Dimebon Attenuates the Aβ -Induced Mitochondrial Permeabilization

ISSN: 1875-5828 (Online)
ISSN: 1567-2050 (Print)

Volume 14, 12 Issues, 2017

Download PDF Flyer

Current Alzheimer Research

This journal supports open access

Aims & ScopeAbstracted/Indexed in

Ranking and Category:
  • 59th of 192 in Clinical Neurology
  • 101st of 256 in Neurosciences

Submit Abstracts Online Submit Manuscripts Online

Prof. Debomoy K. Lahiri
Department of Psychiatry, Indiana University School of Medicine
Neuroscience Research Center
Indianapolis, IN 46202

View Full Editorial Board

Subscribe Purchase Articles Order Reprints

Current: 3.145
5 - Year: 3.58

Dimebon Attenuates the Aβ -Induced Mitochondrial Permeabilization

Current Alzheimer Research, 11(5): 422-429.

Author(s): Elena F. Shevtsova, Daria V. Vinogradova, Elena G. Kireeva, V. Prakash Reddy, Gjumrakch Aliev and Sergey OBachurin.

Affiliation: Institute of Physiologically Active Compounds, Russian Academy of Sciences, Chernogolovka, 142432, Russia.


The currently available experimental data supports the hypothesis that the neuroprotective effect of dimebon is related to the protection of the brain-mitochondria from neurodegeneration. In this study, the influence of dimebon on mitochondria was investigated to gain a better understanding of the neuroprotective effects of this drug. Here, we demonstrate that dimebon enhances the resistance of the isolated rat brain and liver mitochondria to the induction of mitochondrial permeability transition (MPT) by calcium ions even in the presence of atractyloside, a MPT pore (MPTP) opener, but is ineffective against atractyloside-induced mitochondria swelling. Unlike cyclosporine A (CsA), a MPTP inhibitor, Dimebon does not influence the adenine nucleotide translocase (ANT) conformational changes and is not able to prevent the MPT of de-energized mitochondria. Using three different assays, and using amyloid-β peptide for inducing mitochondrial toxicity, we show that the influence of dimebon on the calcium retention capacity (CRC) of mitochondria depends on the mode of calcium addition. No obvious influence of dimebon on CRC was observed under the conditions of calcium infusion in the pump mode but the increase of CRC of rat brain mitochondria was observed when calcium was added in the bolus mode; the addition of calcium in the single pulse mode led to the increase of the lag period of calcium efflux from mitochondria. From these studies it is shown that dimebon is effective against amyloid-β (Aβ ) potentiated mitochondrial swelling and decrease of calcium retention capacity (CRC) of the brain mitochondria.


Alzheimer disease, brain and liver mitochondria, calcium retention capacity, dimebon, mitochondrial permeability transition (MPT).

Purchase Online Order Reprints Order Eprints Rights and Permissions

Article Details

Volume: 11
Issue Number: 5
First Page: 422
Last Page: 429
Page Count: 8
DOI: 10.2174/1567205011666140505094808
Price: $58
Global Biotechnology Congress 2017Drug Discovery and Therapy World Congress 2017

Related Journals

Related eBooks

Webmaster Contact: urooj@benthamscience.org Copyright © 2017 Bentham Science