TAILIEUCHUNG - Báo cáo khoa học: Implication of calpain in neuronal apoptosis A possible regulation of Alzheimer’s disease

Apoptotic neuronal cell death is the cardinal feature of aging and neurode-generative diseases, but its mechanisms remain obscure. Caspases, members of the cysteine protease family, are known to be critical effectors in central nervous system cellular apoptosis. More recently, the calcium-dependent proteases, calpains, have been implicated in cellular apoptotic processes. Indeed, several members of the Bcl-2 family of cell death regulators, nuc-lear transcription factors (p53) and caspases themselves are processed by calpains. . | ềFEBS Journal MINIREVIEW Implication of calpain in neuronal apoptosis A possible regulation of Alzheimer s disease F. Raynaud and A. Marcilhac UMR5539 EPHE-CNRS-UM2 cc107 Université de Montpellier II France Keywords Alzheimer s disease apoptosis calpain neurodegenerative disease neuron Correspondence A. Marcilhac UMR5539 EPHE-CNRS-UM2 cc107 Universite de Montpellier II place E. Bataillon 34095 Montpellier cedex 5 France Fax 33 0467144727 Tel 33 0467144775 E-mail marcilhac@ Received 23 March 2006 accepted 31 May 2006 doi Apoptotic neuronal cell death is the cardinal feature of aging and neurode-generative diseases but its mechanisms remain obscure. Caspases members of the cysteine protease family are known to be critical effectors in central nervous system cellular apoptosis. More recently the calcium-dependent proteases calpains have been implicated in cellular apoptotic processes. Indeed several members of the Bcl-2 family of cell death regulators nuclear transcription factors p53 and caspases themselves are processed by calpains. Progressive regional loss of neurons underlies the irreversible pathogenesis of various neurodegenerative diseases such as Alzheimer s disease in adult brain. Alzheimer s disease is characterized by extracellular plaques of amyloid b peptide aggregates and intracellular neurofibrillary tangles composed of hyperphosphorylated tau leading to apoptotic cell death. In this review we summarize the arguments showing that calpains modulate processes that govern the function and metabolism of these two key proteins in the pathogenesis of Alzheimer s disease. To conclude this article reviews our understanding of calpain-dependent apoptotic neuronal cell death and the ability of these proteases to regulate intracellular signaling pathways leading to chronic neurodegenerative disorders such as Alzheimer s disease. Further research on these calpain-dependent mechanisms which promote or prevent cell .

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