Microglia as potential contributors to motor neuron injury in amyotrophic lateral sclerosis

被引:161
作者
Sargsyan, SA [1 ]
Monk, PN [1 ]
Shaw, PJ [1 ]
机构
[1] Univ Sheffield, Sch Med, Acad Neurol Unit, Sheffield S10 2RX, S Yorkshire, England
基金
英国惠康基金;
关键词
neuroinflammation; cytokines; motor neuron; microglia;
D O I
10.1002/glia.20210
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The central nervous system (CNS) is equipped with a variety of cell types, all of which are assigned particular roles during the development, maintenance, function and repair of neural tissue. One glial cell type, microglia, deserves particular attention, as its role in the healthy or injured CNS is incompletely understood. Evidence exists for both regenerative and degenerative functions of these glial cells during neuronal injury. This review integrates the current knowledge of the role of microglia in an adult-onset neurodegenerative disease, amyotrophic lateral sclerosis (ALS), and pays particular attention to the possible mechanisms of initiation and propagation of neuronal damage during disease onset and progression. Microglial cell properties, behavior and detected inflammatory reactions during the course of the disease are described. The neuroinflammatory changes that occur in a mouse model of ALS are summarized. The understanding of microglial function in the healthy and injured CNS could offer better diagnostic as well as therapeutic approaches for prevention, retardation, or repair of neural tissue degeneration. (C) 2005 Wiley-Liss, Inc.
引用
收藏
页码:241 / 253
页数:13
相关论文
共 142 条
  • [1] Immune reactivity in a mouse model of familial ALS correlates with disease progression
    Alexianu, ME
    Kozovska, M
    Appel, SH
    [J]. NEUROLOGY, 2001, 57 (07) : 1282 - 1289
  • [2] Inducible nitric oxide synthase up-regulation in a transgenic mouse model of familial amyotrophic lateral sclerosis
    Almer, G
    Vukosavic, S
    Romero, N
    Przedborski, S
    [J]. JOURNAL OF NEUROCHEMISTRY, 1999, 72 (06) : 2415 - 2425
  • [3] Increased levels of the pro-inflammatory prostaglandin PGE2 in CSF from ALS patients
    Almer, G
    Teismann, P
    Stevic, Z
    Halaschek-Wiener, J
    Deecke, L
    Kostic, V
    Przedborski, S
    [J]. NEUROLOGY, 2002, 58 (08) : 1277 - 1279
  • [4] Almer G, 2001, ANN NEUROL, V49, P176, DOI 10.1002/1531-8249(20010201)49:2<176::AID-ANA37>3.3.CO
  • [5] 2-O
  • [6] ANDERSEN PM, 2003, MOTOR NEURON DISORDE, P207
  • [7] Glial proliferation and metabotropic glutamate receptor expression in amyotrophic lateral sclerosis
    Anneser, JMH
    Chahli, C
    Ince, PG
    Borasio, GD
    Shaw, PJ
    [J]. JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 2004, 63 (08) : 831 - 840
  • [8] The transcription factor NF-κB and human disease
    Baldwin, AS
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 2001, 107 (01) : 3 - 6
  • [9] BANATI RB, 1995, CLIN NEUROPATHOL, V14, P197
  • [10] PK ('peripheral benzodiazepine') - Binding sites in the CNS indicate early and discrete brain lesions: Microautoradiographic detection of [H-3]PK11195 binding to activated microglia
    Banati, RB
    Myers, R
    Kreutzberg, GW
    [J]. JOURNAL OF NEUROCYTOLOGY, 1997, 26 (02): : 77 - 82