Neuroimmunology of Huntington’s Disease: Revisiting Evidence from Human Studies

Mediators of Inflammation - Tập 2016 - Trang 1-10 - 2016
Natália Pessoa Rocha1, Fabíola M. Ribeiro2, Erin Furr‐Stimming3, Antônio Lúcio Teixeira1
1Neuropsychiatry Program, Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77054, USA
2Department of Biochemistry and Immunology, ICB, Universidade Federal de Minas Gerais, 31270-901 Belo Horizonte, MG, Brazil
3Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, 77030, USA

Tóm tắt

Huntington’s disease (HD) is a neurodegenerative disorder characterized by selective loss of neurons in the striatum and cortex, which leads to progressive motor dysfunction, cognitive decline, and psychiatric disorders. Although the cause of HD is well described—HD is a genetic disorder caused by a trinucleotide (CAG) repeat expansion in the gene encoding for huntingtin (HTT) on chromosome 4p16.3—the ultimate cause of neuronal death is still uncertain. Apart from impairment in systems for handling abnormal proteins, other metabolic pathways and mechanisms might contribute to neurodegeneration and progression of HD. Among these, inflammation seems to play a role in HD pathogenesis. The current review summarizes the available evidence about immune and/or inflammatory changes in HD. HD is associated with increased inflammatory mediators in both the central nervous system and periphery. Accordingly, there have been some attempts to slow HD progression targeting the immune system.

Từ khóa


Tài liệu tham khảo

10.1016/s1474-4422(10)70245-3

10.1016/0092-8674(93)90585-e

10.1016/j.ncl.2009.04.001

10.1038/nrn1806

10.1016/s0962-8924(00)01853-5

10.1016/j.it.2015.04.007

10.2174/18715273113126660170

10.1084/jem.20080178

10.1097/00005072-199111000-00005

10.1093/jnen/60.2.161

10.1097/00005072-198511000-00003

10.1038/nn.3668

10.1002/glia.20526

10.1016/j.brainres.2006.02.102

10.1016/j.nbd.2011.09.003

10.1097/WNR.0b013e32832e34ee

10.1523/jneurosci.0116-08.2008

10.1073/pnas.0911503106

10.1093/hmg/ddt036

10.1016/S1534-5807(02)00188-0

10.1111/j.1460-9568.2005.03985.x

10.1212/01.wnl.0000222734.56412.17

10.1093/brain/awm044

10.1002/hbm.21008

10.1093/brain/awn244

10.1016/j.nbd.2015.08.011

10.1074/mcp.M800231-MCP200

10.1021/pr0700753

10.1016/S1357-2725(01)00155-8

10.3233/JHD-2012-120021

10.1016/j.neuroscience.2016.03.031

10.1016/j.parkreldis.2014.08.011

10.1016/0024-3205(85)90165-1

10.1172/JCI64484

10.1172/JCI64565

10.1093/brain/awt355

10.1212/wnl.28.1.32

10.1371/journal.pone.0141793

1998, Clinical Chemistry and Laboratory Medicine, 36, 747, 10.1515/CCLM.1998.132

10.3389/fphys.2014.00231

10.1371/currents.rrn1231

10.1016/j.nbd.2014.10.012

10.1523/JNEUROSCI.4008-12.2012

10.1111/j.1365-2265.2009.03661.x

10.1002/mds.25752

10.1371/currents.hd.5791c897b5c3bebeed93b1d1da0c0648

10.1523/jneurosci.2675-04.2004

10.1016/j.lfs.2011.02.020

10.1016/j.nbd.2004.07.011

10.1111/bph.12139

10.1515/revneuro-2013-0040

10.1212/01.wnl.0000133403.30559.ff

10.1002/mds.20018

10.2174/157015912800604515

10.1176/appi.neuropsych.18.4.553

10.1016/0091-3057(91)90386-G

10.1212/wnl.0000000000000363

10.1093/hmg/ddu151

10.1111/jnc.13553

10.1016/j.nbd.2015.01.002

10.1001/archneur.65.12.1582

Thông tin
Thông tin xuất bản

Mediators of Inflammation

Tập 2016

1-10

Thông tin tác giả