Current pharmacological interventions for Alzheimer's disease temporarily alleviate the symptoms but do not prevent the disease or its progression. However, a therapy has been discovered that can prevent or delay the onset of Alzheimer's disease and also slow its progression. That therapy is exercise.
A number of epidemiological studies provide evidence for this conclusion. A study in the March 2001 issue of Archives of Neurology, led by Danielle Laurin, found that high levels of physical activity were associated with lower risks of cognitive impairment, Alzheimer disease, and dementia of any type compared with no exercise. In a study published in the Proceedings of the National Academy of the Sciences on March 13, 2001, Robert Friedland and his team found that people who engaged in mentally and physically challenging activities such as reading, walking, gardening, or jogging between young adulthood and middle adulthood reduced their probability of getting Alzheimer's by four times compared to those who did not engage in such activities.
A study presented at the annual meeting of the American Academy of Neurology on April 16, 2008, found that moderate physical exercise between the ages of 50 and 65 was associated with a reduced risk of cognitive impairment. The lead investigator, Dr. Yonas Endale Geda, said that the study did not address how physical exercise may protect against mild cognitive impairment but speculated that exercise might produce chemicals that protect brain cells.
In the July 15, 2008, issue of Neurology, a study led by Dr. Jeffrey Burns found that individuals with Alzheimer's who were less physically fit had quadruple the amount of brain shrinkage compared to normal older adults and that increased cardiorespiratory fitness is associated with reduced brain atrophy in Alzheimer's disease.
Studies With Mice Models of Alzheimer's Disease
A study in The Journal of Neuroscience, April 27, 2005, led by Paul A. Adlard, provided evidence for how physical exercise may protect against Alzheimer's. In this study, a mouse model of Alzheimer's disease was used to examine directly the interaction between exercise and the changes in the brain that occur in the disease. The main marker in the brain for Alzheimer's disease is the existence of amyloid beta-protein plaques. Five months of voluntary exercise resulted in a decrease in amyloid beta-protein plaques in the brains of this Alzheimer's disease mouse model. This reduction was present in both the cortex and hippocampus regions of the brain that are involved in learning and memory. Pharmacological interventions have sought to reduce amyloid beta-protein plaques in Alzheimer's. This study demonstrates that exercise is a simple behavioral intervention sufficient to inhibit the normal progression of Alzheimer's neuropathology in a mouse model of the disease.
Another study with mice was done by William H. Thies, Ph.D., the Alzheimer's Association vice president of medical and scientific affairs. He reported in the Journal of Neuroscience (Thies, 2005) that mice who were given access to a running wheel after reaching old age did better at remembering their way through a maze than those who were not given access to a wheel. He also found that the mice who exercised developed more new brain cells than those mice that were sedentary. He found that the new brain cells that were developed did not differ from those in younger mice. His findings are important because they are evidence that it is never too late to start exercising and that even starting exercise in late adulthood may improve cognition.
Mary Lou Williams, M. Ed., is a writer and lecturer in the field of nutrition. She welcomes inquiries. She can be reached at 267-6480.