The neuronal cell cycle as a mechanism of pathogenesis in Alzheimer's disease.
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.
Department of Neuroscience, MRC Centre for Neurodegeneration Research, Institute of Psychiatry, King's College London, London SE5 8AF, UK.
Antonio
A
Currais
Tibor
T
Hortobágyi
Salvador
S
Soriano
D000544:Alzheimer Disease / Q000378:metabolism / Q000503:physiopathology*; D002453:Cell Cycle / Q000502:physiology*; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation / Q000502:physiology; D006801:Humans; D009474:Neurons / Q000166:cytology* / Q000502:physiology*
D018797:Cell Cycle Proteins