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Cell cycle and Alzheimer's disease: studies in non-neuronal cells

Author(s): Natividad de las Cuevas | Ursula Munoz | Fernando Bartolome | Noemi Esteras | Carolina Alquezar | Angeles Martin-Requero

Journal: Journal of Applied Biomedicine
ISSN 1214-021X

Volume: 8;
Issue: 3;
Start page: 121;
Date: 2010;
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Keywords: Alzheimer’s disease | lymphocytes | cell cycle | cell survival | p27 | p21 | calmodulin | PI3K/Akt | ERK1/2

The most common cause of dementia in the elderly is Alzheimer disease (AD). In Europe, AD is a leadingcause of death. The prevalence of this disease in developed countries is increasing because of very significantshifts in life expectancy and demographic parameters. AD is characterized by progressive cognitiveimpairment, resulting from dysfunction and degeneration of neurons in the limbic and cortical regions of thebrain. Two prominent abnormalities in the affected brain regions are extracellular deposits of β-amyloid, andintracellular aggregates of tau protein in neurofibrillary tangles. The role of these features in AD pathogenesisand progression is not yet completely elucidated. Research over the last decade has revealed that theactivation of cell cycle machinery in postmitotic neurons is one of the earliest events in neuronal degenerationin AD. Here we summarize evidence to support the hypothesis that cell cycle alterations occur in cells otherthan neurons in AD sufferers. Immortalized lymphocytes from AD patients have show an enhanced rate ofproliferation associated with G1/S regulatory failure induced by alterations in the cyclin/CDK/pRb/E2Fpathway. In addition, these cells have a higher resistance to serum deprivation-induced apoptosis. Theseneoplastic-like features, cell cycle dysfunction and impaired apoptosis can be considered systemicmanifestations of AD disease.

Tango Jona
Tangokurs Rapperswil-Jona

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