werth E, et al. Reduced regional NREM sleep slow-wave activity is associated with cognitive impairment in Parkinson disease. Front Neurol. 2021;19(12):618101.\nLatreille V, Carrier J, Lafortune M, Postuma RB, Bertrand JA, Panisset M, et al. Sleep spindles in Parkinson’s disease may predict the development of dementia. Neurobiol Aging. 2015;36(2):1083–90.\nFernández-Arcos A, Morenas-Rodríguez E, Santamaria J, Sánchez-Valle R, Lladó A, Gaig C, et al. Clinical and video-polysomnographic analysis of rapid eye movement sleep behavior disorder and other sleep disturbances in dementia with Lewy bodies. Sleep. 2019;42(7):zsz086.\nStylianou M, Zaaimi B, Thomas A, Taylor JP, LeBeau FEN. Early disruption of cortical sleep-related oscillations in a mouse model of dementia with Lewy bodies (DLB) expressing human mutant (A30P) alpha-synuclein. Front Neurosci. 2020;17(14):579867.\nMassicotte-Marquez J, Carrier J, Décary A, Mathieu A, Vendette M, Petit D, et al. Slow-wave sleep and delta power in rapid eye movement sleep behavior disorder: quantitative NREM EEG in RBD. Ann Neurol. 2005;57(2):277–82.\nChristensen JAE, Kempfner J, Zoetmulder M, Leonthin HL, Arvastson L, Christensen SR, et al. Decreased sleep spindle density in patients with idiopathic REM sleep behavior disorder and patients with Parkinson’s disease. Clin Neurophysiol. 2014;125(3):512–9.\nO’Reilly C, Godin I, Montplaisir J, Nielsen T. REM sleep behaviour disorder is associated with lower fast and higher slow sleep spindle densities. J Sleep Res. 2015;24(6):593–601.\nSunwoo JS, Cha KS, Byun JI, Jun JS, Kim TJ, Shin JW, et al. Nonrapid eye movement sleep electroencephalographic oscillations in idiopathic rapid eye movement sleep behavior disorder: a study of sleep spindles and slow oscillations. Sleep. 2021;44(2):zsaa160.\nIranzo A, Isetta V, Molinuevo JL, Serradell M, Navajas D, Farre R, et al. Electroencephalographic slowing heralds mild cognitive impairment in idiopathic REM sleep behavior disorder. Sleep Med. 2010;11(6):534–9.\nGong SY, Shen Y, Gu HY, Zhuang S, Fu X, Wang QJ, et al. Generalized EEG slowing across phasic REM sleep, not subjective RBD severity, predicts neurodegeneration in idiopathic RBD. NSS. 2022;14:407–18.\nValomon A, Riedner BA, Jones SG, Nakamura KP, Tononi G, Plante DT, et al. A high-density electroencephalography study reveals abnormal sleep homeostasis in patients with rapid eye movement sleep behavior disorder. Sci Rep. 2021;11(1):4758.\nBubu OM, Pirraglia E, Andrade AG, Sharma RA, Gimenez-Badia S, Umasabor-Bubu OQ, et al. Obstructive sleep apnea and longitudinal Alzheimer’s disease biomarker changes. Sleep. 2019;42(6):zsz048.\nLiguori C, Mercuri NB, Izzi F, Romigi A, Cordella A, Sancesario G, Placidi F. Obstructive sleep apnea is associated with early but possibly modifiable alzheimer’s disease biomarkers changes. Sleep. 2017;40(5).\nUlland TK, Ewald AC, Knutson AO, Marino KM, Smith SMC, Watters JJ. Alzheimer’s disease, sleep disordered breathing, and microglia: puzzling out a common link. Cells. 2021;10(11):2907.\nRoy B, Nunez A, Aysola RS, Kang DW, Vacas S, Kumar R. Impaired glymphatic system actions in obstructive sleep apnea adults. Front Neurosci. 2022;6(16):884234.\nLeng Y, Blackwell T, Stone KL, Hoang TD, Redline S, Yaffe K. Periodic limb movements in sleep are associated with greater cognitive decline in older men without dementia. Sleep. 2016;39(10):1807–10.\nWyse CA, Coogan AN. Impact of aging on diurnal expression patterns of CLOCK and BMAL1 in the mouse brain. Brain Res. 2010;14(1337):21–31.\nNakamura TJ, Nakamura W, Yamazaki S, Kudo T, Cutler T, Colwell CS, et al. Age-related decline in circadian output. J Neurosci. 2011;31(28):10201–5.\nPanagiotou M, Michel S, Meijer JH, Deboer T. The aging brain: sleep, the circadian clock and exercise. Biochem Pharmacol. 2021;191:114563.\nWang JL, Lim AS, Chiang WY, Hsieh WH, Lo MT, Schneider JA, et al. Suprachiasmatic neuron numbers and rest-activity circadian rhythms in older humans: SCN and rest-activity rhythms. Ann Neurol. 2015;78(2):317–22.\nKudo T, Loh DH, Truong D, Wu Y, Colwell CS. Circadian dysfunction in a mouse model of Parkinson’s disease. Exp Neurol. 2011;232(1):66–75.\nMaywood ES, Fraenkel E, McAllister CJ, Wood N, Reddy AB, Hastings MH, et al. Disruption of peripheral circadian timekeeping in a mouse model of Huntington’s disease and its restoration by temporally scheduled feeding. J Neurosci. 2010;30(30):10199–204.\nClark GT, Yu Y, Urban CA, Fu G, Wang C, Zhang F, et al. Circadian control of heparan sulfate levels times phagocytosis of amyloid beta aggregates. PLoS Genet. 2022;18(2):e1009994.\nRoh JH, Huang Y, Bero AW, Kasten T, Stewart FR, Bateman RJ, et al. Disruption of the sleep-wake cycle and diurnal fluctuation of β-amyloid in mice with Alzheimer’s disease pathology. Sci Transl Med. 2012;4(150):150ra122.\nGibson EM, Wang C, Tjho S, Khattar N, Kriegsfeld LJ. Experimental “jet lag” inhibits adult neurogenesis and produces long-term cognitive deficits in female hamsters. PLoS One. 2010;5(12):e15267.\nDelorme TC, Srikanta SB, Fisk AS, Cloutier MÈ, Sato M, Pothecary CA, et al. Chronic exposure to dim light at night or irregular lighting conditions impact circadian behavior, motor coordination, and neuronal morphology. Front Neurosci. 2022;16:855154.\nCho K, Ennaceur A, Cole JC, Suh CK. Chronic jet lag produces cognitive deficits. J Neurosci. 2000;20(6):RC66–RC66.\nGan J, Wang XD, Shi Z, Yuan J, Zhang M, Liu S, et al. The impact of rotating night shift work and daytime recharge on cognitive performance among retired nurses. Front Aging Neurosci. 2022;25(13):827772.\n• Musiek ES, Bhimasani M, Zangrilli MA, Morris JC, Holtzman DM, Ju YES. Circadian rest-activity pattern changes in aging and preclinical Alzheimer disease. JAMA Neurol. 2018;75(5):582. Cross-sectional study that demonstrates a relationship between certain circadian alterations and biomarkers of preclinical Alzheimer’s disease.\nTranah GJ, Blackwell T, Stone KL, Ancoli-Israel S, Paudel ML, Ensrud KE, et al. Circadian activity rhythms and risk of incident dementia and mild cognitive impairment in older women. Ann Neurol. 2011;70(5):722–32.\n•• Posner AB, Tranah GJ, Blackwell T, Yaffe K, Ancoli-Israel S, Redline S, et al. Predicting incident dementia and mild cognitive impairment in older women with nonparametric analysis of circadian activity rhythms in the study of osteoporotic fractures. Sleep. 2021;44(10):zsab119. This prospective study, including a large cohort of older female patients, evaluates the risk to develop dementia in those with specific circadian variations assessed with actigraphy.\nLi P, Gao L, Gaba A, Yu L, Cui L, Fan W, et al. Circadian disturbances in Alzheimer’s disease progression: a prospective observational cohort study of community-based older adults. Lancet Health Longev. 2020;1(3):e96-105.\nWaller KL, Mortensen EL, Avlund K, Fagerlund B, Lauritzen M, Gammeltoft S, Jennum P. Melatonin and cortisol profiles in late midlife and their association with age-related changes in cognition. Nat Sci Sleep. 2016;8:47–53.\nSumsuzzman DMD, Choi J, Jin Y, Hong Y. Neurocognitive effects of melatonin treatment in healthy adults and individuals with Alzheimer’s disease and insomnia: a systematic review and meta-analysis of randomized controlled trials. Neurosci Biobehav Rev. 2021;127:459–73.\nWardlaw SM, Phan TX, Saraf A, Chen X, Storm DR. Genetic disruption of the core circadian clock impairs hippocampus-dependent memory. Learn Mem. 2014;21(8):417–23.\nSnider KH, Dziema H, Aten S, Loeser J, Norona FE, Hoyt K, et al. Modulation of learning and memory by the targeted deletion of the circadian clock gene Bmal1 in forebrain circuits. Behav Brain Res. 2016;308:222–35.\nAli AAH, von Gall C. Adult neurogenesis under control of the circadian system. Cells. 2022;11(5):764.\nPallier PN, Maywood ES, Zheng Z, Chesham JE, Inyushkin AN, Dyball R, et al. Pharmacological imposition of sleep slows cognitive decline and reverses dysregulation of circadian gene expression in a transgenic mouse model of Huntington’s disease. J Neurosci. 2007;27(29):7869–78.\n•• Irwin MR, Vitiello MV. Implications of sleep disturbance and inflammation for Alzheimer’s disease dementia. Lancet Neurol. 2019;18(3):296–306. Excellent review that discusses the role of inflammation as a link between sleep disturbances and Alzheimer’s disease pathogenesis.\nBrancaccio M, Wolfes AC, Ness N. Astrocyte circadian timekeeping in brain health and neurodegeneration. Adv Exp Med Biol. 2021;1344:87–110.\nFonken LK, Frank MG, Kitt MM, Barrientos RM, Watkins LR, Maier SF. Microglia inflammatory responses are controlled by an intrinsic circadian clock. Brain Behav Immun. 2015;45:171–9.\nKaneshwaran K, Olah M, Tasaki S, Yu L, Bradshaw EM, Schneider JA, et al. Sleep fragmentation, microglial aging, and cognitive impairment in adults with and without Alzheimer’s dementia. Sci Adv. 2019;5(12):eaax7331.\nMusiek ES, Lim MM, Yang G, Bauer AQ, Qi L, Lee Y, et al. Circadian clock proteins regulate neuronal redox homeostasis and neurodegeneration. J Clin Invest. 2013;123(12):5389–400.