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

被引：69

作者：

Malik, Bilal ^{[1
]}

Currais, Antonio ^{[1
]}

Andres, Ana ^{[1
]}

Towlson, Christopher ^{[1
]}

Pitsi, Didier ^{[1
]}

Nunes, Ana ^{[1
]}

Niblock, Michael ^{[1
]}

Cooper, Jonathan ^{[2
]}

Hortobagyi, Tibor ^{[3
,4
]}

Soriano, Salvador ^{[1
]}

机构：

[1] Kings Coll London, MRC, Ctr Neurodegenerat Res, Dept Neurosci,Inst Psychiat, London SE5 8AF, England

[2] Kings Coll London, MRC, Social Genet & Dev Psychiat Ctr, Paediatr Storage Disorders Lab, London SE5 8AF, England

[3] Kings Coll Hosp London, Acad Neurosci Ctr, Dept Clin Neuropathol, London, England

[4] Univ Szeged, Dept Pathol, Szeged, Hungary

来源：

CELL CYCLE | 2008年 / 7卷 / 05期

基金：

英国医学研究理事会;

关键词：

cell cycle; presenilin; Alzheimer's disease; beta-catenin; apoptosis;

D O I：

10.4161/cc.7.5.5427

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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.

引用

页码：637 / 646

页数：10

共 29 条

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