Exploring the Relation Between Aerobic Exercise, BDNF and Alzheimer’s Disease: A Research Protocol

Abstract

Introduction: Alzheimer's Disease (AD) is a neurodegenerative disease that impacts the aging population by causing severe cognitive decline. Although there is no cure for AD, studies have shown that lifestyle changes may contribute to preventing AD. The purpose of this study is to investigate how regular exercise can influence a positive change in the cognitive decline that is associated with AD in rats, through a rise in BDNF levels. Methods: The study would be performed through a series of procedures and tests. Rats would be surgically induced with AD and separated into groups exposed to different aerobic exercise regiments. Then, they would either complete a novel object recognition test, to assess behavioural components, or magnetic resonance imaging, to assess structural components. Finally, they would have their brains extracted to measure protein levels. Results: The rats who would have been surgically induced with AD and exposed to regular exercise, are anticipated to have performed better on the novel object recognition test, than the rats surgically induced with AD, but not exposed to regular exercise. The rats who would have been surgically induced with AD and exposed to regular exercise, are anticipated to have shown greater gray matter and hippocampal volume on the magnetic resonance imaging, exhibit greater levels of BDNF, and show decreased levels of Aβ peptides and p-tau during the protein level measurement, than the rats induced with AD but not exposed to regular exercise. Discussion: The study would anticipate finding that the increased release of BDNF that occurs through regular exercise, decreases Aβ peptide and p-tau levels. Through decreasing Aβ peptide and p-tau levels, BDNF can be used as a form of neuroprotection in slowing down the cognitive decline that is associated with AD. Conclusion: The measures applied when researching ways in which the cognitive decline brought on by AD in rats can be reduced, could potentially be translated to further studying therapeutic treatments for AD in humans. These results could lead to similar preventative measures for other neurodegenerative diseases. Future directions may include informing the public of the importance that lifestyle changes may have on neurological health.