The neuronal cell cycle as a mechanism of pathogenesis in Alzheimer's disease

Antonio Currais¹, Tibor Hortobágyi², Salvador Soriano¹

¹Department of Neuroscience, MRC Centre for Neurodegeneration Research, Institute of Psychiatry, King's College London, London SE5 8AF, UK
²Department of Clinical Neuropathology, Academic Neuroscience Centre, King's College Hospital, London, UK and Department of Pathology, University of Szeged, Szeged, Hungary

Received: March 18, 2009Accepted: April 27, 2009Published: April 28, 2009

Copyright: © 2009 Currais et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Differentiated neurons display specific biochemical, physiological and morphological properties that apparently prevent them from further cell division. Nevertheless, expression of cell cycle modulators persists after neuronal differentiation and is upregulated under stress conditions, such as trophic factor deprivation, oxidative stress and the presence of DNA damaging agents. This apparent reactivation of the cell cycle has been postulated as a sine qua non for neuronal death in response to those stress conditions, particularly in Alzheimer's disease. However, the physiological and pathogenic implications of a putative neuronal cell cycle are far from clear. Here, we discuss the notion of the neuronal cell cycle as a mediator of cell death, with particular emphasis on Alzheimer's disease.