Physical and cognitive training are able to prevent recognition memory deficits related to amyloid beta neurotoxicity

Abstract Alzheimer's disease (AD) is characterized by the presence of amyloid-β (Aβ), oxidative damage and neuronal degeneration, which, together with other pathological events, promote progressive memory loss and cognitive decline. Non-pharmacological strategies have been study to provide some protection against the development of AD. Considering that physical exercise neuroprotective effects on prevention of cognitive deficits are well elucidate, it is important clarify the effects of cognitive training, and verify if they are similar or comparable to those observed for physical exercise. Here we divided male adult Wistar rats in six groups: control, which rats were not submitted to any intervention; Aβ, which rats were submitted to hippocampal infusion of Aβ; physical exercise (PE), which rats were submitted to 4 weeks of PE training; PE + Aβ, which rats were submitted to 4 weeks of PE training followed by hippocampal infusion of Aβ; cognitive exercise (CE), which rats were submitted to 4 weeks of CE training; and, CE + Aβ, which rats were submitted to 4 weeks of CE training followed by hippocampal infusion of Aβ. Ten days after Aβ infusion, short (STM) and long-term (LTM) object recognition memory, as well as hippocampal oxidative stress (ROS levels by DCFH test), lipid peroxidation (TBARS), total antioxidant capacity (FRAP) and hippocampal histology were evaluated. Both PE and CE were effective in protect cognitive function against memory deficits related to Aβ neurotoxicity, preventing oxidative stress and damage and hippocampal cellular disorganization. So, cognitive training seems to be as good as physical training in the prevention of memory deficits related to Aβ and seems to share some mechanisms of actions, as oxidative stress prevention.