Pathological relationships between microglial cell activity and tau and amyloid β protein in patients with !Alzheimer's disease

被引:49
作者
Hayes, A
Thaker, U
Iwatsubo, T
Pickering-Brown, SM
Mann, DMA
机构
[1] Univ Manchester, Dept Med, Clin Neurosci Res Grp, Manchester M13 9PT, Lancs, England
[2] Univ Tokyo, Dept Neurosci & Neuropathol, Tokyo 113, Japan
[3] Inst Psychiat, Dept Old Age Psychiat, London SE5 8AF, England
关键词
microglial cells; tau protein; amyloid beta protein; neuroinflammation; neurofibrillary degeneration;
D O I
10.1016/S0304-3940(02)00888-1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The extent of microglial cell activation (microglial cell load) was estimated by image analysis of ferritin-immunostained sections of frontal cortex from 72 patients with pathologically confirmed Alzheimer's disease (AD), and correlated with the amount of pathological tau and annyloid beta protein (Abeta), as both Abeta(40) and Abeta(42) load, in adjacent sections of the same cases. Microglial cell load did not correlate with either Abeta(40) or Abeta(42) load but was significantly correlated with pathological tau load. Microglial cell load was unrelated to age at onset of disease or duration of illness. It is possible that because the presence of microglial cells predates that of pathological tau proteins within the cerebral cortex in AD, neurofibrillary damage to nerve cells may stem from the release of proinflammatory and other potentially neurotoxic molecules from microglial cells. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:171 / 174
页数:4
相关论文
共 31 条
[1]   Microglia, amyloid and dementia in Alzheimer disease - A correlative study [J].
Arends, YM ;
Duyckaerts, C ;
Rozemuller, JM ;
Eikelenboom, P ;
Hauw, JJ .
NEUROBIOLOGY OF AGING, 2000, 21 (01) :39-47
[2]   NEUROFIBRILLARY TANGLES BUT NOT SENILE PLAQUES PARALLEL DURATION AND SEVERITY OF ALZHEIMERS-DISEASE [J].
ARRIAGADA, PV ;
GROWDON, JH ;
HEDLEYWHYTE, ET ;
HYMAN, BT .
NEUROLOGY, 1992, 42 (03) :631-639
[3]   Microglial activation by Alzheimer amyloid precursor protein and modulation by apolipoprotein E [J].
Barger, SW ;
Harmon, AD .
NATURE, 1997, 388 (6645) :878-881
[4]   NEUROPATHOLOGICAL STAGING OF ALZHEIMER-RELATED CHANGES [J].
BRAAK, H ;
BRAAK, E .
ACTA NEUROPATHOLOGICA, 1991, 82 (04) :239-259
[5]  
Breitner JCS, 1996, ANNU REV MED, V47, P401
[6]   IMMUNOGLOBULINS AND COMPLEMENT FACTORS IN SENILE PLAQUES - AN IMMUNOPEROXIDASE STUDY [J].
EIKELENBOOM, P ;
STAM, FC .
ACTA NEUROPATHOLOGICA, 1982, 57 (2-3) :239-242
[7]   Association of A beta 40-positive senile plaques with microglial cells in the brains of patients with Alzheimer's disease and in non-demented aged individuals [J].
Fukumoto, H ;
AsamiOdaka, A ;
Suzuki, N ;
Iwatsubo, T .
NEURODEGENERATION, 1996, 5 (01) :13-17
[8]   Are interleukin-1 gene polymorphisms risk factors or disease modifiers in AD? [J].
Green, EK ;
Harris, JM ;
Lemmon, H ;
Lambert, JC ;
Chartier-Harlin, MC ;
St Clair, D ;
Mann, DMA ;
Iwatsubo, T ;
Lendon, CL .
NEUROLOGY, 2002, 58 (10) :1566-1568
[9]   MICROGLIAL INTERLEUKIN-1-ALPHA EXPRESSION IN HUMAN HEAD-INJURY - CORRELATIONS WITH NEURONAL AND NEURITIC BETA-AMYLOID PRECURSOR PROTEIN EXPRESSION [J].
GRIFFIN, WST ;
SHENG, JG ;
GENTLEMAN, SM ;
GRAHAM, DI ;
MRAK, RE ;
ROBERTS, GW .
NEUROSCIENCE LETTERS, 1994, 176 (02) :133-136
[10]  
GRIFFIN WST, 1989, P NATL ACAD SCI USA, V86, P7611