Mechanisms Underlying Inflammation in Neurodegeneration

被引:2879
作者
Glass, Christopher K. [1 ,2 ]
Saijo, Kaoru [1 ]
Winner, Beate [3 ]
Marchetto, Maria Carolina [3 ]
Gage, Fred H. [3 ]
机构
[1] Univ Calif San Diego, Dept Cellular & Mol Med, La Jolla, CA 92093 USA
[2] Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA
[3] Salk Inst Biol Studies, Genet Lab, La Jolla, CA 92037 USA
关键词
AMYOTROPHIC-LATERAL-SCLEROSIS; AMYLOID-BETA-PEPTIDE; GLYCOSYLATION END-PRODUCTS; NITRATED ALPHA-SYNUCLEIN; PLURIPOTENT STEM-CELLS; TUMOR-NECROSIS-FACTOR; MOTOR-NEURON DISEASE; TOLL-LIKE RECEPTORS; NF-KAPPA-B; ALZHEIMERS-DISEASE;
D O I
10.1016/j.cell.2010.02.016
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Inflammation is associated with many neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis. In this Review, we discuss inducers, sensors, transducers, and effectors of neuroinflammation that contribute to neuronal dysfunction and death. Although inducers of inflammation may be generated in a disease-specific manner, there is evidence for a remarkable convergence in the mechanisms responsible for the sensing, transduction, and amplification of inflammatory processes that result in the production of neurotoxic mediators. A major unanswered question is whether pharmacological inhibition of inflammation pathways will be able to safely reverse or slow the course of disease.
引用
收藏
页码:918 / 934
页数:17
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