Increased expression of p130 in Alzheimer disease

Document Type

Article

Abstract

A number of recent findings support the notion of mechanistic parallels between Alzheimer disease (AD) and oncogenic processes, specifically, that neurons in AD, like cancer cells, display aberrant mitotic cell cycle re-entry. However, the mechanism that drives postmitotic neurons to reenter cell cycle remains elusive. In this study, we focused on the retinoblastoma-related protein p130 in AD. p130 is a transcriptional regulator that complexes with E2F4/5 in the nucleus and suppresses genes that regulate entry into the cell cycle. Interestingly, our results show that there are increases in p130 in cytoplasm of susceptible pyramidal neurons as well as neuroglia, often surrounding senile plaques, and within Hirano bodies in AD. By marked contrast, p130 is found at background levels in non-diseased, age-matched controls. Our data suggest that, despite its upregulation, the aberrant localization of p130 to the neuronal cytoplasm facilitates neuronal cell cycle re-entry in AD. © 2006 Springer Science+Business Media, LLC.

Keywords

Alzheimer disease, Apoptosis, Cell cycle, p130, Phosphorylation, Retinoblastoma protein, Tau

Publication Date

4-1-2007

Publication Title

Neurochemical Research

ISSN

03643190

Volume

32

Issue

4-5

First Page

639

Last Page

644

PubMed ID

17006760

Digital Object Identifier (DOI)

10.1007/s11064-006-9146-3

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