Alzheimer's Disease and Physical Fitness

I remember the day my grandfather died. His brain shriveled to the size of an apple, and apple with millions of microscopic holes. His body forgot how to breath, and then he died. Alzheimer's is the most common form of dementia in elderly people. Three genes have been identified that cause early onset: amyloid precursor (APP), being a protein gene on chromosome 21. The presenililin 1 (PSEN!) gene on chromosome 14 and the presenilin 2 gene (PSEN2) on chromosome 1. More than fifty percent of late-onset and related apoliprprotein E affect risk and age of onset of this disease. 

I am studying NSCA (Studying for the National Strength and Conditioning Association) personal trainer examination. One topic peaked my attention - Biological mechanisms, neurotropic factors of exercise. This topic caught my attention because my paternal grandfather died of Alzheimer’s disease. Alzheimer’s disease is a terrible way to die, and it also has an undeniable genetic component. Simply put – there is a very good chance me, my brother and my father will get it.

There are some things we know offset Alzheimer’s. Do mentally challenging activities, take a class at a community college, learn a new language, and challenge your mind to do new and different things. The worst thing a person with a genetic predisposition can do is become mentally lazy.

This essay is meaty, as you are reading it and thinking about the brain, remember the frontal lobe is the last region of the brain to mature and the first to show the effects of advanced age. When alzheimer’s hits – it hits the frontal lobe first, then all the other regions that control motor functions, heart rate, and breathing. The frontal lobe is responsible for the executive processes involved in working memory and the coordination of complex attention functions as well as the inhibition and control of behavior. The frontal lobe is most affected by neurobiological changes of exercise.

There is also a connecting between those who are not physically fit and developing alzheimer's. One postulate is that physical fitness decreases the decline in cerebral blood flow. (note: depending on the exercise, we are not saying fitness increases cerebral blood flow, it simply decrease the decline of cerebral blood flow). A decline in cerebral blood flow is a normal part of aging. Physical exercise has an angiogenic effect – it increases the formation of new blood vessels. Direct evidence for this came from a study of older adults and retirees who differed in their levels of physical activity. [Rogers, R.L.,J.A. Meyer, and K.F. Mortel. 1990]

The retirees who were more active showed both superior cognitive functioning and increased perfusion of the cerebral cortex. Such an exercise-induced change would help to deliver oxygen and nutrients to the neural tissue and thereby support the neural process underlying behavior.

Simply put – you want more blood to flow in your brain.

In addition to causing vascular changes, exercise leads to an increase in the expression of genes that code for neurotropic factors (agents that preserve and nourish brain tissue). An animal study demonstrated that brain-derived neurotrohic factor (BDNF) increased in rats that engaged in voluntary wheel-running to those that were sedentary. Brain-derived neurotropic factor effectively promotes the health of neurons or brain cells and the creation of new synapse or connections between neurons, thus increasing the thickness and integrity of brain tissue. Researchers found increase in BDNF expression in the rat hippocampus, a structure in the brain that is integrally involved in long-term or episodic memory-related processes. In light of such powerful neurobiological influences in animals, it seems likely that similar changes could occur in humans and contribute to the higher cognitive functioning seen in older physically fit participants.

In support of this possibility, researchers reported a positive relationship between aerobic capacity, as measured by VO2 max, and brain tissue density in several regions of the cerebral cortex (grey matter) as well as the white matter tracks, which allow for communication between various brain regions.

Older adults who had greater cardiovascular fitness exhibit denser tissue and reduced age-related decline in critical brain regions such as the prefrontal cortex that underlies executive functioning and reasoning. Importantly, the frontal brain region shows the greatest rate of decline in normal or nondemented aging, and fitness appears to be an effective antedote.

So far, we know exercise improves vascular changes in older adults, it improved BDNF in older adults and slows the aging of the brain. These benefits in combination contribute to a phenomena called Cognitive Reserve. Cognitive Reserve the resistance to age-related decline and pathology associated with forms of dementia like Alzheimer’s disease (forms of plaques and tangles), particularly in the hippocampa region. This resilience to decline or ability to tolerate neurodegenerative process is based on the passive reserve or the biological integrity of the brain (for example, thickness of brain tissue and preservation of vasculature), as well as active reserve or the strategic activation of neural processes to compensate for networks suffering from age-related decline and pathology. Importantly, it appears that exercise may maintain the youthfulness of the brain and the mind by contributing to passive due to neurotrophic and angiogenic effects.

So let’s recap what we learned. Exercise increases brain vascularity which increases oxygen and nutrient exchange in the brain. Exercise increases the expressiom pf agents that preserve and nourish brain tissue – BDNF. Increase brain vascularity, increases oxygen, which increases, nutrient exchange, and increase BDNF exposure. This will not stop Alzheimer’s from killing us, but it delays the onset of Alzheimers by many years. Simply put, if a person combines regular cardiovascular exercise with a diet rich in fatty acids, and lots of cognitive stimulation, they can expect to dely Alsheimers by up to a decade.