Scientists are still not entirely sure what causes Alzheimer's Disease, or how to best prevent (or even delay) its onset. Effectively treating Alzheimer's has proven to be an even more elusive goal. But there is mounting evidence to suggest that exercise could play a crucial role in prevention, delay, and treatment of the disease.
Alzheimher's is the most common form of dementia and effects 26.6 million people worldwide (based on 2006 data). The degenerative disease causes brain cell death that leads to long-term memory loss, confusion, irritability, mood swings, trouble with language and, as bodily functions are lost, death. We all lose a certain amount of brain cells as we age, but the loss is greatly accelerated in Alzheimer's patients.
Though the mechanisms that cause this drastic acceleration is not well understood, a number of factors have been correlated with Alzheimer's:
- An increase of protein fragment clusters. Called amyloid plaques, protein fragment clusters gather amid brain cells, along with tangled "strands" of another protein that begin to appear inside brain cells. In oversimplified terms, the greater the plaques and tangles, the more severe the symptoms of dementia and Alzheimer's.
- A decrease in size of the hippocampus. The hippocampus, responsible for memory formation, organization, and storage, is the first part of the brain to be affected by Alzheimer's. A decrease in hippocampal volume is often present even before behavioral symptoms of the disease are present.
- A sedentary lifestyle. Whether life-long or "adopted" as aging makes exercise more difficult, a sedentary lifestyle is correlated with onset and progression of the disease.
- High blood pressure and diabetes. Both high blood pressure and diabetes contribute to the damage of brain cells. With high blood pressure, capillaries are destroyed, which restricts the flow of blood and nutrients to brain cells. Diabetes worsens blood pressure, exacerbating the issue.
In theory, decreasing any of the above correlated factors should help mitigate the effects (or even prevent onset) of the disease. So, how is exercise related to all this?
In some cases, the connection is obvious. A sedentary lifestyle (number three), for example, is no longer sedentary with the addition of regular exercise. Similarly, regular exercise decreases the likelihood of developing high blood pressure or diabetes.
Digging a bit deeper, researches have found that exercise can slow – and even prevent and/or reverse – the effects of the disease by increasing cognitive plasticity, which is the nervous system's ability to adapt to changes (such as brain injuries, lesions, and cell death) in order to maintain its functions. Cognitive plasticity is often a function of neurons rerouting existing – or creating new – synaptic connections. In this way, neurons unaffected (or even simply less affected) by the disease can compensate for more damaged neurons.
Specifically, exercise has been shown to:
- Increase growth of new capillaries in the brain, which leads to increased blood flow. Normal aging is associated with a reduced resting cerebral blood flow, while increased blood flow to the hippocampus is associated with increased memory retention in adults.
- Increase brain-derived neurotrophic factors (BNDF), a protein that aids the survival, development, and function of neurons. Normal age-related decreases in the volume of BNDF are associated with the decline in hippocampal volume and memory loss. Studies show that aerobic exercise in aging adults increases BNDF levels, which increases cell proliferation in the hippocampus. It also improves spatial memory and the plasticity of brain networks.
- Increase beta-endorphin production. Beta-endorphins are required for hippocampal neurogenesis (the generation of neurons from neural stem cells) during exercise. Normal circulating levels of beta-endorphins are extremely low, but exercise significantly increases their production and volume in circulating blood.
- Increase the length and number of dendritic (the branch-like protrusions of a cell that transmit nerve impulses) connections, which leads to increased plasticity.
- Increase brain uptake of insulin-like growth factor (IGF-1), which is believed to mediate the response to exercise on BDNF, neurogenesis, and cognitive performance.
- Deplete beta-amyloid load (in animal studies). Beta-amyloids are the primary component of amyloid plaques associated with Alzheimer's disease. In human studies, exercise has been shown to decrease PiB uptake - which suggests decreased amyloid plaque deposits (PiB is a compound that is retained only in areas of the brain with significant amyloid deposits).
- Decrease neuroinflammation (a chronic inflammation-like glial response in the central nervous system). Neuroinflammation can cause defective tau proteins that result in the brain cell protein "tangles" that are a hallmark of Alzheimer's disease.
These findings hold true even in people who are genetically predisposed to Alzheimer's!
So, what's the right type and amount of exercise to combat Alzheimer's? Once again: scientists don't know for certain. In older adults, a 10-year history of physical training (30 minutes of moderate exercise 5 days/week) was significantly associated with a lower risk of Alzheimer's. But other studies have shown impressive results from shorter exercise programs (less than 30 minutes or fewer than five days a week), and shorter duration (even just a few months). In nearly all cases, results were most pronounced with aerobic exercise, specifically.
But don't let the lack of an established "sweet spot" stop you, and don't feel like you need to join a gym. Start by taking a brisk 20-minute walk several days a week. While there are many uncertainties (and complete unknowns) in the battle against Alzheimer's, one thing is clearly established: exercise is your brain's armor.
So get moving!