Understanding the Molecular Impact of Physical Exercise on Alzheimer's Disease

Alzheimer's disease is one of the most common neurodegenerative diseases, characterized by a wide range of neurological symptoms that begin with personality changes and psychiatric symptoms, progress to mild cognitive impairment, and eventually lead to dementia. Physical exercise is part of the non-pharmacological treatments used in Alzheimer's disease, as it has been shown to delay the neurodegenerative process by improving the redox state in brain tissue, providing anti-inflammatory effects or stimulating the release of the brain-derived neurotrophic factor that enhances the brain structure and cognitive performance. Here, we reviewed the results obtained from studies conducted in both animal models and human subjects to comprehend how physical exercise interventions can exert changes in the molecular mechanisms underlying the pathophysiological processes in Alzheimer's disease: amyloid β-peptide pathology, tau pathology, neuroglial changes, mitochondrial dysfunction, and oxidative stress. Physical exercise seems to have a protective effect against Alzheimer's disease, since it has been shown to induce positive changes in some of the biomarkers related to the pathophysiological processes of the disease. However, additional studies in humans are necessary to address the current lack of conclusive evidence.