Neuronal death associated to cerebral ischemia is due to a series of pathological events that lead to a decrease in the supply of oxygen and glucose to the brain cells. Traditionally neuronal cell death caused by ischemia has been considered to be necrosis, mainly triggered by an overstimulation, because of increasing extracellular glutamate concentration, of NMDA and AMPA receptors. However, recently several lines of evidence suggest that apoptosis may play an important role in brain damage consequent to ischemic insults, producing a boost in the research of the molecular mechanisms, which could be implicated. By using an "in vitro" model of cerebral ischemia, the oxygen-glucose deprivation-induced cortical cells death, we want to study the possibility that ischemia-mediated release of TNF-alpha by glial cells could be the triggering factor of the apoptotic death. In particular, we are interested in exploring whether activation of NF-kB, the proteolysis-mediated activation of Bid or the inhibition of the survival pathway mediated by Akt/Bad. Events that would activate the caspases involved in apoptosis execution like caspase-3, -7 and/or -8
|Effective start/end date||28/12/01 → 27/12/04|
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