Abstract

Physical activity has been correlated with a reduced incidence of cognitive decline and Alzheimers disease in human populations. Although data from intervention-based randomized trials is scarce, there is some indication that exercise may confer protection against age-related deficits in cognitive function. Data from animal models suggests that exercise, in the form of voluntary wheel running, is associated with reduced amyloid deposition and enhanced clearance of amyloid beta, the major constituent of plaques in Alzheimers disease. Treadmill exercise has also been shown to ameliorate the accumulation of phosphorylated tau, an essential component of neurofibrillary tangles in Alzheimers models. A common therapeutic theme arising from studies of exercise-induced neuroprotection in human populations and in animal models involves reduced inflammation in the central nervous system. In this respect, physical activity may promote neuronal resilience by reducing inflammation.

Keywords: Exercise, running, hippocampus, inflammation, Alzheimer's disease, Aging population, Cardiorespiratory fitness, neurotrophic factor, neuronal dendrites, cholesterol levels