The microglial phagocytic role with specific plaque types in the Alzheimer disease brain

被引：177

作者：

D'Andrea, MR

Cole, GM

Ard, MD

机构：

[1] Johnson & Johnson Pharmaceut Res & Dev, Drug Discovery, Spring House, PA 19477 USA

[2] Univ Calif Los Angeles, Greater Los Angeles VA Med Ctr, GRECC Res, Dept Med,Alzheimers Dis Res Ctr, Los Angeles, CA USA

[3] Univ Calif Los Angeles, Greater Los Angeles VA Med Ctr, GRECC Res, Dept Neurol,Alzheimers Dis Res Ctr, Los Angeles, CA USA

[4] Univ Mississippi, Med Ctr, Dept Anat, Jackson, MS 39216 USA

来源：

NEUROBIOLOGY OF AGING | 2004年 / 25卷 / 05期

关键词：

Alzheimer's disease; amyloid plaques; beta-amyloid; microglia; astrocytes; transgenic mice; neuropathology; inflammation; plaque formation; phagocytosis; dense-core plaques; diffuse plaques; cerebellum; entorhinal cortex;

D O I：

10.1016/j.neurobiolaging.2003.12.026

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

Alzheimer disease (AD) involves glial inflammation associated with amyloid plaques. The role of the microglial cells in the AD brain is controversial, as it remains unclear if the microglia form the amyloid fibrils of plaques or react to them in a macrophage-phagocytic role. Also, it is not known why microglia are preferentially associated with some amyloid plaque types. This review will provide substantial evidence to support the phagocytic role of microglia in the brain as well as explain why microglia are generally associated with specific plaque types that may be explained through their unique mechanisms of formation. In summary, the data presented suggests that plaque associated microglial activation is typically subsequent to specific amyloid plaque formations in the AD brain. (C) 2004 Elsevier Inc. All rights reserved.

引用

页码：675 / 683

页数：9

共 75 条

[1]

Ard MD, 1996, J NEUROSCI RES, V43, P190, DOI 10.1002/(SICI)1097-4547(19960115)43:2<190::AID-JNR7>3.0.CO

[2]

2-B

[3] THE SPATIAL PATTERNS OF BETA-A4 DEPOSIT SUBTYPES IN ALZHEIMERS-DISEASE [J].

ARMSTRONG, RA ;

MYERS, D ;

SMITH, CUM .

ACTA NEUROPATHOLOGICA, 1993, 86 (01) :36-41

[4] Imaging of amyloid-β deposits in brains of living mice permits direct observation of clearance of plaques with immunotherapy [J].

Backskai, BJ ;

Kajdasz, ST ;

Christie, RH ;

Carter, C ;

Games, D ;

Seubert, P ;

Schenk, D ;

Hyman, BT .

NATURE MEDICINE, 2001, 7 (03) :369-372

[5] Lack of apolipoprotein E dramatically reduces amyloid beta-peptide deposition [J].

Bales, KR ;

Verina, T ;

Dodel, RC ;

Du, YS ;

Altstiel, L ;

Bender, M ;

Hyslop, P ;

Johnstone, EM ;

Little, SP ;

Cummins, DJ ;

Piccardo, P ;

Ghetti, B ;

Paul, SM .

NATURE GENETICS, 1997, 17 (03) :263-264

[6]

Bamberger ME, 2003, J NEUROSCI, V23, P2665

[7] Peripherally administered antibodies against amyloid β-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease [J].

Bard, F ;

Cannon, C ;

Barbour, R ;

Burke, RL ;

Games, D ;

Grajeda, H ;

Guido, T ;

Hu, K ;

Huang, JP ;

Johnson-Wood, K ;

Khan, K ;

Kholodenko, D ;

Lee, M ;

Lieberburg, I ;

Motter, R ;

Nguyen, M ;

Soriano, F ;

Vasquez, N ;

Weiss, K ;

Welch, B ;

Seubert, P ;

Schenk, D ;

Yednock, T .

NATURE MEDICINE, 2000, 6 (08) :916-919

[8]

Chen K. S., 1998, Society for Neuroscience Abstracts, V24, P1502

[9]

Cole GM, 2000, MICROSC RES TECHNIQ, V50, P316, DOI 10.1002/1097-0029(20000815)50:4<316::AID-JEMT11>3.0.CO

[10]

2-E

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