New Path For Novel Alzheimer's Therapies
(a major role for changes in Ca)
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Researchers from the University of the Basque Country (UPV/EHU) have found a new Alzheimer's-related mechanism that could give rise to the development of new therapies against this disease. The study was recently published in the Cell Calcium journal, and the authors have already applied for a European patent to protect the commercial exploitation of this new discovery.
The novelty lies in a new mechanism through which the amyloid peptide, the major pathogen in Alzheimer's disease, provokes neuronal death. The Basque researchers have found that this peptide activates some receptors that lead cells to overexcitation and subsequent death; when such receptors are blocked with specific drugs, neurons are protected from the peptide-related lethal effects. This finding is particularly relevant for the development of new therapies slowing down Alzheimer's progression.
Amyloid beta (Aβ) oligomers accumulate in brain tissue of Alzheimer disease patients and are related to pathogenesis. The precise mechanisms by which Aβ oligomers cause neurotoxicity remain unresolved. In this study, we investigated the role of ionotropic glutamate receptors on the intracellular Ca2+ overload caused by Aβ. Using rat cortical neurons in culture and entorhinal–hippocampal organotypic slices, we found that Aβ oligomers significantly induced inward currents, intracellular Ca2+ increases and apoptotic cell death through a mechanism requiring NMDA and AMPA receptor activation. The massive entry of Ca2+ through NMDA and AMPA receptors induced by Aβ oligomers caused mitochondrial dysfunction as indicated by mitochondrial Ca2+ overload, oxidative stress and mitochondrial membrane depolarization. Importantly, chronic treatment with nanomolar concentration of Aβ oligomers also induced NMDA- and AMPA receptor-dependent cell death in entorhinal cortex and hippocampal slice cultures. Together, these results indicate that overactivation of NMDA and AMPA receptor, mitochondrial Ca2+ overload and mitochondrial damage underlie the neurotoxicity induced by Aβ oligomers. Hence, drugs that modulate these events can prevent from Aβ damage to neurons in Alzheimer's disease. Read more: sciencedirect.com
Food Combination and Alzheimer Disease Risk
Simultaneous consideration of previous knowledge regarding potentially AD-related nutrients and multiple food groups can aid in identifying food combinations that are associated with AD risk. Read more: archneur.ama-assn.org
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