\nDoifode T, Giridharan VV, Generoso JS, Bhatti G, Collodel A, Schulz PE, et al. The impact of the microbiota-gut-brain axis on Alzheimer’s disease pathophysiology. Pharmacol Res. 2021;164:105314.\nReynolds AC, Paterson JL, Ferguson SA, Stanley D, Wright KPJ, Dawson D. The shift work and health research agenda: considering changes in gut microbiota as a pathway linking shift work, sleep loss and circadian misalignment, and metabolic disease. Sleep Med Rev. 2017;34:3–9.\nWang Z, Yuan K, Ji YB, Li SX, Shi L, Wang Z, et al. Alterations of the gut microbiota in response to total sleep deprivation and recovery sleep in rats. NSS. 2022;14:121–33.\nZhou J, Wu X, Li Z, Zou Z, Dou S, Li G, et al. Alterations in gut microbiota are correlated with serum metabolites in patients with insomnia disorder. Front Cell Infect Microbiol. 2022;17(12):722662.",{"VOID":1351},"10.1007\u002Fs11910-023-01258-2","2024-12-22T12:16:10.178+00:00","Auto Verify","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11910-023-01258-2",[1356,1371],{"id":1357,"sortIndex":32,"researcher":28,"roles":1358,"affiliations":1359,"properties":1368,"displayName":1370,"givenName":28,"familyName":28},"713f6da0-6d3f-48c3-bc5e-ec83aa292403",[1015],[1360],{"id":1361,"sortIndex":32,"affiliation":1362,"properties":28},"9280a072-32b5-44dd-91db-d5c3d6fae732",{"id":1361,"createTime":28,"updateTime":28,"relativeEntities":1363,"slug":28,"properties":1364,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1367,"statistic":28},[],{"title":1365},{"VI":1366},"Sleep Disorders Centre, Guy’s and St Thomas’ NHS Foundation Trust, London, UK",[],{"title":1369},{"VI":1370},"Laura Pérez-Carbonell",{"id":1372,"sortIndex":40,"researcher":28,"roles":1373,"affiliations":1374,"properties":1383,"displayName":1385,"givenName":28,"familyName":28},"4d9e1ec2-c01a-4209-9582-950f68d6712b",[1015],[1375],{"id":1376,"sortIndex":32,"affiliation":1377,"properties":28},"a1f9a537-2de3-478c-9217-0391852fd9e1",{"id":1376,"createTime":28,"updateTime":28,"relativeEntities":1378,"slug":28,"properties":1379,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1382,"statistic":28},[],{"title":1380},{"VI":1381},"Neurology Service, Hospital Clínic Barcelona, Universitat de Barcelona, IDIBAPS, CIBERNED, Barcelona, Spain",[],{"title":1384},{"VI":1385},"Alex Iranzo",{"url":1354,"publisher":1387,"properties":1433},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1388,"slug":872,"properties":1389,"entityType":25,"verifyStatus":882,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1393,"manageAffiliations":1402,"indexDatabases":1413,"url":28,"thumbnailPath":28,"statistic":1428,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1390,"title":1391,"eissn":1392},{"VOID":877},{"EN":879},{"VOID":875},[1394,1398],{"id":885,"createTime":28,"updateTime":28,"relativeEntities":1395,"label":1396,"description":1397,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":888},{},{"id":891,"createTime":28,"updateTime":28,"relativeEntities":1399,"label":1400,"description":1401,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":894},{},[1403,1408],{"id":898,"createTime":28,"updateTime":28,"relativeEntities":1404,"slug":28,"properties":1405,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1407,"statistic":28},[],{"title":1406},{"EN":902},[],{"id":905,"createTime":28,"updateTime":28,"relativeEntities":1409,"slug":28,"properties":1410,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1412,"statistic":28},[],{"title":1411},{"EN":909},[],[1414,1421],{"id":913,"indexDatabase":1415,"url":925,"indexYears":28,"academicFieldIds":1420,"indexDatabaseRanking":28},{"id":915,"createTime":28,"updateTime":28,"relativeEntities":1416,"label":1417,"description":1418,"key":922,"publicationTags":1419,"standard":28},[],{"EN":918,"VI":918},{"EN":920,"VI":921},[924,813],[927,928],{"id":930,"indexDatabase":1422,"url":936,"indexYears":937,"academicFieldIds":1427,"indexDatabaseRanking":941},{"id":786,"createTime":28,"updateTime":28,"relativeEntities":1423,"label":1424,"description":1425,"key":792,"publicationTags":1426,"standard":28},[],{"EN":789,"VI":789},{"EN":789,"VI":791},[794],[939,940],{"impactFactor":32,"impactFactorByYear":1429,"i10Index":954,"i10IndexLast5Year":136,"totalPublication":955,"totalPublicationByYear":1430,"totalCitation":957,"totalCitationByYear":1431,"totalCitationPerPublication":973,"totalCitationPerPublicationByYear":1432,"hindexLast5Year":689,"hindex":689},{"2012":944,"2013":339,"2014":174,"2015":945,"2016":946,"2017":947,"2018":948,"2019":949,"2020":950,"2021":951,"2022":952,"2023":953},{"2001":157,"2002":328,"2003":688,"2004":151,"2005":281,"2006":50,"2007":152,"2008":161,"2009":139,"2010":50,"2011":328,"2012":160,"2013":560,"2014":161,"2015":281,"2016":611,"2017":161,"2018":600,"2019":611,"2020":152,"2021":279,"2022":280,"2023":50,"2024":45},{"2001":959,"2002":607,"2003":607,"2004":960,"2005":961,"2006":962,"2007":520,"2008":963,"2009":359,"2010":617,"2011":964,"2012":965,"2013":966,"2014":967,"2015":968,"2016":969,"2017":970,"2018":526,"2019":834,"2020":971,"2021":972,"2022":151,"2023":199,"2024":40},{"2001":975,"2002":976,"2003":633,"2004":977,"2005":978,"2006":979,"2007":980,"2008":632,"2009":981,"2010":982,"2011":983,"2012":583,"2013":984,"2014":985,"2015":973,"2016":986,"2017":987,"2018":988,"2019":989,"2020":990,"2021":991,"2022":589,"2023":316,"2024":168},{"pages":1434,"volume":1436},{"VOID":1435},"177-183",{"VOID":1437},"23","2023-03-07",[941,924],{"id":1441,"createTime":1442,"updateTime":1443,"relativeEntities":1444,"slug":1445,"properties":1446,"entityType":1009,"verifyStatus":26,"verifyTime":1455,"verifyNote":1353,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1456,"fullTextUrl":28,"authors":1457,"publicationType":1028,"publisherRelationship":1482,"citationCount":28,"citationInfo":28,"publishDate":1534,"publishYear":1535,"citationAnalyzeStatus":882,"lastCitationAnalyze":28,"indexDatabases":1536,"openAccess":28,"references":28,"isForceReanalyzing":1084},"017133d4-f153-454b-960f-9fe6f65d09ff","2023-12-26T15:33:20.593+00:00","2025-01-05T20:12:24.246+00:00",[],"Cerebral-and-Spinal-Schistosomiasis",{"abstract":1447,"title":1449,"references":1451,"doi":1453},{"EN":1448},"Cerebral schistosomiasis and spinal schistosomiasis are severe underrecognized complications of Schistosoma sp. infection, and can occur at any time during the parasitic infection. Neuroschistosomiasis has been increasingly reported not only in endemic areas but also in Western countries owing to immigration and international travel. Immunogenic interaction between schistosome egg deposition and the delayed hypersensitivity reaction of the host are the main neuropathogenic mechanisms involved. Eggs induce a periovular granulomatous reaction in the tissues. In some cases, schistosome adult worms may aberrantly migrate to the central nervous system via the vertebral venous plexus and place the ova at an ectopic site. Headache and seizures are common in cerebral schistosomiasis, and intracranial hypertension and hydrocephalus may occur in tumour-like and cerebellar schistosomiasis. Spinal schistosomiasis may manifest itself as acute myelitis and\u002For myeloradiculopathy. Recognition of neuroschistosomiasis is important so that early treatment with praziquantel and steroids can be started in an attempt to prevent severe disability.",{"EN":1450},"Cerebral and Spinal Schistosomiasis",{"VOID":1452},"Sun X, Li CP, Zhang JS. Applied medical parasitology. Beijing: People’s Medical Publishing House; 2005. p. 255.\nWorld Health Organization: Schistosomiasis. http:\u002F\u002Fwww.who.int\u002Fmediacentre\u002Ffactsheets\u002Ffs115\u002Fen\u002Findex.html (2012). Accessed Jun 2012.\n•• Gryseels B. Schistosomiasis. Infect Dis Clin North Am. 2012;26:383–97. A comprehensive and updated recent review about systemic schistosomiasis.\nKing CH, Dickman K, Tisch DJ. Reassessment of the cost of chronic helmintic infection: a meta-analysis of disability related outcomes in endemic schistosomiasis. Lancet. 2005;365:1561–9.\nKing CH, Dangerfield-Cha M. The unacknowledged impact of chronic schistosomiasis. Chronic Illn. 2008;4:65–79.\nRoss AG, Bartley PB, Sleigh AC, et al. 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Urology. 