Erschienen in:
01.08.2013 | Original Article
Neuroprotective Effect of Physical Exercise in a Mouse Model of Alzheimer’s Disease Induced by β-Amyloid1–40 Peptide
verfasst von:
Leandro C. Souza, Carlos B. Filho, André T. R. Goes, Lucian Del Fabbro, Marcelo G. de Gomes, Lucielli Savegnago, Mauro Schneider Oliveira, Cristiano R. Jesse
Erschienen in:
Neurotoxicity Research
|
Ausgabe 2/2013
Einloggen, um Zugang zu erhalten
Abstract
This study was designed to investigate the potential neuroprotective effect of exercise in a mouse model of Alzheimer’s disease (AD) induced by intracerebroventricular (i.c.v.) injection of beta-amyloid1–40 (Aβ1–40) peptide. For this aim, male Swiss Albino mice were submitted to swimming training (ST) with progressive increase in intensity and duration for 8 weeks before Aβ1–40 administration (400 pmol/animal; 3 μl/site, i.c.v. route). The cognitive behavioral, oxidative stress, and neuroinflammatory markers in hippocampus and prefrontal cortex of mice were assessed 7 days after Aβ1–40 administration. Our results demonstrated that ST was effective in preventing impairment in short- and long-term memories in the object recognition test. ST attenuated the increased levels of reactive species and decreased non-protein thiol levels in hippocampus and prefrontal cortex induced by Aβ1–40. Also, Aβ1–40 inhibited superoxide dismutase activity and increased glutathione peroxidase, glutathione reductase, and glutathione S-transferase activities in hippocampus and prefrontal cortex—alterations that were mitigated by ST. In addition, ST was effective against the increase of tumor necrosis factor-alpha and interleukin-1 beta levels and the decrease of interleukin-10 levels in hippocampus and prefrontal cortex. This study confirmed the hypothesis that exercise is able to protect against some mechanisms of Aβ1–40-induced neurotoxicity. In conclusion, we suggest that exercise can prevent the cognitive decline, oxidative stress, and neuroinflammation induced by Aβ1–40 in mice supporting the hypothesis that exercise can be used as a non-pharmacological tool to reduce the symptoms of AD.