期刊
NEUROBIOLOGY OF DISEASE
卷 15, 期 3, 页码 553-562出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2003.12.011
关键词
cell death; tau; tauopathy; TUNEL; caspase-3; Alzheimer's disease; frontotemporal dementia with parkinsonism linked to chromosome-17
资金
- NIA NIH HHS [P01 AG17216] Funding Source: Medline
Transgenic mice overexpressing human tau with the P301L mutation develop neurofibrillary tangles, extensive gliosis, adult-onset motor abnormalities, and neuronal loss in affected brain regions. We investigated the mechanism of neuronal cell death in this model of tauopathy. There was no evidence of neuronal apoptosis at any age; however, a population of oligodendorocytes was immunopositive for TUNEL and activated caspase-3. EM confirmed that these oligodendrocytes were undergoing apoptosis. These data suggest that classical apoptosis is not a major mechanism of neuronal cell death associated with the tau dysfunction in this mouse model; however, prominent white matter pathology in the spinal cord suggests that axonal degeneration in dying neurons causes oligodendrocytes to undergo apoptosis. It is unknown if loss of oligodendrocytes either through apoptosis or through the formation of intracellular tau lesions further contributes to the neurodegeneration seen in these mice. (C) 2004 Elsevier Inc. All rights reserved.
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