The effect of exercise on hippocampal integrity: review of recent research

To review salient basic research regarding physical exercise as a major protective factor against hippocampal degradation and to emphasize its relevance to humans.

Recent mammalian and human research literature search and theoretical discussion.

The cascade of cellular damages from oxidative stress, nitrosative stress and gluco-corticoid effects are cumulative and age related. Exercise training reduces oxidative stress, nitro-sative stress and improves neuroendocrine autoregulation which counteracts damages from stress- and age-related neuronal degeneration, brain ischemia and traumatic brain injury. Conversely, lack of exercise and motility restrictions are associated with increased vulnerability from oxidative stress, nitrosative stress and glucocorticoid excesses, all of which precede amyloid deposition and are fundamental in the cascade of events resulting in neuronal degradation, especially in the hippocampi.

Despite the paucity of human research, basic animal models and clinical data overwhelmingly support the notion that exercise treatment is a major protective factor against neurodegeneration of varied etiologies. The final common pathway of degradation is clearly related to oxidative stress, nitrosative stress, glucocorticoid dysregulation, inflammation and amyloid deposition. We conclude that people prone to chronic distress, brain ischemia, brain trauma, and the aged are at increased risk for neurodegenerative diseases such as Alzheimer's. Exercise training may be a major protective factor but without clinical guidelines, its prescription and success with treatment adherence remain elusive.