Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9435154 | Progress in Neurobiology | 2005 | 22 Pages |
Abstract
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, TNFα, NO, PGE2, 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.
Keywords
PGE2phagocytic oxidaseLipopolysacharide1-methyl-4-phenylpyridinium ionMMP-3VTAMPTPIL-1βFTDECMiNOSDEP6-HydroxydopamineAβNADPHTNFαLPSNSAID6-OHDA1-methyl-4-phenyl-1,2,3,6-tetrahydropyridineMPP+NFκBROSHIV associated dementiaAIDSimmunoreactiveInterleukin-1 betaBeta-amyloidAlzheimer's diseaseParkinson's diseasesubstantia nigratumor necrosis factor-alphatyrosine hydroxylaseHADCNSDopamineDiesel exhaust particlesparticulate matterinducible nitric oxide synthaseacquired immune deficiency syndromecentral nervous systemNon-steroidal anti-inflammatory drugnuclear factor-κBPhoxExtracellular matrixmatrix metalloproteinase-3Multiple sclerosisventral tegmental areaNitric oxidenicotinamide adenine dinucleotide phosphatehuman immunodeficiency virusHIVProstaglandin E2Reactive oxygen species
Related Topics
Life Sciences
Neuroscience
Neuroscience (General)
Authors
Michelle L. Block, Jau-Shyong Hong,