2002;59:195–200.",{"VOID":1454},"10.1007\u002Fs11910-012-0305-4","2025-01-05T20:12:24.245+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11910-012-0305-4",[1458],{"id":1459,"sortIndex":32,"researcher":28,"roles":1460,"affiliations":1461,"properties":1479,"displayName":1481,"givenName":28,"familyName":28},"253ee17c-55e1-4a85-b725-5f3c77210ab1",[1015],[1462,1470],{"id":1463,"sortIndex":32,"affiliation":1464,"properties":28},"d058edf3-3dec-4def-9e23-25b5535473fd",{"id":1463,"createTime":28,"updateTime":28,"relativeEntities":1465,"slug":28,"properties":1466,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1469,"statistic":28},[],{"title":1467},{"VI":1468},"Medicine and Health Sciences Faculty, Universitat Internacional de Catalunya (UIC), Barcelona, Spain",[],{"id":1471,"sortIndex":40,"affiliation":1472,"properties":1478},"0290d15d-6558-48a9-8e6e-2bc820a91290",{"id":1471,"createTime":28,"updateTime":28,"relativeEntities":1473,"slug":28,"properties":1474,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1477,"statistic":28},[],{"title":1475},{"EN":1476},"Zaragoza, Spain",[],{},{"title":1480},{"VI":1481},"Francisco Javier Carod Artal",{"url":1456,"publisher":1483,"properties":1529},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1484,"slug":872,"properties":1485,"entityType":25,"verifyStatus":882,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1489,"manageAffiliations":1498,"indexDatabases":1509,"url":28,"thumbnailPath":28,"statistic":1524,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1486,"title":1487,"eissn":1488},{"VOID":877},{"EN":879},{"VOID":875},[1490,1494],{"id":885,"createTime":28,"updateTime":28,"relativeEntities":1491,"label":1492,"description":1493,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":888},{},{"id":891,"createTime":28,"updateTime":28,"relativeEntities":1495,"label":1496,"description":1497,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":894},{},[1499,1504],{"id":898,"createTime":28,"updateTime":28,"relativeEntities":1500,"slug":28,"properties":1501,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1503,"statistic":28},[],{"title":1502},{"EN":902},[],{"id":905,"createTime":28,"updateTime":28,"relativeEntities":1505,"slug":28,"properties":1506,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1508,"statistic":28},[],{"title":1507},{"EN":909},[],[1510,1517],{"id":913,"indexDatabase":1511,"url":925,"indexYears":28,"academicFieldIds":1516,"indexDatabaseRanking":28},{"id":915,"createTime":28,"updateTime":28,"relativeEntities":1512,"label":1513,"description":1514,"key":922,"publicationTags":1515,"standard":28},[],{"EN":918,"VI":918},{"EN":920,"VI":921},[924,813],[927,928],{"id":930,"indexDatabase":1518,"url":936,"indexYears":937,"academicFieldIds":1523,"indexDatabaseRanking":941},{"id":786,"createTime":28,"updateTime":28,"relativeEntities":1519,"label":1520,"description":1521,"key":792,"publicationTags":1522,"standard":28},[],{"EN":789,"VI":789},{"EN":789,"VI":791},[794],[939,940],{"impactFactor":32,"impactFactorByYear":1525,"i10Index":954,"i10IndexLast5Year":136,"totalPublication":955,"totalPublicationByYear":1526,"totalCitation":957,"totalCitationByYear":1527,"totalCitationPerPublication":973,"totalCitationPerPublicationByYear":1528,"hindexLast5Year":689,"hindex":689},{"2012":944,"2013":339,"2014":174,"2015":945,"2016":946,"2017":947,"2018":948,"2019":949,"2020":950,"2021":951,"2022":952,"2023":953},{"2001":157,"2002":328,"2003":688,"2004":151,"2005":281,"2006":50,"2007":152,"2008":161,"2009":139,"2010":50,"2011":328,"2012":160,"2013":560,"2014":161,"2015":281,"2016":611,"2017":161,"2018":600,"2019":611,"2020":152,"2021":279,"2022":280,"2023":50,"2024":45},{"2001":959,"2002":607,"2003":607,"2004":960,"2005":961,"2006":962,"2007":520,"2008":963,"2009":359,"2010":617,"2011":964,"2012":965,"2013":966,"2014":967,"2015":968,"2016":969,"2017":970,"2018":526,"2019":834,"2020":971,"2021":972,"2022":151,"2023":199,"2024":40},{"2001":975,"2002":976,"2003":633,"2004":977,"2005":978,"2006":979,"2007":980,"2008":632,"2009":981,"2010":982,"2011":983,"2012":583,"2013":984,"2014":985,"2015":973,"2016":986,"2017":987,"2018":988,"2019":989,"2020":990,"2021":991,"2022":589,"2023":316,"2024":168},{"pages":1530,"volume":1532},{"VOID":1531},"666-674",{"VOID":1533},"12","2012-08-19",2012,[941,924],{"id":1538,"createTime":1539,"updateTime":1540,"relativeEntities":1541,"slug":1542,"properties":1543,"entityType":1009,"verifyStatus":26,"verifyTime":1540,"verifyNote":1353,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1552,"fullTextUrl":28,"authors":1553,"publicationType":1028,"publisherRelationship":1617,"citationCount":28,"citationInfo":28,"publishDate":1668,"publishYear":1535,"citationAnalyzeStatus":882,"lastCitationAnalyze":28,"indexDatabases":1669,"openAccess":28,"references":28,"isForceReanalyzing":1084},"01be891e-99ba-42ff-90a9-ae64b2f4bf47","2024-01-12T03:45:40.852+00:00","2024-12-27T19:15:45.130+00:00",[],"Redefining-Parkinson-s-Disease-Research-Using-Induced-Pluripotent-Stem-Cells",{"abstract":1544,"title":1546,"references":1548,"doi":1550},{"EN":1545},"Parkinson’s disease (PD) is a movement disorder associated with the degeneration of nigral dopaminergic (DA) neurons. One of the greatest obstacles for PD research is the lack of patient-specific nigral DA neurons for mechanistic studies and drug discovery. The advent of induced pluripotent stem cells (iPSCs) has overcome this seemingly intractable problem and changed PD research in many profound ways. In this review, we discuss recent development in the generation and analyses of patient-specific iPSC-derived midbrain DA neurons. Results from this novel platform of human cellular models of PD have offered a tantalizing glimpse of the promising future of PD research. With the development of the latest genomic modification technologies, dopaminergic neuron differentiation methodologies, and cell transplantation studies, PD research is poised to enter a new phase that utilizes the human model system to identify the unique vulnerabilities of human nigral DA neurons and disease-modifying therapies based on such mechanistic studies.",{"EN":1547},"Redefining Parkinson’s Disease Research Using Induced Pluripotent Stem Cells",{"VOID":1549},"Langston JW. Parkinson’s disease: current and future challenges. Neurotoxicology. 2002;23:443–50.\nSavitt JM, Dawson VL, Dawson TM. Diagnosis and treatment of Parkinson disease: molecules to medicine. J Clin Invest. 2006;116:1744–54.\nDawson TM, Dawson VL. Rare genetic mutations shed light on the pathogenesis of Parkinson disease. J Clin Invest. 2003;111:145–51.\nKlein C, Schlossmacher MG. Parkinson disease, 10 years after its genetic revolution: multiple clues to a complex disorder. 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Science. 2004;304:1158–60.\nBonifati V, Rizzu P, van Baren MJ, et al. Mutations in the DJ-1 gene associated with autosomal recessive early-onset parkinsonism. Science. 2003;299:256–9.\nHardy J. Genetic analysis of pathways to Parkinson disease. Neuron. 2010;68:201–6.\nDawson TM, Ko HS, Dawson VL. Genetic animal models of Parkinson’s disease. Neuron. 2010;66:646–61.\nTakahashi K, Tanabe K, Ohnukl M, et al. Induction of pluripotent stem cells from adult human fibroblasts by defined factors. Cell. 2007;131:861–72. This is the first paper to report the reprogramming of human somatic cells to iPSCs, a landmark breakthrough in biomedical research.\nYu JY, Vodyanik MA, Smuga-Otto K, et al. Induced pluripotent stem cell lines derived from human somatic cells. Science. 2007;318:1917–20. This independent study shows that derivation of iPSCs from human somatic cells is possible using a different set of transcription factors.\nPark IH, Arora N, Huo H, et al. 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Proc Natl Acad Sci U S A. 2010;107:378–83.\n• Seibler P, Graziotto J, Jeong H, et al. Mitochondrial Parkin recruitment is impaired in neurons derived from mutant PINK1 induced pluripotent stem cells. J Neurosci. 2011;31(16):5970–6. This is the first paper on iPSCs from PD patients with PINK1 mutations.\nBarbeau A. Parkinson’s disease: clinical features and etiopathology. In: Viken PJ, Bruyn GW, Klawans HL, editors. Handbook of clinical neurology. Amsterdam: Elsevier Science Publishers; 1986. p. 87–108.\nBraak H, Del Tredici K. Assessing fetal nerve cell grafts in Parkinson’s disease. Nat Med. 2008;14:483–5.\nZhao T, Zhang ZN, Rong Z, et al. Immunogenicity of induced pluripotent stem cells. Nature. 2011;474(7350):212–5.\nMatsuda W, Furuta T, Nakamura KC, et al. Single nigrostriatal dopaminergic neurons form widely spread and highly dense axonal arborizations in the neostriatum. J Neurosci. 2009;29(2):444–53.\nLi JY, Englund E, Holton JL, et al. Lewy bodies in grafted neurons in subjects with Parkinson’s disease suggest host-to-graft disease propagation. Nat Med. 2008;14(5):501–3.\nKordower JH, Chu Y, Hauser RA, et al. Lewy body-like pathology in long-term embryonic nigral transplants in Parkinson’s disease. Nat Med. 2008;14(5):504–6.\nDesplats P, Lee HJ, Bae EJ, et al. Inclusion formation and neuronal cell death through neuron-to-neuron transmission of alpha-synuclein. Proc Natl Acad Sci USA. 2009;106(31):13010–5.\n• Hockemeyer D, Soldner F, Beard C, et al. Efficient targeting of expressed and silent genes in human ESCs and iPSCs using zinc-finger nucleases. Nat Biotechnol. 2009;27:851–7. This is the first study to use ZFN to target GFP to the Pitx3 locus for the genetic labeling of midbrain DA neurons differentiated from iPSCs.\n• Hockemeyer D, Wang H, Kiani S, et al. Genetic engineering of human pluripotent cells using TALE nucleases. Nat Biotechnol. 2011;29:731–4. This is the first study to use TALEN to target GFP to the Pitx3 locus for the genetic labeling of midbrain DA neurons differentiated from iPSCs.\nNichols J, Smith A. Naive and primed pluripotent states. Cell Stem Cell. 2009;4(6):487–92.\nHanna J, Cheng AW, Saha K, et al. Human embryonic stem cells with biological and epigenetic characteristics similar to those of mouse ESCs. Proc Natl Acad Sci U S A. 2010;107(20):9222–7.