Cardiorespiratory Fitness Attenuates Association between Poor Sleep and Alzheimer’s Disease

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foot on treadmill

Researchers from the University of Wisconsin-Madison completed a study that offers clues into how sleep and exercise affect Alzheimer’s disease risk. 

The study, “Cardiorespiratory Fitness Modifies Influence of Sleep Problems on Cerebrospinal Fluid Biomarkers in an At-Risk Cohort,” was published online in the Journal of Alzheimer’s disease. The research was led by Lena Law and members of the Ozioma Okonkwo lab, which studies exercise and Alzheimer’s disease risk. 

Law explains, “Alzheimer’s disease is a devastating condition and unfortunately, its prevalence is increasing with little to no options for effective treatment. Because of this, discovering preventative measures to delay the onset of disease is of high importance. By studying modifiable risk factors that can be targeted in mid-life or earlier, such as physical activity and sleep, our research has the potential to have a large impact on the incidence of Alzheimer’s disease and hopefully provide a better quality of life to those who may otherwise be affected.”

Previous studies have shown that better sleep and cardiorespiratory fitness are protective against Alzheimer’s disease pathophysiology. However, there have been few studies examining how both sleep and exercise affect the changes that occur in cerebrospinal fluid in preclinical Alzheimer’s disease: an early stage of the disease where patients have changes in their brain, but no or little cognitive impairment. Law et al. studied this association. 

Changes in cerebrospinal fluid can be detected years before people experience Alzheimer’s disease symptoms. For example, levels of the proteins amyloid and tau in the cerebrospinal fluid correspond with the risk of developing Alzheimer’s disease in the future. These researchers found that participants who had problems sleeping had higher levels of the protein p-tau in their cerebrospinal fluid. However, they found that participants who were more aerobically fit were protected from the protein increase related to poor sleep. That means that if participants slept poorly but exercised, they were less likely to have elevated p-tau in their cerebrospinal fluid. 

This information shows that improving sleep and increasing aerobic exercise may be practical targets to protect against Alzheimer’s disease pathophysiology. More research needs to be done about the association of exercise, sleep, and Alzheimer’s disease biomarkers. But, Law et. al’s findings are an important step in determining how to slow the progression of Alzheimer’s disease in at-risk individuals. 

About the study

Participants from this study were from the Wisconsin Registry for Alzheimer’s Prevention (WRAP), a registry of over 1,500 late-middle-aged adults. WRAP is one of the world’s largest and longest-running studies of individuals at risk for Alzheimer’s disease. Law et al. included 74 participants from WRAP in their study. All participants were cognitively healthy, but many had risk factors for Alzheimer’s disease, meaning that they had a parent who had Alzheimer’s or that they had genetic risk for the disease.

Story by Emma Zalog