It is well understood that exercise exerts multiple positive effects on our body and mind, but aside from prolonging our life expectancy, it has been postulated that exercise can improve our cognition and memory. This doesn’t mean that the average person should train like a Division 1 athlete to reap the cognitive benefits of exercise. The precise mechanism of how such cognitive changes come to be are yet to be clearly understood, but studies on humans and mice have shown that the protein BDNF (Brain-derived neurotrophic factor) plays a crucial role in neurogenesis, the growth and maturation of neurons, and synaptic plasticity. BDNF belongs to a family of neurotrophins, which are proteins that support neurons and increase their proliferation.

Plasticity is the key for learning and memory, and is defined as the brain’s adaptability to environmental changes. For example, synaptic plasticity is the making and breaking of connections between neurons. The synapse is the location where two neurons communicate with each other via neurotransmitters (chemicals in the brain). The importance of BDNF is due to its ability to regulate synaptic plasticity. Low levels of BDNF are associated with neurodegenerative diseases, such as Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, and multiple sclerosis - all of which involve a decrease in the number of neurons. Therefore, multiple studies are attempting to utilize BDNF in order to treat these diseases. The entire mechanism of BDNF is a lengthy one, but in short, once BDNF is activated, it may act on other proteins to indirectly regulate neural plasticity, resistance to stress, and improve cell survival. 

It is not enough to solely introduce new neurons to a diseased brain. The new neurons must survive and mature which is facilitated by BDNF, as shown by Rudolph Tanzi, a neurologist who conducted a study on the effect of neurogenesis on Alzheimer’s disease. When exercising, the body is producing proteins from the muscle, liver, and fat in order to increase the speed of which neurons mature, increase blood flow to the brain through the formation of blood vessels (known as vascularization), and increase the volume of the hippocampus. The hippocampus is a region of the brain that is vital for memory formation and learning. 

A study conducted in the 1990s by Henriette van Praag found that mice that were housed in cages with running wheels had double the number of neurons than mice that were placed in open water and in water mazes. It was also found that the offspring of mice had a slightly greater cognitive advantage than the offspring of sedentary mice. Another study showed that male mice whose fathers exercised and had subsequent genetic changes to their sperm were found to have decreased anxiety levels, leading to the possible conclusion that the benefits of exercise can be transferred to offspring. Because these studies have been conducted primarily on mice, it is still uncertain whether these benefits are applicable to humans, but the positive physical and mental changes that exercise brings about have been positively correlated with exercise in humans in many studies. 

BDNF also plays an important role in depression and anxiety management. The great feeling that most of us get after exercising is due to the release of endorphins, which are neurotransmitters that give us a sensation of euphoria. This release of endorphins is also known as the “runner’s high”, but can actually be released with any form of physical exercise. BDNF plays a more permanent role than endorphins. Studies involving mutations of the BDNF, rendering it non-functional, have resulted in decreased memory, performance, hippocampus volume, and increased prevalence of major depressive disorders, anxiety disorders, and depressive symptoms in those with bipolar disorder and Alzheimer’s disease. 

Exercise will not automatically improve our cognition and restore the capacity of an elderly person suffering from dementia. It also is definitely not guaranteed that exercising while we are young will prevent us from having dementia, Alzheimer’s disease, or other neurocognitive diseases when we age. However, this doesn’t mean that we shouldn’t try to exercise with moderation. 

References:

Bathina, Siresha, and Undurti N Das. “Brain-derived neurotrophic factor and its clinical implications.” Archives of medical science : AMS vol. 11,6 (2015): 1164-78. doi:10.5114/aoms.2015.56342 

“BDNF Gene - Genetics Home Reference - NIH.” U.S. National Library of Medicine, National Institutes of Health, ghr.nlm.nih.gov/gene/BDNF.

Liu, Patrick Z., and Robin Nusslock. “Exercise-Mediated Neurogenesis in the Hippocampus via BDNF.” Frontiers, Frontiers, 23 Jan. 2018, www.frontiersin.org/articles/10.3389/fnins.2018.00052/full .

Mayo Clinic Staff. “Exercise and Stress: Get Moving to Manage Stress.” Mayo Clinic, Mayo Foundation for Medical Education and Research, 8 Mar. 2018, www.mayoclinic.org/healthy-lifestyle/stress-management/in-depth/exercise-and-stress/art-20044469.

Sleiman, Sama F, et al. “Exercise Promotes the Expression of Brain Derived Neurotrophic Factor (BDNF) through the Action of the Ketone Body β-Hydroxybutyrate.” ELife, ELife Sciences Publications, Ltd, 2 June 2016, elifesciences.org/articles/15092.

Williams, Ruth. “Exercise's Benefits to Dementia Can Be Made Chemically.” The Scientist Magazine®, The Scientist, 6 Sept. 2018, www.the-scientist.com/news-opinion/exercises-benefits-to-dementia-can-be-made-chemically-64761

Yeager, Ashley. “How Exercise Reprograms the Brain.” The Scientist Magazine®, The Scientist, 31 Oct. 2018, www.the-scientist.com/features/this-is-your-brain-on-exercise-64934#:~:text=Exercise%2C%20studies%20have%20shown%2C%20leads,of%20the%20hippocampus%20in%20humans.