\nBuecker C, Chen HH, Polo JM, et al. A murine ESC-like state facilitates transgenesis and homologous recombination in human pluripotent stem cells. Cell Stem Cell. 2010;6(6):535–46.",{"VOID":1551},"10.1007\u002Fs11910-012-0288-1","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11910-012-0288-1",[1554,1578,1591,1604],{"id":1555,"sortIndex":32,"researcher":28,"roles":1556,"affiliations":1557,"properties":1575,"displayName":1577,"givenName":28,"familyName":28},"92f106a2-d637-47e6-9df8-04316b0100b1",[1015],[1558,1566],{"id":1559,"sortIndex":32,"affiliation":1560,"properties":28},"53f4defc-55fc-4bae-90b6-1ff0a76fa98f",{"id":1559,"createTime":28,"updateTime":28,"relativeEntities":1561,"slug":28,"properties":1562,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1565,"statistic":28},[],{"title":1563},{"VI":1564},"Department of Physiology and Biophysics, State University of New York at Buffalo, Buffalo, USA",[],{"id":1567,"sortIndex":40,"affiliation":1568,"properties":1574},"0c16d58b-1282-4cfe-838e-0d4f188e618b",{"id":1567,"createTime":28,"updateTime":28,"relativeEntities":1569,"slug":28,"properties":1570,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1573,"statistic":28},[],{"title":1571},{"VI":1572},"Department of Neurology, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China",[],{},{"title":1576},{"VI":1577},"Jiali 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Jiang",{"id":1592,"sortIndex":123,"researcher":28,"roles":1593,"affiliations":1594,"properties":1601,"displayName":1603,"givenName":28,"familyName":28},"5eca0d5e-862a-4828-adc6-f005d5fafa17",[1015],[1595],{"id":1567,"sortIndex":32,"affiliation":1596,"properties":28},{"id":1567,"createTime":28,"updateTime":28,"relativeEntities":1597,"slug":28,"properties":1598,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1600,"statistic":28},[],{"title":1599},{"VI":1572},[],{"title":1602},{"VI":1603},"Baorong Zhang",{"id":1605,"sortIndex":42,"researcher":28,"roles":1606,"affiliations":1607,"properties":1614,"displayName":1616,"givenName":28,"familyName":28},"29abff42-6239-4fcb-b0f3-85ba12802d1b",[1015],[1608],{"id":1559,"sortIndex":32,"affiliation":1609,"properties":28},{"id":1559,"createTime":28,"updateTime":28,"relativeEntities":1610,"slug":28,"properties":1611,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1613,"statistic":28},[],{"title":1612},{"VI":1564},[],{"title":1615},{"VI":1616},"Jian 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of headache dates back thousands of years, and to date, tension-type headache (TTH) remains the most common form of headache. We will review the history and current understanding of the pathophysiology of TTH and discuss the recommended clinical evaluation and management for this syndrome. Despite being the most prevalent headache disorder, TTH pathophysiology remains poorly understood. Patients with TTH tend to have muscles that are harder, more tender to palpation, and may have more frequent trigger points of tenderness than patients without headache. However, cause and effect of these muscular findings are unclear. Studies support both peripheral and central mechanisms contributing to the pain of TTH. Diagnosis is based on clinical presentation, while the focus of evaluation is to rule out possible secondary causes of headache. Treatment options have remained similar over the course of the past decade, with some additional studies supportive of both pharmacological and non-pharmacological options. An approach to TTH has been outlined including historical context, evolution over time, and the best evidence regarding our current understanding of the complex pathophysiology and treatment of this disease.","Mô tả về đau đầu đã tồn tại hàng ngàn năm, và cho đến nay, đau đầu kiểu căng thẳng (TTH) vẫn là loại đau đầu phổ biến nhất. Chúng tôi sẽ xem xét lịch sử và sự hiểu biết hiện tại về sinh lý bệnh của TTH và thảo luận về đánh giá lâm sàng và quản lý được khuyến nghị cho hội chứng này. Mặc dù là rối loạn đau đầu phổ biến nhất, sinh lý bệnh của TTH vẫn chưa được hiểu rõ. Bệnh nhân mắc TTH có xu hướng có cơ bắp cứng hơn, nhạy cảm hơn khi sờ nắn, và có thể có nhiều điểm kích thích nhạy cảm hơn so với bệnh nhân không bị đau đầu. Tuy nhiên, mối quan hệ giữa nguyên nhân và tác động của những phát hiện về cơ bắp này vẫn chưa rõ ràng. Các nghiên cứu hỗ trợ cả các cơ chế ngoại vi và trung ương góp phần vào cơn đau của TTH. Chẩn đoán dựa trên hình thức lâm sàng, trong khi mục tiêu của việc đánh giá là loại trừ các nguyên nhân thứ cấp có thể của đau đầu. Các lựa chọn điều trị vẫn tương tự trong suốt thập kỷ qua, với một số nghiên cứu bổ sung ủng hộ cả các phương pháp điều trị dược lý và phi dược lý. Một cách tiếp cận đối với TTH đã được nêu rõ bao gồm bối cảnh lịch sử, sự phát triển theo thời gian, và bằng chứng tốt nhất liên quan đến sự hiểu biết hiện tại của chúng tôi về sinh lý bệnh phức tạp và điều trị bệnh này.",{"EN":1681,"VI":1682},"Current Understanding of the Pathophysiology and Approach to Tension-Type Headache","Hiểu Biết Hiện Tại Về Đường Sinh Lý Bệnh và Cách Tiếp Cận Đau Đầu Tension-Type",{"VI":1684},"Đau đầu kiểu căng thẳng, sinh lý bệnh, đánh giá lâm sàng, quản lý bệnh, cơ chế đau",{"VOID":1686},"Dalessio, D., Headache mechanisms in handbook of clinical neurology: headaches and cranial neuralgias P.J.a.B. 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Epidemiology of chronic daily headache in the general population. Headache, 1999. 39(3): p. 190–6.\nScher AI, et al. Prevalence of frequent headache in a population sample. Headache. 1998;38(7):497–506.\nPascual J, Colas R, Castillo J. Epidemiology of chronic daily headache. Curr Pain Headache Rep. 2001;5(6):529–36.\nUlrich V, Gervil M, Olesen J. The relative influence of environment and genes in episodic tension-type headache. Neurology. 2004;62(11):2065–9.\nOstergaard S, et al. Comparison of first degree relatives and spouses of people with chronic tension headache. BMJ. 1997;314(7087):1092–3.\nRussell MB, Saltyte-Benth J, Levi N. Are infrequent episodic, frequent episodic and chronic tension-type headache inherited? A population-based study of 11 199 twin pairs. J Headache Pain. 2006;7(3):119–26.\nPark JW, et al. Serotonin transporter polymorphism and harm avoidance personality in chronic tension-type headache. Headache. 2004;44(10):1005–9.\nFernandez-de-Las-Penas C, et al. Catechol-O-Methyltransferase (COMT) rs4680 Val158Met polymorphism is associated with widespread pressure pain sensitivity and depression in women with chronic, but not episodic, tension-type headache. Clin J Pain. 2019;35(4):345–52.\nSong, T.J., et al., Anxiety and depression in tension-type headache: a population-based study. PLoS One, 2016. 11(10): p. e0165316.\nAshina S, et al. Prevalence of neck pain in migraine and tension-type headache: a population study. Cephalalgia. 2015;35(3):211–9.\nAshina S, et al. Increased pain sensitivity in migraine and tension-type headache coexistent with low back pain: a cross-sectional population study. Eur J Pain. 2018;22(5):904–14.\nJensen, R. and J. Olesen, Initiating mechanisms of experimentally induced tension-type headache. Cephalalgia, 1996. 16(3): p. 175–82; discussion 138–9.\nSchoenen J, et al. Cephalic and extracephalic pressure pain thresholds in chronic tension-type headache. Pain. 1991;47(2):145–9.\n•• Buchgreitz L, et al. Increased pain sensitivity is not a risk factor but a consequence of frequent headache: a population-based follow-up study. Pain. 2008;137(3):623–30.. (This was a longitudinal study following TTH patients for 12 years, demonstrating that increased pain sensitivity was a consequence and not merely a risk factor for development of chronic headache.)\nSandrini G, et al. Abnormal modulatory influence of diffuse noxious inhibitory controls in migraine and chronic tension-type headache patients. Cephalalgia. 2006;26(7):782–9.\nWoolf CJ, Doubell TP. The pathophysiology of chronic pain–increased sensitivity to low threshold A beta-fibre inputs. Curr Opin Neurobiol. 1994;4(4):525–34.\nAshina M, et al. Muscle hardness in patients with chronic tension-type headache: relation to actual headache state. Pain. 1999;79(2–3):201–5.\nCouppe C, et al. Myofascial trigger points are very prevalent in patients with chronic tension-type headache: a double-blinded controlled study. Clin J Pain. 2007;23(1):23–7.\nFernandez-de-las-Penas C, et al. Referred pain from myofascial trigger points in head and neck-shoulder muscles reproduces head pain features in children with chronic tension type headache. J Headache Pain. 2011;12(1):35–43.\nFernandez-de-Las-Penas C, Cuadrado ML, Pareja JA. Myofascial trigger points, neck mobility, and forward head posture in episodic tension-type headache. Headache. 2007;47(5):662–72.\nFernandez de las Penas, C., et al., Referred pain from the trochlear region in tension-type headache: a myofascial trigger point from the superior oblique muscle. Headache, 2005. 45(6): p. 731–7.\nFernandez-de-las-Penas C, et al. Trigger points in the suboccipital muscles and forward head posture in tension-type headache. Headache. 2006;46(3):454–60.\nFernandez-de-Las-Penas C, et al. The local and referred pain from myofascial trigger points in the temporalis muscle contributes to pain profile in chronic tension-type headache. Clin J Pain. 2007;23(9):786–92.