Loss of neuronal cell cycle control as a mechanism of neurodegeneration in the presenilin-1 alzheimer's disease brain

Bilal Malik, Antonio Currais, Ana Andres, Christopher Towlson, Didier Pitsi, Ana Nunes, Michael Niblock, Jonathan Cooper, Tibor Hortobágyi, Salvador Soriano

Research output: Contribution to journalArticle

49 Citations (Scopus)

Abstract

Presenilin-1 (PS1) is a component of the β-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.

Original languageEnglish
Pages (from-to)637-646
Number of pages10
JournalCell Cycle
Volume7
Issue number5
DOIs
Publication statusPublished - Mar 1 2008

Keywords

  • Alzheimer's disease
  • Apoptosis
  • Cell cycle
  • Presenilin
  • β-catenin

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology

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    Malik, B., Currais, A., Andres, A., Towlson, C., Pitsi, D., Nunes, A., Niblock, M., Cooper, J., Hortobágyi, T., & Soriano, S. (2008). Loss of neuronal cell cycle control as a mechanism of neurodegeneration in the presenilin-1 alzheimer's disease brain. Cell Cycle, 7(5), 637-646. https://doi.org/10.4161/cc.7.5.5427