Neurobiological role and therapeutic potential of exercise-induced irisin in Alzheimer's disease management

Abstract

Alzheimer's disease (AD) poses a significant obstacle in today's healthcare landscape, with limited effective treatments. Recent studies have revealed encouraging findings about how exercise-triggered irisin might help slow down the advancement of AD. Irisin, a myokine, released during physical activity, has garnered significant attention for its pleiotropic effects, extending beyond its traditional role in metabolic regulation. This review explores irisin's multifaceted potential in combating AD. Research indicates that irisin enhances synaptic plasticity, crucial for learning and memory, and exhibits neuroprotective properties that may slow AD progression by safeguarding neurons from degeneration. Additionally, irisin's ability to modulate inflammatory responses is significant, as neuroinflammation is a key feature of AD pathology. Irisin may also influence the metabolism and clearance of amyloid-beta plaques and tau tangles, hallmark pathological markers of AD. Furthermore, irisin boosts brain-derived neurotrophic factor expression, vital for neuronal health, and improves insulin glucose regulation, addressing impaired brain insulin signaling observed in AD. Exercise-induced irisin presents a non-pharmacological strategy, leveraging physical activity’s brain health benefits. Future research should focus on elucidating irisin’s mechanisms and conducting clinical trials to assess its therapeutic efficacy and safety in AD patients. Overall, irisin therapy offers a promising avenue for AD treatment, potentially slowing disease progression and enhancing cognitive function, paving the way for innovative therapeutic strategies in the fight against AD.