What questions have you been tackling in your research?
One consequence of increasing life expectancy is that more and more people are at risk of age-related neurodegenerative disorders, such as Alzheimer’s disease (AD). Indeed, the prevalence of AD is projected to rise more than 140% by 2050. Repeated clinical trial failures over the last decade further underscore the critical need for prevention. Thus, big questions in my lab center on modifiable factors that influence brain and cognitive aging. In addition to protective factors that can increase resilience to age-related neuropathology, we are interested in characterizing social contextual factors that create and sustain racial and ethnic inequalities in AD.
What are some of the most important findings from your work?
Existing models of AD risk and resilience are not sufficient to explain the vast degree of variability in brain aging, cognitive aging, and the strength of associations between brain and cognitive aging. Therefore, our work seeks to promote more comprehensive models that incorporate life course biopsychosocial factors. For example, we have shown that even very early life experiences (e.g., social support received during childhood) can influence physical, mental, and cognitive health decades later. We have also shown that racially-patterned social stress (e.g., everyday discrimination) independent predicts faster late-life memory decline.
How can we use this knowledge in our everyday lives?
Some people dismiss AD as a disease of old age, but we now know that subclinical disease begins 20-30 years prior to diagnosis. Our research highlights potential avenues for prevention that can be targeted throughout the life course in order to optimize cognitive aging. Our research also helps to reveal the causes and consequences of inequality, an important step toward achieving health justice.