The principal mental disorders affecting late life are dementias such as Alzheimer disease (AD) and the primary mood disorder, depression. In addition to cognitive falloff, some of the most common symptoms in the dementing and neurodegenerative diseases are depressed mood, apathy and anxiety. There is overlap between these symptoms and those seen in depression. Loss of neurons and nerve cell connections is characteristically seen in AD. Many investigators have theorized that neuronal atrophy and death in these disorders results, in part, from a lack of of trophic support. For healthy existence, cells in every location in the body depend on chemicals called trophic factors that protect them and allow them to function optimally. In the brain, neurotrophins are the compounds neurons rely on for this cellular support. The primary one is called BDNF (Brain-Derived Neurotrophic Factor). BDNF is present in the highest concentrations in the hippocampus, a brain region with vital functions in both learning and memory.

Hippocampal BDNF levels fall in response to stress.  Stress plays a key role in the development of depression and other psychiatric illnesses. Shrinkage of the hippocampus associated with nerve cell loss and atrophy has been observed in animals exposed to chronic stress. These animals manifest behavioral alterations associated with a depressive state. Consistent with these observations is the fact that humans with a history of chronic, recurrent depression, or post-traumatic stress disorder have shown significant hippocampal atrophy (shrinkage) in brain imaging studies.

One approach used in treating depressive symptoms is the administration of antidepressant medication. Recent evidence suggests that these drugs produce a downstream elevation of BDNF in association with their mood elevating properties. In this context, it is interesting to note that current research studies provide evidence that our daily behavior and lifestyle choices influence the level of BDNF expression in the brain. Exercise and participation in an enlightened environment are often linked with up-regulation of synthesis of this important neurotrophin. They also modulate neurogenesis, or production of new nerve cells within the hippocampus.

The ability of exercise to improve the psychiatric status of depressed patients has been observed for some time. As has already been discussed in previous posts, physical activity upregulates the production of BDNF. This suggests that exercise and antidepressant therapy activate similar molecular pathways in the brain. 

Three recent articles have assessed the effects of exercise on patients with major depressive illness. Several conclusions can be made from these studies. One, that exercise improves the symptoms of depression. Second, exercise improves the outcome in patients being treated with antidepressants. Third, moderate intensity exercise is more effective than low intensity exercise in alleviation of depressive symptoms.

Another significant observation regarding the impact of exercise on depressive symptomatology is that its antidepressant effects endure after the period of exercise is terminated. Effects of depression on executive function are exceedingly problematic for many depressed patients. Exercise has been shown to improve reaction times and other parameters of executive function.

There are very few downsides to exercising. It is good for prevention of obesity, blood pressure control, improvement of cardiovascular risk profile and now it is known to be beneficial for mental health and cognition.