Aging and Alzheimer's disease pathology

Neuropathology - Tập 40 Số 1 - Trang 22-29 - 2020
Renpei Sengoku1
1Departments of Neurology and Neuropathology Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology Tokyo Japan

Tóm tắt

The number of people with dementia worldwide is predicted to increase to 131.5 million by 2050. When studying dementia, understanding the basis of the neuropathological background is very important. Taking Alzheimer's disease (AD) neuropathology as an example, we know that the accumulation of abnormal structures such as senile plaques and neurofibrillary tangles is a hallmark. Macroscopic atrophy affects the entorhinal area and hippocampus, amygdala, and associative regions of the neocortex. Braak advocates the spread of tau deposits from the entorhinal to associative regions of the neocortex as the disease progresses. If the AD has only tau pathology, the degree and distribution of tau deposition may be associated with clinical symptoms. However, AD is also accompanied by amyloid‐β deposition and even atrophy. Although it is possible to make a neuropathological diagnosis of AD from the spread of amyloid and tau depositions, neuropathological abnormal protein accumulation cannot explain all clinical symptoms of AD. There is an ambiguity between clinical symptoms and neuropathological findings. It is important to understand neuropathological findings while understanding that this ambiguity exists. So, for the reader's help, first we briefly explain the changes in the brain with age, and then describe AD as a typical disease of dementia; finally we will describe the diseases that mimic AD for neurologists who are not experts in neuropathology.

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Tài liệu tham khảo

KYODO. New dementia strategy to cope with projected rise in cases.The Japan Times2015 27 Jan. Available from URL:https://www.japantimes.co.jp/news/2015/01/27/national/science-health/new-dementia-strategy-to-cope-with-projected-rise-in-cases/.

2013, G8 Dementia Summit Communique

10.3233/JAD-180843

10.1002/ana.410040410

10.1007/s00401-016-1562-0

10.1007/BF00304627

10.1007/s00401-011-0871-6

10.1097/00005072-196804000-00001

10.1111/j.1365-2990.1994.tb00951.x

10.1111/j.1365-2990.2011.01208.x

10.1097/00005072-198703000-00006

10.31887/DCNS.2003.5.1/hhippius

Alzheimer A, 1907, Über eine eigenartige Erkrankung der Hirnrinde, Allg Zschr Psychiatr Psych Gerichtl Med, 64, 146

10.1001/archneur.1976.00500040001001

10.1212/WNL.34.7.939

10.3233/JAD-2012-120223

10.1083/jcb.101.4.1371

10.1016/S1471-4914(02)02440-1

10.1126/science.282.5395.1914

10.1093/oxfordjournals.jbchem.a135662

10.1093/brain/awv316

10.1159/000076344

10.1097/00005072-199704000-00001

Yamaguchi H, 1988, Diffuse type of senile plaques in the brains of Alzheimer‐type dementia, Acta Neuropathol, 77, 113, 10.1007/BF00687420

10.1007/BF00308809

10.1007/s00401-006-0127-z

10.1111/j.1750-3639.2008.00147.x

10.1212/WNL.58.12.1791

10.1016/S0197-4580(97)00056-0

Ikeda K, 2000, Clinical aspects of argyrophilic grain disease, Clin Neuropathol, 19, 278

10.1097/00019442-200512000-00008

10.1001/archneur.63.5.665

10.1111/j.1440-1789.2007.00806.x

10.1111/j.1365-2990.1989.tb01146.x

10.1097/NEN.0b013e3181e5ae5c

10.1016/0304-3940(87)90204-7

10.1046/j.1365-2990.1998.00090.x

10.1093/jnen/61.6.547

10.1093/jnen/63.9.911

10.5414/NPP29271

10.1097/00005072-199702000-00006

10.1097/NEN.0000000000000022

10.1111/neup.12429

10.1111/j.1440-1789.1996.tb00162.x

10.1007/s00401-006-0156-7

10.1007/BF00296494

10.1016/0197-4580(95)00021-6

10.1007/s00401-014-1349-0

10.1046/j.1440-1789.2003.00522.x