Dimebon inhibits calcium-induced swelling of rat brain mitochondria but does not alter calcium retention or cytochrome C release.

Neuromolecular Medicine
Kranthi Kumari Naga, James W Geddes

Abstract

Dimebon was originally introduced as an antihistamine and subsequently investigated as a possible therapeutic for a variety of disorders, including Alzheimer's disease. One putative mechanism underlying the neuroprotective properties of Dimebon is inhibition of mitochondrial permeability transition, based on the observation that Dimebon inhibited the swelling of rat liver mitochondria induced by calcium and other agents that induce permeability transition. Because liver and brain mitochondria differ substantially in their properties and response to conditions associated with opening of the permeability transition pore, we sought to determine whether Dimebon inhibited permeability transition in brain mitochondria. Dimebon reduced calcium-induced mitochondrial swelling but did not enhance the calcium retention capacity or impair calcium-induced cytochrome C release from non-synaptic mitochondria isolated from rat brain cerebral cortex. These findings indicate that Dimebon does not inhibit mitochondrial permeability transition, induced by excessive calcium uptake, in brain mitochondria.

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Citations

Dec 20, 2011·Neurotoxicity Research·Sergey O BachurinNatalia N Ninkina
Dec 8, 2015·Journal of Alzheimer's Disease : JAD·Carola StockburgerWalter E Müller
Jul 1, 2015·Molecular Neurobiology·Aleksey UstyugovSergey Bachurin
Jun 20, 2012·Neurochemistry International·Werner J GeldenhuysDean E Dluzen
Sep 12, 2019·Frontiers in Pharmacology·Giovanna Cenini, Wolfgang Voos
Jul 16, 2014·Biomedit︠s︡inskai︠a︡ khimii︠a︡·T A ShelkovnikovaN N Ninkina
Nov 9, 2020·Trends in Neurosciences·Maria Calvo-Rodriguez, Brian J Bacskai

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