You are viewing a javascript disabled version of the site. Please enable Javascript for this site to function properly.
Go to headerGo to navigationGo to searchGo to contentsGo to footer
In content section. Select this link to jump to navigation

Alzheimer's Disease-Like Pathology in Senescence-Accelerated OXYS Rats can be Partially Retarded with Mitochondria-Targeted Antioxidant SkQ1

Article type: Research Article

Authors: Stefanova, Natalia A.a; * | Muraleva, Natalia A.a | Skulachev, Vladimir P.b; c | Kolosova, Nataliya G.a; b

Affiliations: [a] Institute of Cytology and Genetics, Novosibirsk, Russia | [b] Institute of Mitoengineering, Moscow, Russia | [c] Belozersky Institute of Physico-Chemical Biology and Faculty of Bioengineering and Bioinformatics, Lomonosov Moscow State University, Moscow, Russia

Correspondence: [*] Correspondence to: Natalia A. Stefanova, Institute of Cytology and Genetics, Prospekt Lavrentyeva 10, 630090 Novosibirsk, Russia. Tel.: +7 383 363 49 80; Fax: +7 383 333 12 78; E-mail: [email protected].

Keywords: Alzheimer's disease, brain aging, mitochondria-targeted antioxidant SkQ1, senescence-accelerated OXYS rats

DOI: 10.3233/JAD-131034

Journal: Journal of Alzheimer's Disease, vol. 38, no. 3, pp. 681-694, 2014

Accepted 3 August 2013
|
Published: 25 November 2013
Get PDF open access

Abstract

We previously showed that mitochondria-targeted antioxidant SkQ1 (plastoquinonyl-decyltriphenylphosphonium) at nanomolar concentrations is capable of preventing and slowing down some cerebral dysfunctions in accelerated-senescence OXYS rats. Here we demonstrate that OXYS rats develop behavior, learning, and memory deficits against a background of neurodegeneration signs detected by magnetic resonance tomography and amyloid-β (Aβ) pathology similar to those seen in Alzheimer's disease (AD). Long-term treatment with SkQ1 (250 nmol/kg body weight daily from the age of 1.5 to 23 months) reduced the age-related alterations in behavior and spatial memory deficit in Morris water maze in OXYS and Wistar rats. Furthermore, this is the first report that SkQ1 treatment slows down pathological accumulation of AβPP, Aβ, and hyperphosphorylation of tau-protein in OXYS rats, as well as age-dependent changes in healthy Wistar rats. Our results support the possibility of using the OXYS strain as a rat model of AD-like pathology. It seems probable that the mitochondria-targeted antioxidant SkQ1 can be a good prophylactic strategy to maintain brain health and to treat AD.

Show more