Regular Exercise Slows Cognitive Decline and Age-Related Damage to the Brain

Maintaining fitness through the practice of regular exercise improves health in old age, slowing the pace of damage to the brain and consequent cognitive decline. While there is largely only correlational data in humans to show a link between exercise and a slower pace of neurodegeneration, many animal studies make it clear that exercise causes an improved trajectory for health in later life. It does not extend overall life span in mice, as is the case for calorie restriction, but is otherwise very effective for an intervention that is essentially free.

This beneficial outcome is likely due to a combination of overlapping mechanisms, and it is presently hard to say which of those mechanisms are more important. Exercise upregulates cellular maintenance processes such as autophagy, and it is well demonstrated in animal studies that more autophagy improves long term health. Exercise also reduces chronic inflammation, and, when present, that inflammation drives a more rapid progression of all of the common age-related conditions. Fitter people tend to carry less visceral fat tissue, and excess visceral fat accelerates the pace of aging through a more rapid creation of senescent cells, as well as other processes that increase chronic inflammation. Fitter people also exhibit better cardiovascular function and lesser degrees of age-related hypertension, both of which are important when it comes to avoiding structural damage and functional decline in brain tissue.

Researchers examined 317 participants enrolled in the Wisconsin Registry for Alzheimer's Prevention, an ongoing observational study of more than 1,500 people with a history of parents with probable Alzheimer's dementia. Registrants were cognitively healthy and between the ages of 40 and 65 years at the time of enrollment. Participation in the registry included an initial assessment of biological, health and lifestyle factors associated with the disease and follow-up assessments every two to four years.

All participants completed a questionnaire about their physical activity and underwent neuropsychological testing and brain scans to measure several biomarkers associated with Alzheimer's disease. The researchers compared data from individuals younger than 60 years with older adults and found a decrease in cognitive abilities as well as an increase in biomarkers associated with the disease in the older individuals. However, the effects were significantly weaker in older adults who reported engaging in the equivalent of at least 30 minutes of moderate exercise five days a week.

In another study, researchers studied 95 people, also from the registry, who were given scores called polygenic risk scores, based on whether they possessed certain genetic variants associated with Alzheimer's. Similar to the previous research, the researchers also looked at how biomarkers changed with genetic risk and what role, if any, aerobic fitness might play. Not surprisingly, people with higher risk scores also showed increased biomarkers for the disease. Again, the researchers found that the effect was weaker in people with greater aerobic fitness, a score incorporating age, sex, body mass index, resting heart rate, and self-reported physical activity.

A third study examined MRIs from 107 individuals from the registry who were asked to run on a treadmill to determine their oxygen uptake efficiency slope, a measure of aerobic fitness. In line with previous studies, the researchers again found that an indicator of Alzheimer's disease, known as white matter hyperintensities, significantly increased in the brain with age, but not so much in participants with high levels of aerobic fitness.