Microglia and inflammation-mediated neurodegeneration: Multiple triggers with a common mechanism

被引:1259
作者
Block, ML [1 ]
Hong, JS [1 ]
机构
[1] NIEHS, Neuropharmacol Sect, Res Triangle Pk, NC 27709 USA
关键词
D O I
10.1016/j.pneurobio.2005.06.004
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Inflammation, a common denominator among the diverse list of neurodegenerative diseases, has recently been implicated as a critical mechanism responsible for the progressive nature of neurodegeneration. Microglia are the resident innate immune cells in the central nervous system and produce a barrage of factors (IL-1 TNF alpha, NO, PGE(2), superoxide) that are toxic to neurons. Evidence supports that the unregulated activation of microglia in response to environmental toxins, endogenous proteins, and neuronal death results in the production of toxic factors that propagate neuronal injury. In the following review, we discuss the common thread of microglial activation across numerous neurodegenerative diseases, define current perceptions of how microglia are damaging neurons, and explain how the microglial response to neuronal damage results in a self-propelling cycle of neuron death. circle star 2005 Elsevier Ltd. All rights reserved.
引用
收藏
页码:77 / 98
页数:22
相关论文
共 223 条
  • [21] DNA damage in nasal and brain tissues of canines exposed to air pollutants is associated with evidence of chronic brain inflammation and neurodegeneration
    Calderón-Garcidueñas, L
    Maronpot, RR
    Torres-Jardon, R
    Henríquez-Roldán, C
    Schoonhoven, R
    Acuña-Ayala, H
    Villarreal-Calderón, A
    Nakamura, J
    Fernando, R
    Reed, W
    Azzarelli, B
    Swenberg, JA
    [J]. TOXICOLOGIC PATHOLOGY, 2003, 31 (05) : 524 - 538
  • [22] Air pollution and brain damage
    Calderón-Garcidueñas, L
    Azzarelli, B
    Acuna, H
    Garcia, R
    Gambling, TM
    Osnaya, N
    Monroy, S
    Tizapantzi, MD
    Carson, JL
    Villarreal-Calderon, A
    Rewcastle, B
    [J]. TOXICOLOGIC PATHOLOGY, 2002, 30 (03) : 373 - 389
  • [23] Particulate matter in polluted air may increase biomarkers of inflammation in mouse brain
    Campbell, A
    Oldham, M
    Becaria, A
    Bondy, SC
    Meacher, D
    Sioutas, C
    Misra, C
    Mendez, LB
    Kleinman, A
    [J]. NEUROTOXICOLOGY, 2005, 26 (01) : 133 - 140
  • [24] Identification of two distinct mechanisms of phagocytosis controlled by different Rho GTPases
    Caron, E
    Hall, A
    [J]. SCIENCE, 1998, 282 (5394) : 1717 - 1721
  • [25] Prenatal exposure to the bacteriotoxin lipopolysaccharide leads to long-term losses of dopamine neurons in offspring: A potential, new model of Parkinson's disease
    Carvey, PM
    Chang, Q
    Lipton, JW
    Ling, ZD
    [J]. FRONTIERS IN BIOSCIENCE-LANDMARK, 2003, 8 : S826 - S837
  • [26] CHAKRABARTI L, 1991, AM J PATHOL, V139, P1273
  • [27] Influence of neurons on lipopolysaccharide-stimulated production of nitric oxide and tumor necrosis factor-α by cultured glia
    Chang, RCC
    Hudson, P
    Wilson, B
    Haddon, L
    Hong, JS
    [J]. BRAIN RESEARCH, 2000, 853 (02) : 236 - 244
  • [28] A novel effect of an opioid receptor antagonist, naloxone, on the production of reactive oxygen species by microglia: a study by electron paramagnetic resonance spectroscopy
    Chang, RCC
    Rota, C
    Glover, RE
    Mason, RP
    Hong, JS
    [J]. BRAIN RESEARCH, 2000, 854 (1-2) : 224 - 229
  • [29] CHAO CC, 1992, J IMMUNOL, V149, P2736
  • [30] PRODUCTION OF SUPEROXIDE ANIONS BY A CNS MACROPHAGE, THE MICROGLIA
    COLTON, CA
    GILBERT, DL
    [J]. FEBS LETTERS, 1987, 223 (02) : 284 - 288