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In situ hybridization analysis of presenilin 1 mRNA in Alzheimer disease and in lesioned rat brain.

ABSTRACT: 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.

SUBMITTER: Page K

PROVIDER: S-EPMC19487 | biostudies-literature | 1996 Nov

REPOSITORIES: biostudies-literature

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In situ hybridization analysis of presenilin 1 mRNA in Alzheimer disease and in lesioned rat brain.

Page K K Hollister R R Tanzi R E RE Hyman B T BT

Proceedings of the National Academy of Sciences of the United States of America 19961101 24

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 p ...[more]

PMID: 8943053

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