Up-regulation of Bcl-2 in APP transgenic mice is associated with neuroprotection.

ABSTRACT: Abeta-induced neurodegeneration is limited in APP and APP+PS1 transgenic mice. In middle-aged APP + PS1 transgenic mice, we found significantly increased Bcl-2 expression. The increase in Bcl-2 is restricted to amyloid-containing brain regions and is not found at young ages, suggesting that Abeta deposition is the stimulus for increased Bcl-2. Western blot results were confirmed with immunohistochemistry and qRT-PCR. In addition, we found that APP transgenic mice were protected from neurotoxicity caused by an injection of bak BH3 fusion peptides, known to induce apoptosis by antagonizing bcl protein activity. Nissl and fluorojade-stained slides showed that the active bak BH3 peptide caused substantial neuronal loss in the dentate gyrus and CA3 regions of nontransgenic, but not APP mice. Th

SUBMITTER: Karlnoski R 

PROVIDER: S-EPMC1885419 | biostudies-literature | 2007 Jan

REPOSITORIES: biostudies-literature