Journal
CELL CYCLE
Volume 7, Issue 5, Pages 637-646Publisher
LANDES BIOSCIENCE
DOI: 10.4161/cc.7.5.5427
Keywords
cell cycle; presenilin; Alzheimer's disease; beta-catenin; apoptosis
Categories
Funding
- MRC [G0600676] Funding Source: UKRI
- Medical Research Council [G0600676] Funding Source: Medline
- Alzheimers Research UK [ART-EG2003B-1] Funding Source: researchfish
- Medical Research Council [G0600676] Funding Source: researchfish
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Presenilin-1 (PS1) is a component of the beta-catenin degradation machinery, and PS1 mutations linked to familial Alzheimer's disease (FAD) represent a loss of this function, leading, in non-neuronal cells, to accumulation of cyclin D1, aberrant cell cycle activation and hyperproliferation. In post-mitotic neurons, cell cycle activation is thought to be abortive and initiate apoptosis, thus contributing to AD pathogenesis. Consequently, we tested here the hypothesis that, in the PS1 FAD brain, cyclin D1 accumulation may occur and lead to neuronal apoptosis secondary to an abortive entry into the cell cycle.
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