Elisabete Ferreiro

TL;DR: It is observed that oligomeric Abeta1-42 depletes ER Ca(2+) levels leading to intracellular Ca( 2+) dyshomeostasis involving phospholipase C activation and in the presence of dantrolene, an inhibitor of ERCa(2+) release through ryanodine receptors, the oligomer-induced apoptosis was prevented demonstrating the involvement of ER Ca (2+) release.

TL;DR: It is demonstrated that the early PrP- and Abeta-induced perturbation of ER Ca(2+) homeostasis is a death message that leads to neuronal loss, suggesting that the regulation of ER calcium levels may be a potential therapeutical target for PrD and AD.

TL;DR: It is demonstrated that the early Abeta- and PrP -induced perturbation of ER Ca2+ homeostasis affects mitochondrial function, activating the mitochondrial-mediated apoptotic pathway and help to clarify the mechanism implicated in neuronal death that occurs in AD and PrD.

TL;DR: The evidences that link the 'metabolic syndrome' with increased risk for developing AD are resumed and the major changes occurring on both extra-mitochondrial and mitochondrial metabolic pathways are revisited, as revealed by imaging studies and biochemical analysis of brain and peripheral samples obtained from AD patients.

TL;DR: It is demonstrated that the release of Ca2+ from the ER, mediated by both RyR and IP3R, is involved in Aβ toxicity and can contribute, together with the activation of other intracellular neurotoxic mechanisms, to Aβ‐induced neuronal death.