期刊
JOURNAL OF NEUROTRAUMA
卷 27, 期 11, 页码 1983-1995出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/neu.2010.1396
关键词
Alzheimer's disease; amyloid; apolipoprotein E; microglia; pharmacogenomics; tau
资金
- Institute for the Study of Aging
- Alzheimer's Association
Cognitive impairment is common following traumatic brain injury (TBI), and neuroinflammatory mechanisms may predispose to the development of neurodegenerative disease. Apolipoprotein E (apoE) polymorphisms modify neuroinflammatory responses, and influence both outcome from acute brain injury and the risk of developing neurodegenerative disease. We demonstrate that TBI accelerates neurodegenerative pathology in double-transgenic animals expressing the common human apoE alleles and mutated amyloid precursor protein, and that pathology is exacerbated in the presence of the apoE4 allele. The administration of an apoE-mimetic peptide markedly reduced the development of neurodegenerative pathology in mice homozygous for apoE3 as well as apoE3/E4 heterozygotes. These results demonstrate that TBI accelerates the cardinal neuropathological features of neurodegenerative disease, and establishes the potential for apoE mimetic therapies in reducing pathology associated with neurodegeneration.
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