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Hippocampal mRNA profiles of transgenic mice expressing comparable levels of wildtype or Alzheimer-mutant human amyloid protein precursors


, : Hippocampal mRNA profiles of transgenic mice expressing comparable levels of wildtype or Alzheimer-mutant human amyloid protein precursors. Society for Neuroscience Abstracts 27(1): 332

Increased cerebral levels of beta-amyloid peptides (Abeta) are associated with Alzheimer's disease (AD). Mutations in the human beta-amyloid protein precursor (hAPP) alter Abeta production and cause autosomal dominant familial AD (FAD). How Abeta induces neurodegeneration or cognitive decline is unknown. Previously, we showed that age-dependent hippocampal decreases in presynaptic terminal density and synaptic transmission strength in hAPP transgenic (tg) mice depended on Abeta levels but not on Abeta deposition into plaques (J. Neurosci. 20: 4050). hAPP-FAD tg mice typically had higher Abeta levels and more prominent synaptic deficits than hAPP-wildtype (WT) tg mice. We hypothesized that the underlying mechanisms would be reflected, in part, in changes of hippocampal gene expression. Hippocampal RNA from individual hAPP-WT and hAPP-FAD mice was analyzed with microarrays representing over 13,000 sequences. Potentially significant differences between groups were found for 367 sequences. The 20 genes and 14 ESTs with the greatest changes belonged to the following clusters: extracellular matrix components, adhesion molecules, enzymes involved in neurotransmitter turnover, transcription factors, growth factors, and synaptic proteins. We are confirming these molecular leads by quantitative fluorogenic PCR and immunochemistry. In parallel studies, we are examining the precise role of validated targets in Abeta-dependent neurodegeneration and cognitive decline.

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