Systemic and acquired immune responses in alzheimer's disease

被引:94
作者
Britschgi, Markus [1 ]
Wyss-Coray, Tony [1 ]
机构
[1] Stanford Univ, Sch Med, Dept Neurol & Neurol Sci, Stanford, CA 94305 USA
来源
NEUROINFLAMMATION IN NEURONAL DEATH AND REPAIR | 2007年 / 82卷
关键词
D O I
10.1016/S0074-7742(07)82011-3
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Alzheimer's disease (AD) is a neurodegenerative disorder characterized clinically by a progressive cognitive decline and dementia. AD brains are marked by amyloid plaques and neurofibrillary tangles, neuronal cell loss, and a prominent activation of glial cells, and innate immune responses. A growing number of studies in AD have also reported alterations in systemic immune responses including changes in lymphocyte and macrophage distribution and activation, the presence of autoantibodies, or abnormal cytokine production. Studies in animal models for AD support the notion that immune cells infiltrate the brain and may modulate the disease. Here we will review evidence for systemic alterations in immune responses and a role for acquired immunity in AD and discuss their potential contribution to the disease.
引用
收藏
页码:205 / 233
页数:29
相关论文
共 180 条
[41]   The ins and outs of T-lymphocyte trafficking to the CNS: anatomical sites and molecular mechanisms [J].
Engelhardt, B ;
Ransohoff, RM .
TRENDS IN IMMUNOLOGY, 2005, 26 (09) :485-495
[42]   Aβ-specific T-cells reverse cognitive decline and synaptic loss in Alzheimer's mice [J].
Ethell, Douglas W. ;
Shippy, Daniel ;
Cao, Chuanhai ;
Cracchiolo, Jennifer R. ;
Runfeldt, Melissa ;
Blake, Brett ;
Arendash, Gary W. .
NEUROBIOLOGY OF DISEASE, 2006, 23 (02) :351-361
[43]   Neuropathology and pathogenesis of encephalitis following amyloid-β immunization in Alzheimer's disease [J].
Ferrer, I ;
Rovira, MB ;
Guerra, MLS ;
Rey, MJ ;
Costa-Jussá, F .
BRAIN PATHOLOGY, 2004, 14 (01) :11-20
[44]   BDNF and full-length and truncated TrkB expression in Alzheimer disease.: Implications in therapeutic strategies [J].
Ferrer, I ;
Marín, C ;
Rey, MJ ;
Ribalta, T ;
Goutan, E ;
Blanco, R ;
Tolosa, E ;
Martí, E .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1999, 58 (07) :729-739
[45]   Ineffective phagocytosis of amyloid-β by macrophages of Alzheimer's disease patients [J].
Fiala, M ;
Lin, J ;
Ringman, J ;
Kermani-Arab, V ;
Tsao, G ;
Patel, A ;
Lossinsky, AS ;
Graves, MC ;
Gustavson, A ;
Sayre, J ;
Sofroni, E ;
Suarez, T ;
Chiappelli, F ;
Bernard, G .
JOURNAL OF ALZHEIMERS DISEASE, 2005, 7 (03) :221-232
[46]  
Fitzgerald K.A., 2001, CYTOKINE FACTSBOOK
[47]   ALTERED EXPRESSION OF TRANSFORMING GROWTH-FACTOR-BETA IN ALZHEIMERS-DISEASE [J].
FLANDERS, KC ;
LIPPA, CF ;
SMITH, TW ;
POLLEN, DA ;
SPORN, MB .
NEUROLOGY, 1995, 45 (08) :1561-1569
[48]   Absence of C1q leads to less neuropathology in transgenic mouse models of Alzheimer's disease [J].
Fonseca, MI ;
Zhou, J ;
Botto, M ;
Tenner, AJ .
JOURNAL OF NEUROSCIENCE, 2004, 24 (29) :6457-6465
[49]   Neuronal localization of C1q in preclinical Alzheimer's disease [J].
Fonseca, MI ;
Kawas, CH ;
Troncoso, JC ;
Tenner, AJ .
NEUROBIOLOGY OF DISEASE, 2004, 15 (01) :40-46
[50]   Chemokines in serum and cerebrospinal fluid of Alzheimer's disease patients [J].
Galimbert, D ;
Schoonenboom, N ;
Scarpini, E ;
Scheltens, P .
ANNALS OF NEUROLOGY, 2003, 53 (04) :547-548