\nFernandez-de-Las-Penas C, et al. Myofascial trigger points in the suboccipital muscles in episodic tension-type headache. Man Ther. 2006;11(3):225–30.\nFernandez-de-Las-Penas C, et al. Myofascial trigger points and their relationship to headache clinical parameters in chronic tension-type headache. Headache. 2006;46(8):1264–72.\nFernandez-de-Las-Penas C, et al. Referred pain from trapezius muscle trigger points shares similar characteristics with chronic tension type headache. Eur J Pain. 2007;11(4):475–82.\nSohn JH, Choi HC, Jun AY. Differential patterns of muscle modification in women with episodic and chronic tension-type headache revealed using surface electromyographic analysis. J Electromyogr Kinesiol. 2013;23(1):110–7.\nPalacios-Cena M, et al. Trigger points are associated with widespread pressure pain sensitivity in people with tension-type headache. Cephalalgia. 2018;38(2):237–45.\nSchmidt-Hansen PT, et al. Patterns of experimentally induced pain in pericranial muscles. Cephalalgia. 2006;26(5):568–77.\nHubbard, D.R. and G.M. Berkoff, Myofascial trigger points show spontaneous needle EMG activity. Spine (Phila Pa 1976), 1993. 18(13): p. 1803–7.\nDo TP, et al. Myofascial trigger points in migraine and tension-type headache. J Headache Pain. 2018;19(1):84.\nArendt-Nielsen L, et al. Muscle triggers as a possible source of pain in a subgroup of tension-type headache patients? Clin J Pain. 2016;32(8):711–8.\nHarden RN, et al. Botulinum toxin a in the treatment of chronic tension-type headache with cervical myofascial trigger points: a randomized, double-blind, placebo-controlled pilot study. Headache. 2009;49(5):732–43.\nKaradas O, et al. Efficacy of local lidocaine application on anxiety and depression and its curative effect on patients with chronic tension-type headache. Eur Neurol. 2013;70(1–2):95–101.\nMoraska AF, et al. Myofascial trigger point-focused head and neck massage for recurrent tension-type headache: a randomized, placebo-controlled clinical trial. Clin J Pain. 2015;31(2):159–68.\nFernandez-De-Las-Penas C, Arendt-Nielsen L. Improving understanding of trigger points and widespread pressure pain sensitivity in tension-type headache patients: clinical implications. Expert Rev Neurother. 2017;17(9):933–9.\nFernandez-de-Las-Penas C. Myofascial head pain. Curr Pain Headache Rep. 2015;19(7):28.\nLangemark M, Jensen K, Olesen J. Temporal muscle blood flow in chronic tension-type headache. Arch Neurol. 1990;47(6):654–8.\nAshina M, et al. In vivo evidence of altered skeletal muscle blood flow in chronic tension-type headache. Brain. 2002;125(Pt 2):320–6.\n•• Ashina S, et al. Tension-type headache. Nat Rev Dis Primers. 2021;7(1):24.. (This is a recently published comprehensive review of TTH including integration of multiple proposed pathophysiologic mechanisms contributing to chronification of TTH.)\nWang P, et al. Regional homogeneity abnormalities in patients with tension-type headache: a resting-state fMRI study. Neurosci Bull. 2014;30(6):949–55.\nChen B, et al. Cortical plasticity between the pain and pain-free phases in patients with episodic tension-type headache. J Headache Pain. 2016;17(1):105.\nChen WT, et al. Comparison of gray matter volume between migraine and “strict-criteria” tension-type headache. J Headache Pain. 2018;19(1):4.\nSchmidt-Wilcke T, et al. Gray matter decrease in patients with chronic tension type headache. Neurology. 2005;65(9):1483–6.\nRasmussen BK. Migraine and tension-type headache in a general population: precipitating factors, female hormones, sleep pattern and relation to lifestyle. Pain. 1993;53(1):65–72.\nUlrich V, et al. A comparison of tension-type headache in migraineurs and in non-migraineurs: a population-based study. Pain. 1996;67(2–3):501–6.\nSpierings EL, Ranke AH, Honkoop PC. Precipitating and aggravating factors of migraine versus tension-type headache. Headache. 2001;41(6):554–8.\nLeistad RB, et al. Stress-induced pain and muscle activity in patients with migraine and tension-type headache. Cephalalgia. 2006;26(1):64–73.\nRossi P, et al. The contribution of clinical neurophysiology to the comprehension of the tension-type headache mechanisms. Clin Neurophysiol. 2011;122(6):1075–85.\nAshina M, et al. Possible mechanisms of action of nitric oxide synthase inhibitors in chronic tension-type headache. Brain. 1999;122(Pt 9):1629–35.\nAshina M, et al. Possible mechanisms of glyceryl-trinitrate-induced immediate headache in patients with chronic tension-type headache. Cephalalgia. 2000;20(10):919–24.\nAshina M, et al. Nitric oxide-induced headache in patients with chronic tension-type headache. Brain. 2000;123(Pt 9):1830–7.\nAshina M, et al. Effect of inhibition of nitric oxide synthase on chronic tension-type headache: a randomised crossover trial. Lancet. 1999;353(9149):287–9.\nAshina M. Neurobiology of chronic tension-type headache. Cephalalgia. 2004;24(3):161–72.\nBendtsen L, et al. Serotonin metabolism in chronic tension-type headache. Cephalalgia. 1997;17(8):843–8.\nBendtsen L, Mellerup ET. The platelet serotonin transporter in primary headaches. Eur J Neurol. 1998;5(3):277–82.\nBach FW, et al. Effect of sulpiride or paroxetine on cerebrospinal fluid neuropeptide concentrations in patients with chronic tension-type headache. Neuropeptides. 1994;27(2):129–36.\nAshina M, et al. Plasma levels of calcitonin gene-related peptide in chronic tension-type headache. Neurology. 2000;55(9):1335–40.\nAshina M, et al. Plasma levels of substance P, neuropeptide Y and vasoactive intestinal polypeptide in patients with chronic tension-type headache. Pain. 1999;83(3):541–7.\nAshina M, et al. Tender points are not sites of ongoing inflammation -in vivo evidence in patients with chronic tension-type headache. Cephalalgia. 2003;23(2):109–16.\nMork, H., et al., Possible mechanisms of pain perception in patients with episodic tension-type headache. A new experimental model of myofascial pain. Cephalalgia, 2004. 24(6): p. 466–75.\nHeadache Classification Committee of the International Headache Society (IHS) The international classification of headache disorders, 3rd edition. Cephalalgia, 2018. 38(1): p. 1–211.\nTerrin A, et al. A prospective study on osmophobia in migraine versus tension-type headache in a large series of attacks. Cephalalgia. 2020;40(4):337–46.\n• Bendtsen L, et al. EFNS guideline on the treatment of tension-type headache - report of an EFNS task force. Eur J Neurol. 2010;17(11):1318–25.. (These are the most recent evidence-based guidelines for treatment of TTH.)\nRobbins MS. Diagnosis and management of headache: a review. JAMA. 2021;325(18):1874–85.\nLoder E, Rizzoli P. Tension-type headache. BMJ. 2008;336(7635):88–92.\nStephens, G., S. Derry, and R.A. Moore, Paracetamol (acetaminophen) for acute treatment of episodic tension-type headache in adults. Cochrane Database Syst Rev, 2016(6): p. CD011889.\nDerry, S., P.J. Wiffen, and R.A. Moore, Aspirin for acute treatment of episodic tension-type headache in adults. Cochrane Database Syst Rev, 2017. 1: p. CD011888.\nDerry, S., et al., Ibuprofen for acute treatment of episodic tension-type headache in adults. Cochrane Database Syst Rev, 2015(7): p. CD011474.\nPrior, M.J., et al., Efficacy and safety of acetaminophen and naproxen in the treatment of tension-type headache. A randomized, double-blind, placebo-controlled trial. Cephalalgia, 2002. 22(9): p. 740–8.\nVeys, L., S. Derry, and R.A. Moore, Ketoprofen for episodic tension-type headache in adults. Cochrane Database Syst Rev, 2016. 9: p. CD012190.\nKubitzek F, et al. Low-dose diclofenac potassium in the treatment of episodic tension-type headache. Eur J Pain. 2003;7(2):155–62.\nDiener HC, Gold M, Hagen M. Use of a fixed combination of acetylsalicylic acid, acetaminophen and caffeine compared with acetaminophen alone in episodic tension-type headache: meta-analysis of four randomized, double-blind, placebo-controlled, crossover studies. J Headache Pain. 2014;15:76.\nBendtsen L, Jensen R, Olesen J. A non-selective (amitriptyline), but not a selective (citalopram), serotonin reuptake inhibitor is effective in the prophylactic treatment of chronic tension-type headache. J Neurol Neurosurg Psychiatry. 1996;61(3):285–90.\nLexicomp Facts and Comparisons, Amitriptyline. 2021, Wolters Kluwer Health, Inc.\nBanzi, R., et al., Selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) for the prevention of tension-type headache in adults. Cochrane Database Syst Rev, 2015(5): p. CD011681.\nBendtsen L, Jensen R. Mirtazapine is effective in the prophylactic treatment of chronic tension-type headache. Neurology. 2004;62(10):1706–11.\nMartin-Araguz A, Bustamante-Martinez C, de Pedro-Pijoan JM. Treatment of chronic tension type headache with mirtazapine and amitriptyline. Rev Neurol. 2003;37(2):101–5.\nZissis NP, et al. A randomized, double-blind, placebo-controlled study of venlafaxine XR in out-patients with tension-type headache. Cephalalgia. 2007;27(4):315–24.\nYurekli VA, et al. The effect of sodium valproate on chronic daily headache and its subgroups. J Headache Pain. 2008;9(1):37–41.