EXERKINES PREVENTED EFFECT ON NEUROINFLAMMATION INDUCED BY Aβ OLIGOMERS IN A PRECLINICAL MODEL OF ALZHEIMER`S DISEASE

Alzheimer`s disease (AD) is a neurodegenerative disorder characterized by deposits of soluble amyloid-β oligomers (AβO) and plaques, neuroinflammation, and cognitive decline affecting about 50 million people worldwide. Currently, there is no effective treatment for AD and notable efforts are aimed at developing strategies to counteract the mechanisms leading to the development of the disease. Evidence suggests that physical exercise (PE) can reduce the risk of developing AD or attenuate its progression; however, the molecular mechanisms that underlie its beneficial effects remain poorly understood. An increasing number of exercise-associated signaling molecules with potential roles in improving brain functions have been identified in the last few years. Irisin has been described as an important myokine capable of mediating the beneficial effects of PE on synaptic plasticity and memory in animal models of AD. Additionally, growing evidence points out that irisin promotes an increase in osteocalcin release by osteoblasts. This osteokine plays a pivotal role in the central nervous system and has been recognized as an anti-gerontic hormone that could prevent age-related cognitive decline. Despite recent findings showing the potential neuroprotective effects of irisin and osteocalcin, the role of these exerkines on neuroinflammation involved in the neurodegenerative process of AD remains to be determined.