Editorial: Brain adaptations to exercise in health and neurodegenerative diseases: considerations and future perspectives on the underlying mechanisms

Physical exercise is known to have numerous benefits for the central nervous system (CNS), improving cognitive function and counteracting the onset and progression of neurodegenerative diseases. However, the molecular mechanisms underlying these positive effects have not been fully elucidated, highlighting the need for further research in the field of exercise physiology [1].The available evidence suggests a multi-pathway effect of exercise, capable of influencing neuronal redox status, neurotrophic factor synthesis, neurogenesis, synaptic transmission and plasticity, as well as cerebral blood flow and oxygenation [2-4]. Particularly, Xu et al. investigated the role of physical exercise in modulating the mitochondrial mechanisms involved in the pathogenesis of Parkinson's disease, highlighting how alterations in mitochondrial biogenesis, mitophagy and neuronal redox balance contribute to the degeneration of dopaminergic neurons. Specifically, exercise appears to restore mitochondrial homeostasis by regulating the production of reactive oxygen species (ROS), activating neuroprotective exerkine-mediated signals and increasing the expression of neurotrophic factors, supporting its potential as a complementary non-pharmacological intervention in the management of the disease [5]. These observations are consistent with previous studies that have shown that exercise stimulates the production of neurotrophins, key molecules in protecting neurons and counteracting neurodegenerative processes [6,7]. Among the exercise-induced neurotrophins, brain-derived neurotrophic factor (BDNF) has attracted considerable interest both for its role in neuronal survival and for its involvement in depressive disorders. In this regard, the systematic review with meta-analysis by Fang