In addition to keeping the brain’s lobes healthier and more intact, physical exercise can act directly on the brain’s molecular machinery. There is increasing recognition that physical activity can help relieve the effects of deterioration of nerve cell function. Numerous scientific studies with animals have reported that voluntary exercise leads to an increase in production of Brain-Derived Neurotrophic Factor (BDNF). This is a kind of protein that aids in the growth and survival of nerve cells during development, and in the maintenance of adult nerve cells. Because BDNF has both neurotrophic and neuroprotective properties, it is able to significantly influence brain plasticity. (For more information on BDNF, click here.)
HD invariably leads to decreased levels of BDNF, leaving nerve cells more vulnerable and prone to injury or death. In people without HD who have the normal huntingtin protein, the huntingtin protein indirectly activates the promoter, or the "on" switch, of the gene that encodes BDNF. When this gene is turned on, it prompts nerve cells to make more BDNF. In people who have HD, mutant huntingtin indirectly inactivates the "on" switch so that BDNF can no longer be produced. In the absence of BDNF, the cell’s ability to survive is markedly decreased.
Currently, scientists are looking for ways to harness neurotrophic factors such as BDNF so they can be administered to patients. This treatment would theoretically improve the symptoms of people with neurological disorders because it would dramatically improve the health and survival of the person’s nerve cells. Animal studies and in vitro models both indicate that BDNF is capable of making damaged nerve cells regrow. Because of this capability, BDNF represents an exciting possibility for reversing brain disorders, such as HD. The fascinating part of BDNF is that the protein can naturally be increased through exercise. In one rat study, several days of voluntary wheel-running increased levels of BDNF. The changes in BDNF levels were found in nerve cells within days in both male and female rats and were sustained for several weeks after exercise.
In particular, running activity increases levels of BDNF in the lumbar spinal cord, cerebellum, and cortex, but not in the striatum. Since the main site of neurodegeneration in people with HD is the striatum, exercise alone will likely not be able to prevent many of the symptoms of the disease. However, exercise can help preserve cognitive function and promote the general health of the brain, as well as the general health of the body overall. Although exercise may not be able to promote neurogenesis (the growth of nerve cells) in the striatum, it may promote neurogenesis in other areas of the brain and body by increasing the vitality of nerve cells. These changes may be enough to delay the onset and progression of various HD symptoms.
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Last Modified: 05/22/2009
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