\nLampl C, et al. A prospective, open-label, long-term study of the efficacy and tolerability of topiramate in the prophylaxis of chronic tension-type headache. Cephalalgia. 2006;26(10):1203–8.\nAleksic-Shihabi A, Lojen G, Vukovic V. Prevention of tension type headache with topiramate. Acta Med Croatica. 2008;62(2):145–9.\nFogelholm R, Murros K. Tizanidine in chronic tension-type headache: a placebo controlled double-blind cross-over study. Headache. 1992;32(10):509–13.\nMurros K, et al. Modified-release formulation of tizanidine in chronic tension-type headache. Headache. 2000;40(8):633–7.\nGhadiri-Sani, M. and N. Silver, Headache (chronic tension-type). BMJ Clin Evid, 2016. 2016.\nKaradas O, Gul HL, Inan LE. Lidocaine injection of pericranial myofascial trigger points in the treatment of frequent episodic tension-type headache. J Headache Pain. 2013;14:44.\nHolroyd KA, et al. Management of chronic tension-type headache with tricyclic antidepressant medication, stress management therapy, and their combination: a randomized controlled trial. JAMA. 2001;285(17):2208–15.\nNestoriuc Y, et al. Biofeedback treatment for headache disorders: a comprehensive efficacy review. Appl Psychophysiol Biofeedback. 2008;33(3):125–40.\nGu Q, Hou JC, Fang XM. Mindfulness meditation for primary headache pain: a meta-analysis. Chin Med J (Engl). 2018;131(7):829–38.\nFalsiroli Maistrello, L., M. Rafanelli, and A. Turolla, Manual therapy and quality of life in people with headache: systematic review and meta-analysis of randomized controlled trials. Curr Pain Headache Rep, 2019. 23(10): p. 78.\nLinde, K., et al., Acupuncture for the prevention of tension-type headache. Cochrane Database Syst Rev, 2016. 4: p. CD007587.\nKolokotsios, S., et al., The effectiveness of acupuncture on headache intensity and frequency in patients with tension-type headache: a systematic review and meta-analysis. Cureus, 2021. 13(4): p. e14237.\nGildir, S., et al., A randomized trial of trigger point dry needling versus sham needling for chronic tension-type headache. Medicine (Baltimore), 2019. 98(8): p. e14520.\nLyngberg AC, et al. Prognosis of migraine and tension-type headache: a population-based follow-up study. Neurology. 2005;65(4):580–5.",{"VOID":1688},"10.1007\u002Fs11910-021-01138-7","2025-01-14T13:45:29.900+00:00",[30],"https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11910-021-01138-7",[1693,1711,1726],{"id":1694,"sortIndex":32,"researcher":28,"roles":1695,"affiliations":1696,"properties":1708,"displayName":1710,"givenName":28,"familyName":28},"38f8956b-35a5-4f18-9741-c504f1e29c1a",[1015],[1697],{"id":1698,"sortIndex":32,"affiliation":1699,"properties":1705},"42d01ce3-8a72-40ed-976e-fdd740e73453",{"id":1698,"createTime":28,"updateTime":28,"relativeEntities":1700,"slug":28,"properties":1701,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1704,"statistic":28},[],{"title":1702},{"EN":1703},"Department of Neurology, Mayo Clinic, Rochester, United States",[],{"title":1706},{"VI":1707},"Department of Neurology, Mayo Clinic, Rochester, USA",{"title":1709},{"VI":1710},"Stephanie J. Steel",{"id":1712,"sortIndex":40,"researcher":28,"roles":1713,"affiliations":1714,"properties":1723,"displayName":1725,"givenName":28,"familyName":28},"feb66713-23c6-45ef-b3a7-ed3d42a148f3",[1015],[1715],{"id":1698,"sortIndex":32,"affiliation":1716,"properties":1721},{"id":1698,"createTime":28,"updateTime":28,"relativeEntities":1717,"slug":28,"properties":1718,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1720,"statistic":28},[],{"title":1719},{"EN":1703},[],{"title":1722},{"VI":1707},{"title":1724},{"VI":1725},"Carrie E. 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Symptomatic treatment has been available for decades, but to date there is no treatment retarding disease progression. Over the past decade several genes causing parkinsonism have been identified in families with a mendelian pattern of inheritance. The most recent is the leucine-rich repeat kinase 2 (LRRK2) gene. Pathogenic mutations in the LRRK2 gene cause a significant proportion of clinically typical, late-onset PD. This review summarizes the current knowledge on the contribution of LRRK2 mutations in understanding parkinsonism.",{"EN":1804},"PARK8 LRRK2 parkinsonism",{"VOID":1806},"Ferri CP, Prince M, Brayne C, et al.: Global prevalence of dementia: a Delphi consensus study. Lancet 2005, 366:2112.\nAarsland D, Zaccai J, Brayne C: A systematic review of prevalence studies of dementia in Parkinson’s disease. Mov Disord 2005, 20:1255.\nZaccai J, McCracken C, Brayne C: A systematic review of prevalence and incidence studies of dementia with Lewy bodies. Age Ageing 2005, 34:561.\nde RijkMC, Launer LJ, Berger K, et al.: Prevalence of Parkinson’s disease in Europe: a collaborative study of population-based cohorts. Neurologic Diseases in the Elderly Research Group. Neurology 2000; 54:S21.\nAarsland D, Larsen JP, Lim NG, et al.: Range of neuropsychiatric disturbances in patients with Parkinson’s disease. J Neurol Neurosurg Psychiatry 1999, 67:492.\nChaudhuri KR, Healy DG, Schapira AH: Non-motor symptoms of Parkinson’s disease: diagnosis and management. Lancet Neurol 2006, 5:235. A review of the nonmotor complications in PD.\nBraak H, Del Tredici K, Rub U, et al.: Staging of brain pathology related to sporadic Parkinson’s disease. Neurobiol Aging 2003, 24:197.\nGasser T: Genetics of Parkinson’s disease. Curr Opin Neurol 2005, 18:363. Review of genes involved in parkinsonism.\nLewthwaite AJ, Nicholl DJ: Genetics of parkinsonism. Curr Neurol Neurosci Rep 2005, 5:397. Review of genes involved in parkinsonism.\nFunayama M, Hasegawa K, Kowa H, et al.: A new locus for Parkinson’s disease (PARK8) maps to chromosome 12p11.2-q13.1. Ann Neurol 2002, 51:296. The first article establishing linkage to the PARK8 locus.\nZimprich A, Muller-Myhsok B, Farrer M, et al.: The PARK8 locus in autosomal dominant parkinsonism: confirmation of linkage and further delineation of the disease-containing interval. Am J Hum Genet 2004, 74:11.\nPaisan-Ruiz C, Saenz A, Lopez de Munain A, et al.: Familial Parkinson’s disease: clinical and genetic analysis of four Basque families. Ann Neurol 2005, 57:365.\nZimprich A, Biskup S, Leitner P, et al.: Mutations in LRRK2 Cause Autosomal-Dominant Parkinsonism with Pleomorphic Pathology. Neuron 2004, 44:601. One of the to back-to-back papers describing LRRK2 as the gene causing autosomal dominant PD linked to PARK8.\nPaisan-Ruiz C, Jain S, Evans EW, et al.: Cloning of the gene containing mutations that cause PARK8-linked Parkinson’s disease. Neuron 2004, 44:595. The other back-to-back paper describing LRRK2 as the gene causing autosomal dominant PD linked to PARK8.\nAasly JO, Toft M, Fernandez-Mata I, et al.: Clinical features of LRRK2-associated Parkinson’s disease in central Norway. Ann Neurol 2005, 57:762. One of the early clinical descriptions of Lrrk2 G2019S substitution carriers.\nInfante J, Rodriguez E, Combarros O, et al.: LRRK2 G2019S is a common mutation in Spanish patients with late-onset Parkinson’s disease. Neurosci Lett 2006, 395:224–226.\nLesage S, Durr A, Tazir M, et al.: LRRK2 G2019S as a cause of Parkinson’s disease in North African Arabs. N Engl J Med 2006, 354:422. One of the first reports on very high frequencies of G2019S in North African Arabs.\nDi Fonzo A, Tassorelli C, De Mari M, et al.: Comprehensive analysis of the LRRK2 gene in sixty families with Parkinson’s disease. Eur J Hum Genet 2006, 14:322–331.\nGilks WP, Abou-Sleiman PM, Gandhi S, et al.: A common LRRK2 mutation in idiopathic Parkinson’s disease. Lancet 2005, 365:415.\nKachergus J, Mata IF, Hulihan M, et al.: Identification of a novel LRRK2 mutation linked to autosomal dominant parkinsonism: evidence of a common founder across European populations. Am J Hum Genet 2005, 76:672. One of the first reports identifying the G2019S substitution and describing a common haplotype that indicates a common founder of the G2019S substitution.\nGalpern WR, Lang AE: Interface between tauopathies and synucleinopathies: A tale of two proteins. Ann Neurol 2006, 59:449.\nBosgraaf L, Van HaastertPJ: Roc, a Ras\u002FGTPase domain in complex proteins. Biochim Biophys Acta 2003; 1643:5.\nFunayama M, Hasegawa K, Ohta E, et al.: An LRRK2 mutation as a cause for the parkinsonism in the original PARK8 family. Ann Neurol 2005, 57:918.\nMata IF, Kachergus JM, Taylor JP, et al.: Lrrk2 pathogenic substitutions in Parkinson’s disease. Neurogenetics 2005, 6:171.\nKhan NL, Jain S, Lynch JM, et al.: Mutations in the gene LRRK2 encoding dardarin (PARK8) cause familial Parkinson’s disease: clinical, pathological, olfactory and functional imaging and genetic data. Brain 2005, 128:2786. This report includes PET findings associated with LRRK2 mutations.\nSkipper L, Shen H, Chua E, et al.: Analysis of LRRK2 functional domains in nondominant Parkinson disease. Neurology 2005, 65:1319.\nPaisan-Ruiz C, Lang AE, Kawarai T, et al.: LRRK2 gene in Parkinson disease: mutation analysis and case control association study. Neurology 2005, 65:696.\nZabetian CP, Samii A, Mosley AD, et al.: A clinic-based study of the LRRK2 gene in Parkinson disease yields new mutations. Neurology 2005, 65:741.