Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12104/44323
Title: Role of cell cycle re-entry in neurons: A common apoptotic mechanism of neuronal cell death
Author: Folch, J.
Junyent, F.
Verdaguer, E.
Auladell, C.
Pizarro, J.G.
Beas-Zárate, Carlos
Pallas, M.
Camins, A.
Issue Date: 2012
Abstract: Currently, there is no effective treatment for neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease. Thus, a major focus of neuroscience research is to examine the mechanisms involved in neuronal loss in order to identify potential drug targets. Recent results indicate that DNA damage and re-entry into the cell cycle may constitute a common pathway in apoptosis in neurological diseases. The role of the cell cycle in such disorders is supported by data on the brain of patients who showed an increase in cell-cycle protein expression. Indeed, studies performed in neuronal cell preparations indicate that oxidative stress could be the main mechanism responsible for cell cycle re-entry. DNA damage and repair after oxidative stress may activate the enzyme ataxia telangiectasia mutated, which is a cell-cycle regulator. Once the cell cycle is activated, the increase in the expression of transcription factor E2F-1 could induce neuronal apoptosis. Furthermore, the potential routes involved in E2F-1 induced apoptosis could be p53-dependent or p53-independent. Under this E2F-1 hypothesis of cell death, multiple mitochondria-dependent pathways may be activated, including caspase and caspase-independent signaling cascades. Finally, given that cyclin-dependent kinase inhibitory drugs have neuroprotective and anti-apoptotic effects in experimental models, their potential application for the treatment of neurological disorders should be taken into account. © 2011 Springer Science+Business Media, LLC.
URI: http://www.scopus.com/inward/record.url?eid=2-s2.0-84865403573&partnerID=40&md5=6685246a3988bdb40fb7a08af4d39840
http://hdl.handle.net/20.500.12104/44323
Appears in Collections:Producción científica UdeG

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