Abstract
Amyloid β-peptide (Aβ) is widely held to be associated with Alzheimer's disease. It was previously demonstrated by our group that Aβ induces cell death by an apoptotic process. We report here that activation of the caspase-3 apoptotic cascade is regulated by calcineurin-mediated BAD dephosphorylation. Calcineurin inhibitors were also proven to be effective by preventing the loss of mitochondrial membrane potential (ΔΨm) induced by Aβ, not allowing cytochrome c release from mitochondria and subsequently caspase-3 activation. Considering the results presented, we argue that calcineurin activation and BAD dephosphorylation are upstream in premitochondrial signaling events leading to caspase-3 activation in Aβ-peptide-treated cells.
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