In situ hybridization analysis of presenilin 1 mRNA in Alzheimer disease and in lesioned rat brain.
Presenilin-1 ( PS-1) gene mutations are responsible for the majority of the early onset familial forms of Alzheimer disease (AD). Neither PS-1's anatomic distribution in brain nor expression in AD have been reported. Using in situ hybridization in the rat forebrain, we show that PS-1 mRNA expression is primarily in cortical and hippocampal neurons, with less expression in subcortical structures, in a regional pattern similar to APP695. Excitotoxic lesions lead to loss of PS-1 signal. A neuronal pattern of expression of PS-1 mRNA was also observed in the human hippocampal formation. AD and control levels did not differ. PS-1 is expressed in brain areas vulnerable to AD changes more so than in areas spared in AD; however, PS-1 expression is not sufficient to mark vulnerable regions. Collectively, these data suggest that the neuropathogenic process consequent to PS-1 mutations begins in neuronal cell populations.[1]References
- In situ hybridization analysis of presenilin 1 mRNA in Alzheimer disease and in lesioned rat brain. Page, K., Hollister, R., Tanzi, R.E., Hyman, B.T. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
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