Efeitos do treinamento físico e cognitivo nos déficits de memória relacionados a neurotoxicidade induzida pela proteína beta-amiloide

Abstract

Alzheimer’s disease (AD) is the biggest cause of dementia, accounting for 50%–75% of dementia cases in the world. 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. Currently, an AD has no cure and treatment is limited. Researches focused on non-pharmacological treatment have been developed with the aim to act in brain plasticity and to minimize the neurotoxicity caused by Aβ peptide. Considering that physical exercise neuroprotective effects on the prevention of cognitive deficits are well elucidated, it is important to clarify the effects of cognitive training. Our hypothesis is that cognitive exercise has preventive and therapeutic effects similar or comparable effects to those observed in physical exercise, considering that it can promote the plasticity stimulation. The regular practice of physical exercise is a consolidated strategy on the prevention of cognitive deficits; however, little is known about the effects of acute exercise on memory. We hypothesize that one physical exercise session could act as a modulator of learning. So, our other hypothesis is that one single session of physical exercise performed after learning can modulate learning, improving consolidation of memory, even in deficits situation. To test these hypothesis, using an animal model Aβ-induced neurotoxicity, the present study shows that the physical and cognitive exercise are strategies able to prevent and to reverse the recognition memory deficits, to decrease the hippocampal ROS levels and lipid peroxidation, to restore the acetylcholinesterase activity in the hippocampus, parameters altered by Aβ-induced neurotoxicity. In addition, physical and cognitive training were able to reorganize, at least in part, the hippocampal morphological organization. In our third study, we demonstrated that one physical exercise session, performed after learning is able to improve recognition memory persistence in control rats and the memory consolidation in animals with cognitive deficit related to amyloid-β neurotoxicity. We verified that between the mechanisms involved in the effects of acute exercise on memory is the dopaminergic syst em activation. Based on our findings, we can conclude that cognitive exercise is as good as physical exercise as prevention and therapy for memory deficits related to Aβ-induced neurotoxicity, which act through oxidative balance. It is still possible to conclude that acute exercise is an effective strategy as a learning modulator, promoting memory consolidation in animals with cognitive deficits. More studies are necessary to investigate additional mechanisms that can help explain: (i) additional mechanisms to explain the effects of cognitive exercise; (ii) its effects on memory persistence; and, (iii) its effects in other experimental models related to AD. It is also important to investigate other mechanisms that may be involved in the benefits of acute exercise and to investigate whether the association of physical and cognitive exercise could enhance the effects observed in individual therapies.