Exercise encourages the brain to work at optimum capacity, causing nerve cells to multiply, strengthening the neurons interconnections, and protecting them from damage associated with Alzheimer’s Disease (AD). Exercise can also help diseased and damaged nerves.
Exercising causes nerve cells to release proteins called neurotrophic factors. One in particular, brain-derived neurotrophic factor (BDNF), triggers numerous other chemicals that promote neural health. Simply adding BDNF to neurons in a lab causes them to grow, sprout branches, and extend rapidly. BDNF has been shown to have direct benefits on brain functions, including repairing neural illnesses like AD.
Other studies have found that exercise can delay the onset of AD. A 2006 study in Seattle monitored 1,740 persons 65 and older without cognitive impairment for 6 years. At the end of the study, it was determined that 107 participants had developed AD and 158 dementia.
The incidence rate for developing dementia was 13.0 per 1,000 person-years for participants who exercised 3 or more times per week compared with 19.7 per 1,000 person-years for those who exercised fewer than 3 times per week. Similar results were observed in analyses pertaining to the participants with AD. The investigators concluded that “These results suggest that regular exercise is associated with a delay in onset of dementia and AD, further supporting its value for elderly persons.”
In a study at the University of Illinois, magnetic resonance imaging (MRI) showed that aerobic fitness reduces brain tissue loss in aging humans. The researchers used MRI to demonstrate that aging correlates with it a loss of both gray and white matter in multiple areas of the brain, especially in areas associated with cognitive functions. Researchers demonstrated that cardiovascular fitness protected against the loss of brain tissue. The areas most protected by aerobic fitness are those that play central roles in successful everyday functioning.