Journal
JOURNAL OF NEUROSCIENCE
Volume 25, Issue 6, Pages 1571-1578Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4145-04.2005
Keywords
presenilin; DNA microarray; Alzheimer's disease; gene expression; transcriptome; animal model
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Funding
- NIA NIH HHS [AG021494, R01 AG021494] Funding Source: Medline
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Familial forms of Alzheimer's disease (FADs) are caused by the expression of mutant presenilin 1 (PS1) or presenilin 2. Using DNA microarrays, we explored the brain transcription profiles of mice with conditional knock-out of PS1 ( cKO PS1) in the forebrain. In parallel, we performed a transcription profiling of the hippocampus and frontal cortex of the FAD-linked DeltaE9 mutant transgenic ( TG) mice and matched controls [ TG mice expressing wild-type human PS1 (hPS1)]. When the TG and cKO datasets were cross-compared, the majority of the 30 common expression alterations were in opposite direction, suggesting that the FAD-linked PS1 variant produces transcriptome changes primarily by gain of aberrant function. Our microarray studies also revealed an unanticipated inverse correlation of transcript levels between the brains of mice that coexpress DeltaE9 hPS1+ amyloid precursor protein (APP)(695) Swe and DeltaE9 hPS1 single transgenic mice. The opposite directionality of these changes in transcript levels must be a function of APP and/or APP derivatives.
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