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An AÎ242 double mutant inhibits AÎ242-induced plasma and mitochondrial membrane disruption in artificial membranes, isolated organs and intact cells by Oren, Ofek; Ben Zichri, Shani; Taube, Ran; Jelinek, Raz; Papo, Niv is a Neuroscience article available to read on EtoBox.

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Destabilization of plasma and inner mitochondrial membranes by extra- and intracellular amyloid β peptide (Aβ42) aggregates may lead to dysregulated calcium flux through the plasma membrane, mitochondrial-mediated apoptosis, and neuronal cell death in patients with Alzheimer's disease. In the current study, experiments performed with artificial membranes, isolated mitochondria, and neuronal cells allowed us to understand the mechanism by which a nonaggregating Aβ42 double mutant (designated Aβ42) exerts its neuroprotective effects. Specifically, we showed that Aβ42 protected neuronal cells from Aβ42-induced accumulation of toxic intracellular levels of calcium and from apoptosis. Aβ42 also inhibited Aβ42-induced mitochondrial membrane potential depolarization in the cells and abolished the Aβ42-mediated decrease in cytochrome oxidase activity in purified mitochondrial particles. These results can be explained in terms of the amelioration by Aβ42 of Aβ42-mediated changes in membrane fluidity in DOPC and cardiolipin/DOPC phospholipid vesicles, mimicking plasma and mitochondrial membranes, respectively. These observations are also in agreement with the inhibition by Aβ42 of phospholip

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Author

Oren, Ofek; Ben Zichri, Shani; Taube, Ran; Jelinek, Raz; Papo, Niv

Publisher

American Chemical Society; American Chemical Society (ACS) (ISSN 1948-7193)

Published

2020

Language

EN

Field

Neuroscience (Life Sciences)