Volunteering, polygenic risk for Alzheimer's disease, and cognitive functioning among older adults
Sae Hwang Han1, J Scott Roberts2, Jan E Mutchler3
1Department of Human Development and Family Sciences, College of Natural Sciences, University of Texas at Austin, 108 E. Dean Keeton St., Stop A2702, Austin, TX, 78712-1248, United States.
Objective:
In the context of the public health burden posed by increases in Alzheimer's Disease (AD) prevalence around the globe and the related research efforts to identify modifiable risk factors for the disease, we sought to provide an empirical test of earlier claims that volunteering may be considered as a health intervention that could help to prevent or delay the onset of AD.
Method:
Using nine waves of panel data from the U.S. Health and Retirement Study (n=9,697), we examined whether volunteering conferred cognitive health benefits in later life and whether volunteering served a gene-regulatory function to help alleviate cognitive decline associated with polygenic risk for AD. Multilevel models were used to estimate associations between volunteering, polygenic risk for AD, and cognitive functioning over time.
Results:
We found robust within-person associations between volunteering (assessed as volunteer status and time commitment) and cognitive functioning over time, such that volunteering was associated with higher levels of cognitive functioning and slower cognitive decline. The findings also provided evidence that the within-person associations for volunteering and cognitive decline were more pronounced for older adults at higher genetic risk for developing AD.
Conclusions:
Our findings are in line with a growing body of theoretical frameworks and empirical evidence suggesting that prosocial behaviors are directly associated with biological systems and may modify gene regulation to confer health benefits. The analytic approach taken in this study also provided a useful framework for investigating the effectiveness of other modifiable risk factors that vary over time in the context of cognitive decline related to genetic risk for AD.
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