of exercise. Obesity. 2006;14:345-356. Voluntary physical activity and exercise training can favorably influence brain plasticity by facilitating neurogenerative, neuroadaptive, and neuroprotective processes. At least some of the processes are mediated by neurotrophic factors. Motor skill training and regular exercise enhance executive functions of cognition and some types of learning, including motor learning in the spinal cord. These adaptations in the central nervous system have implications for the prevention and treatment of obesity, cancer, depression, the decline in cognition associated with aging, and neurological disorders such as Parkinson's disease, Alzheimer's dementia, ischemic stroke, and head and spinal cord injury. Chronic voluntary physical activity also attenuates neural responses to stress in brain circuits responsible for regulating peripheral sympathetic activity, suggesting constraint on sympathetic responses to stress that could plausibly contribute to reductions in clinical disorders such as hypertension, heart failure, oxidative stress, and suppression of immunity. Mechanisms explaining these adaptations are not as yet known, but metabolic and neurochemical pathways among skeletal muscle, the spinal cord, and the brain offer plausible, testable mechanisms that might help explain effects of physical activity and exercise on the central nervous system.

Physical activity and antidepressant treatment have each separately been of significant interest for the management of Alzheimer's disease (AD);In recent years, great strides have been made in understanding the regulation of growth factors at the molecular level. We report, for the first time, an apparent interaction between two distinct interventions, a pharmacological agent and a behavioral change, leading to a potentiation of brain-derived neurotrophic factor (BDNF) expression. As discussed below, this observation may have important applications to neurodegenerative/behavioral disorder treatment investigation and development.

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