Alzheimer’s Disease and Exercise
Cogs 163: Week 6
By: Nana Pearson
sLeptin is back at it again! Since our group presented this week about the role of myokines in exercise, we thought it would only be appropriate to revisit the topic of exercise and further highlight its importance in exercise’s therapeutic potentials in preventing a horribly enigmatic, neurodegenerative disease: Alzheimer’s Disease (AD).
This blog post will provide some interesting insight into how exercise can possibly serve as a preventative measure against Alzheimer’s Disease, as scientists are scrambling to find a cure for this horrible affliction.
It is common knowledge that exercise has a myriad of positive benefits. As a 24/7 stressed out college student, that is always struggling to keep afloat in a sea of assignments, tests, and seemingly never-ending stream of midterms, I always resort to exercise, even just a quick run on the treadmill, to blow off some steam. The rush of endorphins that I feel post-exercise is definitely one of the many tangible benefits of exercise in addition to maintaining and regulating your physical wellbeing. The benefits of exercise, however, extends far beyond that as it even potentially offers an avenue to stave off a neurodegenerative disease that doesn’t currently have a cure.
In the “Neurological Health” section of the Scientific American, an article titled “How Exercise Might “Clean” the Alzheimer’s Brain”, explored how the effects of exercise on the brain can shed light to potential therapeutic treatments of AD (Alzheimer’s Disease).
But first, let me explain what is going on in the brains of those who suffer from AD. If one picks up a microscope and analyzes the effects of AD on the brain, one will notice that AD will cause an accumulation of toxic nerve cell waste, in the form of amyloid plaques and neurofibrillary tangles.
The notorious formation and accumulation of these toxic amyloid plaques between neurons are one of the primary hallmarks of AD. “Amyloid” is just a general term for protein fragments that the body produces on its own. The amyloid specific to AD that gets tangled is called “Beta-Amyloid”. Beta-amyloid is a protein fragment that gets removed from an amyloid precursor protein (APP). In a normal, healthy brain these amyloids are broken down and removed from the brain, but in those suffering from AD, we see a buildup of them, resulting in the formation of insoluble, hard plaques.
The neurofibrillary tangles are another major hallmark of AD. In a normal healthy brain, the tau protein, which the tangles are primarily composed of, isn’t abnormal, and the microtubule, which the tau protein aids in forming a crucial part of its structure, isn’t structurally compromised. The microtubule is so important because it facilitates nerve cells to transport essential nutrients to one another.
These two forces together cause an array of problems for the brain such as severe cognitive decline including memory loss. So with that being said, we will now get to how exercise can create a very positive environment for our brain that can potentially lead to a therapeutic treatment for AD.
Though more research needs to be done on the exact mechanisms and role exercise can contribute to preventing AD, research has shown that exercise induces biochemical changes in the brain, creating an optimal environment for the restoration of nerve cell health. Moreover, exercise can help facilitate a restorative process called “adult hippocampal neurogenesis”, which enhances connectivity and nerve cell growth in the hippocampus.
Given this result through research, the researchers mentioned in the article sought to explore this finding further in their research. They discovered through mouse models of AD, that exercised mice exhibited greater memory capacity than sedentary ones (no exercise), as the brains displayed an increase in BDNF and improved adult hippocampal neurogenesis. BDNF, an exercise induced myokine that was discussed in our presentation, is a molecule that aids in promoting brain cell growth. Even more impressive was the researchers’ finding that with the combination of genetic (injection of a virus) and pharmacological measures/techniques, increasing both BDNF levels and hippocampal cell growth to restore brain function, primarily memory, in mice with AD without exercise is possible! Here, we can see the importance of exercise reflected here, as this finding couldn’t have been possible without the effects of exercise on the brain.
It should be noted, however, that we still don’t know the extent to how well these mice model results will translate into humans. There is still far more research that needs to be conducted to ensure a significant efficacy of these results in humans. Though AD and the therapeutic solutions to it are still shrouded in a lot of mystery, this hopeful finding will hopefully inspire researchers and scientists to further explore this option as a way to treat AD. Moreover, it will also hopefully inspire a lot more people to get outside or hit the gym to exercise as exercise stimulates the brain in highly positive ways as we explored earlier in this blog post.
Now everyone, get out there and start exercising!!
References:
“Amyloid Plaques and Neurofibrillary Tangles.” BrightFocus Foundation, 1 July 2015, www.brightfocus.org/alzheimers-disease/infographic/amyloid-plaques-and-neurofibrillary-tangles.
Grinstein, Jonathan D. “How Exercise Might ‘Clean’ the Alzheimer’s Brain.” Scientific American, Scientific American, 16 Oct. 2018, www.scientificamerican.com/article/how-exercise-might-clean-the-alzheimers-brain1/.