\nTomiyama H, Li Y, Funayama M, et al.: Clinicogenetic study of mutations ini LRRK2 exon 41 in Parkinson’s disease patients from 18 countries. Mov Disord 2006, [e-pub ahead of print].\nBiskup S, Mueller JC, Sharma M, et al.: Common variants of LRRK2 are not associated with sporadic Parkinson’s disease. Ann Neurol 2005, 58:905. A comprehensive evaluation of common variants within the LRRK2 gene.\nPaisan-Ruiz C, Evans EW, Jain S, et al.: Testing association between LRRK2 and Parkinson’s disease and investigating linkage disequilibrium 10.1136\u002Fjmg.2005.036889. J Med Genet 2006, 43:e09.\nSkipper L, Li Y, Bonnard C, et al.: Comprehensive evaluation of common genetic variation within LRRK2 reveals evidence for association with sporadic Parkinson’s disease. Hum Mol Genet 2005, 14:3549.\nDi Fonzo A, Rohe CF, Ferreira J, et al.: A frequent LRRK2 gene mutation associated with autosomal dominant Parkinson’s disease. Lancet 2005, 365:412.\nFarrer M, Stone J, Mata IF, et al.: LRRK2 mutations in Parkinson disease. Neurology 2005, 65:738.\nNichols WC, Pankratz N, Hernandez D, et al.: Genetic screening for a single common LRRK2 mutation in familial Parkinson’s disease. Lancet 2005, 365:410.\nKay DM, Zabetian CP, Factor SA, et al.: Parkinson’s disease and LRRK2: Frequency of a common mutation in U.S. movement disorder clinics. Mov Disord 2005, 20:1077–1078.\nTan EK, Shen H, Tan LC, et al.: The G2019S LRRK2 mutation is uncommon in an Asian cohort of Parkinson’s disease patients. Neurosci Lett 2005, 384:327.\nLu CS, Simons EJ, Wu-Chou YH, et al.: The LRRK2 I2012T, G2019S, and I2020T mutations are rare in Taiwanese patients with sporadic Parkinson’s disease. Parkinsonism Relat Disord 2005, 11:521.\nOzelius LJ, Senthil G, Saunders-Pullman R, et al.: LRRK2 G2019S as a cause of Parkinson’s disease in Ashkenazi Jews. N Engl J Med 2006; 354:424. Reporting very high frequencies of G2019S in Ashkenazi Jews.\nMata IF, Ross OA, Kachergus J, et al.: LRRK2 mutations are a common cause of Parkinson’s disease in Spain. Eur J Neurol 2006, 13:391–394.\nBras JM, Guerreiro RJ, Ribeiro MH, et al.: G2019S dardarin substitution is a common cause of Parkinson’s disease in a Portuguese cohort. Mov Disord 2005, 20:1653.\nLesage S, Leutenegger AL, Ibanez P, et al.: LRRK2 haplotype analyses in European and North African families with Parkinson disease: a common founder for the G2019S mutation dating from the 13th century. Am J Hum Genet 2005, 77:330.\nMata IF, Taylor JP, Kachergus J, et al.: LRRK2 R1441G in Spanish patients with Parkinson’s disease. Neurosci Lett 2005, 382:309.\nWszolek ZK, Pfeiffer RF, Tsuboi Y, et al.: Autosomal dominant parkinsonism associated with variable synuclein and tau pathology. Neurology 2004, 62:1619.\nWszolek ZK, Vieregge P, Uitti RJ, et al.: German-Canadian family (family A) with parkinsonism, amyotrophy, and dementia: longitudinal observations. Parkinsonism Relat Disord 1997, 3:125.\nRoss OA, Toft M, Whittle AJ, et al.: Lrrk2 and Lewy body disease. Ann Neurol 2006, 59:388. A report on pathologic features in G2019S substitution carriers.\nGiasson BI, Covy JP, Bonini NM, et al.: Biochemical and pathological characterization of Lrrk2. Ann Neurol 2006, 59:315.\nHernandez DG, Paisan-Ruiz C, McInerney-Leo A, et al.: Clinical and positron emission tomography of Parkinson’s disease caused by LRRK2. Ann Neurol 2005, 57:453. Clinical and PET features of LRRK2.\nAdams JR, van Netten H, Schulzer M, et al.: PET in LRRK2 mutations: comparison to sporadic Parkinson’s disease and evidence for presymptomatic compensation. Brain 2005, 128:2777. PET findings in LRRK2 mutation carriers, including evidence of presymptomatic compensation in mutation carriers.\nToft M, Sando SB, Melquist S, et al.: LRRK2 mutations are not common in Alzheimer’s disease. Mech Ageing Dev 2005, 126:1201.\nZabetian CP, Lauricella CJ, Tsuang DW, et al.: Analysis of the LRRK2 G2019S mutation in Alzheimer Disease. Arch Neurol 2006, 63:156.\nRoss OA, Whittle AJ, Cobb SA, et al.: Lrrk2 R1441 substitution and progressive supranuclear palsy. Neuropathol Appl Neurobiol 2006, 32:23.\nKay DM, Kramer P, Higgins D, et al.: Escaping Parkinson’s disease: a neurologically healthy octogenarian with the LRRK2 G2019S mutation. Mov Disord 2005, 20:1077.\nGloeckner CJ, Kinkl N, Schumacher A, et al.: The Parkinson disease causing LRRK2 mutation I2020T is associated with increased kinase activity. Hum Mol Genet 2006; 15:223. One of the initial reports on functional research on LRRK2 mutations.\nWest AB, Moore DJ, Biskup S, et al.: Parkinson’s diseaseassociated mutations in leucine-rich repeat kinase 2 augment kinase activity. Proc Natl Acad Sci U S A 2005, 102:16842. The first report showing that the LRRK2 mutations enhance kinase activity.\nSilva RM, Kuan CY, Rakic P, Burke RE: Mixed lineage kinase-c-jun N-terminal kinase signaling pathway: a new therapeutic target in Parkinson’s disease. Mov Disord 2005, 20:653.\nBialecka M, Hui S, Klodowska-Duda G, et al.: Analysis of LRRK 2 G 2019 S and I 2020 T mutations in Parkinson’s disease. Neurosci Lett 2005, 390:1.\nGosal D, Ross OA, Wiley J, et al.: Clinical traits of LRRK2-associated Parkinson’s disease in Ireland: a link between familial and idiopathic PD. Parkinsonism Relat Disord 2005, 11:349.\nGoldwurm S, Di Fonzo A, Simons EJ, et al.: The G6055A (G2019S) mutation in LRRK2 is frequent in both early and late onset Parkinson’s disease and originates from a common ancestor. J Med Genet 2005, 42:e65.",{"VOID":1808},"10.1007\u002Fs11910-006-0020-0","2024-12-13T04:48:22.918+00:00","Author affiliation is blank","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs11910-006-0020-0",[1813,1820],{"id":1814,"sortIndex":32,"researcher":28,"roles":1815,"affiliations":1816,"properties":1817,"displayName":1819,"givenName":28,"familyName":28},"769ee18e-426a-47ff-ac32-45099c2e1fa4",[1015],[],{"title":1818},{"VI":1819},"Kristoffer Haugarvoll",{"id":1821,"sortIndex":40,"researcher":28,"roles":1822,"affiliations":1823,"properties":1832,"displayName":1834,"givenName":28,"familyName":28},"a816e5d8-36d9-422e-ad29-f97ccdd821da",[1015],[1824],{"id":1825,"sortIndex":32,"affiliation":1826,"properties":28},"f1b889df-577d-4213-b4c9-0271af30116f",{"id":1825,"createTime":28,"updateTime":28,"relativeEntities":1827,"slug":28,"properties":1828,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1831,"statistic":28},[],{"title":1829},{"VI":1830},"Department of Neuroscience and Neurology, Mayo Clinic College of Medicine, Jacksonville, USA",[],{"title":1833},{"VI":1834},"Zbigniew K. Wszolek",{"url":1811,"publisher":1836,"properties":1882},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1837,"slug":872,"properties":1838,"entityType":25,"verifyStatus":882,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1842,"manageAffiliations":1851,"indexDatabases":1862,"url":28,"thumbnailPath":28,"statistic":1877,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1839,"title":1840,"eissn":1841},{"VOID":877},{"EN":879},{"VOID":875},[1843,1847],{"id":885,"createTime":28,"updateTime":28,"relativeEntities":1844,"label":1845,"description":1846,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":888},{},{"id":891,"createTime":28,"updateTime":28,"relativeEntities":1848,"label":1849,"description":1850,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":894},{},[1852,1857],{"id":898,"createTime":28,"updateTime":28,"relativeEntities":1853,"slug":28,"properties":1854,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1856,"statistic":28},[],{"title":1855},{"EN":902},[],{"id":905,"createTime":28,"updateTime":28,"relativeEntities":1858,"slug":28,"properties":1859,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1861,"statistic":28},[],{"title":1860},{"EN":909},[],[1863,1870],{"id":913,"indexDatabase":1864,"url":925,"indexYears":28,"academicFieldIds":1869,"indexDatabaseRanking":28},{"id":915,"createTime":28,"updateTime":28,"relativeEntities":1865,"label":1866,"description":1867,"key":922,"publicationTags":1868,"standard":28},[],{"EN":918,"VI":918},{"EN":920,"VI":921},[924,813],[927,928],{"id":930,"indexDatabase":1871,"url":936,"indexYears":937,"academicFieldIds":1876,"indexDatabaseRanking":941},{"id":786,"createTime":28,"updateTime":28,"relativeEntities":1872,"label":1873,"description":1874,"key":792,"publicationTags":1875,"standard":28},[],{"EN":789,"VI":789},{"EN":789,"VI":791},[794],[939,940],{"impactFactor":32,"impactFactorByYear":1878,"i10Index":954,"i10IndexLast5Year":136,"totalPublication":955,"totalPublicationByYear":1879,"totalCitation":957,"totalCitationByYear":1880,"totalCitationPerPublication":973,"totalCitationPerPublicationByYear":1881,"hindexLast5Year":689,"hindex":689},{"2012":944,"2013":339,"2014":174,"2015":945,"2016":946,"2017":947,"2018":948,"2019":949,"2020":950,"2021":951,"2022":952,"2023":953},{"2001":157,"2002":328,"2003":688,"2004":151,"2005":281,"2006":50,"2007":152,"2008":161,"2009":139,"2010":50,"2011":328,"2012":160,"2013":560,"2014":161,"2015":281,"2016":611,"2017":161,"2018":600,"2019":611,"2020":152,"2021":279,"2022":280,"2023":50,"2024":45},{"2001":959,"2002":607,"2003":607,"2004":960,"2005":961,"2006":962,"2007":520,"2008":963,"2009":359,"2010":617,"2011":964,"2012":965,"2013":966,"2014":967,"2015":968,"2016":969,"2017":970,"2018":526,"2019":834,"2020":971,"2021":972,"2022":151,"2023":199,"2024":40},{"2001":975,"2002":976,"2003":633,"2004":977,"2005":978,"2006":979,"2007":980,"2008":632,"2009":981,"2010":982,"2011":983,"2012":583,"2013":984,"2014":985,"2015":973,"2016":986,"2017":987,"2018":988,"2019":989,"2020":990,"2021":991,"2022":589,"2023":316,"2024":168},{"pages":1883,"volume":1885},{"VOID":1884},"287-294",{"VOID":1886},"6","2006-07-01",2006,[941,924],{"id":1891,"createTime":1892,"updateTime":1893,"relativeEntities":1894,"slug":1895,"properties":1896,"entityType":1009,"verifyStatus":26,"verifyTime":1893,"verifyNote":1353,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1905,"fullTextUrl":28,"authors":1906,"publicationType":1028,"publisherRelationship":1944,"citationCount":28,"citationInfo":28,"publishDate":1996,"publishYear":1997,"citationAnalyzeStatus":882,"lastCitationAnalyze":28,"indexDatabases":1998,"openAccess":28,"references":28,"isForceReanalyzing":1084},"026787fc-0474-4b3c-ae9f-c748b8addd1e","2023-12-09T04:11:41.349+00:00","2025-02-15T23:30:26.368+00:00",[],"Neurostimulation-for-Memory-Enhancement-in-Epilepsy",{"abstract":1897,"title":1899,"references":1901,"doi":1903},{"EN":1898},"Memory