Literature search services are currently unavailable. During our hosting provider's UPS upgrade we experienced a hardware failure and are currently working to resolve the issue.

Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Overexpression of wild type but not an FAD mutant presenilin-1 promotes neurogenesis in the hippocampus of adult mice.

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.

Pubmed ID: 12079399


  • Wen PH
  • Shao X
  • Shao Z
  • Hof PR
  • Wisniewski T
  • Kelley K
  • Friedrich VL
  • Ho L
  • Pasinetti GM
  • Shioi J
  • Robakis NK
  • Elder GA


Neurobiology of disease

Publication Data

June 24, 2002

Associated Grants

  • Agency: NIA NIH HHS, Id: AG05138
  • Agency: NIA NIH HHS, Id: AG08200
  • Agency: NIA NIH HHS, Id: AG14392
  • Agency: NIA NIH HHS, Id: AG17926

Mesh Terms

  • Aging
  • Alzheimer Disease
  • Animals
  • Cell Count
  • Cell Differentiation
  • Cell Survival
  • Hippocampus
  • Humans
  • Membrane Proteins
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred DBA
  • Mice, Transgenic
  • Mutation
  • Neurons
  • Presenilin-1
  • Stem Cells