Journal
NEUROBIOLOGY OF DISEASE
Volume 10, Issue 1, Pages 8-19Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1006/nbdi.2002.0490
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Funding
- NIA NIH HHS [AG17926, AG14392, AG08200, AG05138] Funding Source: Medline
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Mutations in the presenilin-1 (PS-1) gene are one cause of familial Alzheimer's disease (FAD). However, the functions of the PS-1 protein as well as how PS-1 mutations cause FAD are incompletely understood. Here we investigated if neuronal overexpression of wild-type or FAD mutant PS-1 in transgenic mice affects neurogenesis in the hippocampus of adult animals. We show that either a wild-type or an FAD mutant PS-1 transgene reduces the number of neural progenitors in the dentate gyrus. However, the wild-type, but not the FAD mutant PS-1 promoted the survival and differentiation of progenitors leading to more immature granule cell neurons being generated in PS-1 wild type expressing animals. These studies suggest that PS-1 plays a role in regulating neurogenesis in adult hippocampus and that FAD mutants may have deleterious properties independent of their effects on amyloid deposition. (C) 2002 Elsevier Science (USA).
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