is one of the top concerns of epilepsy patients, but there are no known treatments to directly alleviate the memory deficits associated with epilepsy. Neurostimulation may provide new therapeutic tools to enhance memory in epilepsy patients. Here, we critically review recent investigations of memory enhancement using transcranial electrical stimulation (tES), transcranial magnetic stimulation (TMS), vagus nerve stimulation (VNS), chronic intracranial stimulation, and acute intracranial stimulation. Existing literature suggests that transcranial direct current stimulation (tDCS) produces a small enhancement in memory in neuropsychological patients, but transcranial alternating current stimulation (tACS) and transcranial random noise stimulation (tRNS) have not been found to have an effect on memory. Most studies of transcranial magnetic stimulation (TMS) have found that TMS has no positive effect on memory. Vagus nerve stimulation can acutely enhance memory, while chronic therapy does not appear to alter memory performance. We found that there is the most evidence for significant memory enhancement using intracranial stimulation techniques, especially chronic stimulation of the fornix and task-responsive stimulation of the lateral temporal lobe. Presently, there are no existing therapeutic options for directly treating epilepy-related memory deficits. While neurostimulation technologies for memory enhancement are largely still in the experimental phase, neurostimulation appears promising as a future technique for treating epilepsy-related memory deficits.",{"EN":1900},"Neurostimulation for Memory Enhancement in Epilepsy",{"VOID":1902},"McAuley JW, Elliott JO, Patankar S, Hart S, Long L, Moore JL, et al. Comparing patients’ and practitioners’ views on epilepsy concerns: a call to address memory concerns. Epilepsy Behav. 2010;19:580–3.\nBlake RV, Wroe SJ, Breen EK, McCarthy RA. Accelerated forgetting in patients with epilepsyEvidence for an impairment in memory consolidation. Brain. 2000;123:472–83.\nWilkinson H, Holdstock JS, Baker G, Herbert A, Clague F, Downes JJ. Long-term accelerated forgetting of verbal and non-verbal information in temporal lobe epilepsy. Cortex. 2012;48:317–32.\nDavidson M, Dorris L, O’Regan M, Zuberi SM. Memory consolidation and accelerated forgetting in children with idiopathic generalized epilepsy. Epilepsy Behav. 2007;11:394–400.\nSidhu MK, Stretton J, Winston GP, Symms M, Thompson PJ, Koepp MJ, et al. Factors affecting reorganisation of memory encoding networks in temporal lobe epilepsy. Epilepsy Res. 2015;110:1–9.\nHorak PC, Meisenhelter S, Song Y, Testorf ME, Kahana MJ, Viles WD, et al. Interictal epileptiform discharges impair word recall in multiple brain areas. Epilepsia. 2017;58:373–80.\nParadiso S, Hermann BP, Blumer D, Davies K, Robinson RG. Impact of depressed mood on neuropsychological status in temporal lobe epilepsy. J Neurol Neurosurg Psychiatry. 2001;70:180–5.\nMeador KJ, Loring DW, Moore E, Thompson WO, Nichols ME, Oberzan R, et al. Comparative cognitive effects of phenobarbital, phenytoin, and valproate in healthy adults. Neurology. 1995;45:1494–9.\nMeador KJ, Loring DW, Abney OL, Allen ME, Moore EE, Zamrini EY, et al. Effects of carbamazepine and phenytoin on EEG and memory in healthy adults. Epilepsia. 1993;34:153–7.\nHermann B, Meador KJ, Gaillard WD, Cramer JA. Cognition across the lifespan: antiepileptic drugs, epilepsy, or both? Epilepsy Behav. 2010;17:1–5.\nNitsche MA, Paulus W. Excitability changes induced in the human motor cortex by weak transcranial direct current stimulation. J Physiol. 2000;527:633–9.\nKeeser D, Meindl T, Bor J, Palm U, Pogarell O, Mulert C, et al. Prefrontal transcranial direct current stimulation changes connectivity of resting-state networks during fMRI. J Neurosci. 2011;31:15284–93.\nHill AT, Fitzgerald PB, Hoy KE. Effects of anodal transcranial direct current stimulation on working memory: a systematic review and meta-analysis of findings from healthy and neuropsychiatric populations. Brain Stimul. 2016;9:197–208.\n•• Karvigh SA, Motamedi M, Arzani M, Roshan JHN. HD-tDCS in refractory lateral frontal lobe epilepsy patients. Seizure. 47:74–80. The authors found in an uncontrolled study that tDCS could dramatically and chronically enhance memory in epilepsy patients. Further investigation of this method using a more controlled study design is needed.\nSan-Juan D, Morales-Quezada L, Orozco Garduño AJ, Alonso-Vanegas M, González-Aragón MF, Espinoza López DA, et al. Transcranial direct current stimulation in epilepsy. Brain Stimul. 2015;8:455–64.\nFregni F, Boggio PS, Nitsche M, Bermpohl F, Antal A, Feredoes E, et al. Anodal transcranial direct current stimulation of prefrontal cortex enhances working memory. 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Epilepsy Behav. 2007;10:521–8.\nRossi S, Cappa SF, Babiloni C, Pasqualetti P, Miniussi C, Carducci F, et al. Prefontal cortex in long-term memory: an “interference” approach using magnetic stimulation. Nat Neurosci. 2001;4:948.\nGagnon G, Blanchet S, Grondin S, Schneider C. Paired-pulse transcranial magnetic stimulation over the dorsolateral prefrontal cortex interferes with episodic encoding and retrieval for both verbal and non-verbal materials. Brain Res. 1344:148–58.\nKöhler S, Paus T, Buckner RL, Milner B. Effects of left inferior prefrontal stimulation on episodic memory formation: a two-stage fMRI. J Cogn Neurosci. 2004;16:178–88.\nBlumenfeld RS, Lee TG, D’Esposito M. The effects of lateral prefrontal transcranial magnetic stimulation on item memory encoding. Neuropsychologia. 2014;53:197–202.\nKahn I, Pascual-Leone A, Theoret H, Fregni F, Clark D, Wagner AD. Transient disruption of ventrolateral prefrontal cortex during verbal encoding affects subsequent memory performance. 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The influence of vagus nerve stimulation on memory. Cogn Behav Neurol: Off J Soc Behav Cogn Neurol. 2006;19:119–22.\n•• Sun L, Peräkylä J, Holm K, Haapasalo J, Lehtimäki K, Ogawa KH, et al. Vagus nerve stimulation improves working memory performance. J Clin Exp Neuropsychol. 39:954–64. The authors found that VNS stimulation acutely improved response accuracy in a working memory task.\nHoppe C, Helmstaedter C, Scherrmann J, Elger CE. No evidence for cognitive side effects after 6 months of vagus nerve stimulation in epilepsy patients. Epilepsy Behav. 2001;2:351–6.\nMcGlone J, Valdivia I, Penner M, Williams J, Sadler RM, Clarke DB. Quality of life and memory after vagus nerve stimulator implantation for epilepsy. Can J Neurol Sci. 2008;35:287–96.\nMuller L, Hamilton LS, Edwards E, Bouchard KE, Chang EF. Spatial resolution dependence on spectral frequency in human speech cortex electrocorticography. J Neural Eng. 2016;13:056013.\nHamani C, McAndrews MP, Cohn M, Oh M, Zumsteg D, Shapiro CM, et al. Memory enhancement induced by hypothalamic\u002Ffornix deep brain stimulation. Ann Neurol. 2008;63:119–23.\nLaxton AW, Tang-Wai DF, McAndrews MP, Zumsteg D, Wennberg R, Keren R, et al. A phase I trial of deep brain stimulation of memory circuits in Alzheimer’s disease. Ann Neurol. 2010;68:521–34.\nKoubeissi MZ, Kahriman E, Syed TU, Miller J, Durand DM. Low-frequency electrical stimulation of a fiber tract in temporal lobe epilepsy. Ann Neurol. 74:223–31.\nMiller JP, Sweet JA, Bailey CM, Munyon CN, Luders HO, Fastenau PS. Visual-spatial memory may be enhanced with theta burst deep brain stimulation of the fornix: a preliminary investigation with four cases. Brain. 2015;138:1833–42.\nVelasco AL, Velasco F, Velasco M, Trejo D, Castro G, Carrillo-Ruiz JD. Electrical stimulation of the hippocampal epileptic foci for seizure control: a double-blind, long-term follow-up study. 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