LAUSR

Fewer births, declines in mortality related to cardiovascular disease and cancer, and international migration are contributing to unprecedented demographic shifts in the United States. Increasingly, the population is older and more diverse, and in the next 2 decades, racial and ethnic minorities will compose 42% of older adults. Without intervention, existing racial and ethnic health disparities among minority older adults are likely to be exacerbated. The pressing need to address these health disparities is perhaps most evident in Alzheimer disease (AD), which increases in prevalence with age and is disproportionately more prevalent among African American and Hispanic/Latino individuals. Alzheimer disease prevalence is expected to triple by 2050 and threatens to overwhelm the health system unless significant advances are made. Despite numerous failures of AD drug trials, there remains optimism that some AD treatments may be effective, if started very early, likely in the preclinical (asymptomatic) period. Diagnosis of preclinical AD currently relies on cerebrospinal fluid (CSF) biomarkers and/or molecular or functional neuroimaging, and much of the evidence supporting this approach was generated from studies with fewer than 5% racial and ethnic minorities.1 Diagnostic tools and therapeutic strategies developed using evidence with so little racial and ethnic diversity could lead to inaccurate diagnosis and/or ineffective treatment for minority patients, thus worsening disparities. For example, studies have found lower CSF tau2 and higher uptake of radioligands for amyloid3 in African American individuals compared with white individuals. If these findings are replicated and confirmed in larger studies, there could be implications for use of biomarkers in diagnosis and management of AD. However, even if differences between racial/ethnic groups are confirmed, these findings could reflect differences in risk owing to comorbidities and/or unexamined social factors. Persistent disparities in AD outcomes have heightened calls for more minority participation in research, which remains low despite the decades-old National Institutes of Health guidelines on inclusion of minority individuals in clinical research and the 2017 National Institutes of Health requirements that phase III clinical trials include valid analyses by race/ethnicity. Researchers are keenly aware of the imperative to increase minority enrollment, but lack of trust, prior research abuses, and ineffective communication with minority communities contribute to low participation.4 Despite the barriers, successful minority recruitment has occurred using strategies such as hiring staff experienced working with diverse communities, partnering with community organizations, and using communication channels known to reach diverse communities.4 While inclusion of minority populations in research is critical, minority recruitment alone is unlikely to provide the evidence needed to understand and address health disparities. Many studies have found an association between AD and years of education, quality of education, socioeconomic status, and neighborhood characteristics.5,6 Thus, AD studies should be expected to consider these contextual and life experiences, especially among racial and ethnic minority patients who disproportionately are more likely to be socioeconomically disadvantaged. Many studies comparing groups by race/ethnicity use few variables to adjust for socioeconomic factors (eg, years of education and income level), and these insufficiently capture important differences in life experiences between races/ethnicities that could affect risk of disease. Unfortunately, analyzing findings by race/ethnicity without appropriate contextual data could lead to inaccurate, misleading, or stigmatizing conclusions that may detract from the overall goals of diversity in research: to enhance the accuracy, utility, and generalizability of scientific evidence. Studies of race and ethnicity demonstrate greater genetic heterogeneity within than between racial/ ethnic groups,7 yet there is a common misperception that groups are more genetically homogeneous within racial/ethnic groups. Race, as defined by the US Census and Office of Management and Budget, is a sociocultural construct that is not biologically, anthropologically, or genetically based. Because race is socially determined and dependent on self-identification, it is a fluid construct that can change over time and vary by location and culture. Although substantial evidence exists to contradict claims that race is biologically based and without evidence that genetic or biological characteristics can be inherently structured into racial categories,8 long-held assumptions about innate biological differences between races continue to permeate medicine and biomedical research.9 This is in part because minority race/ ethnicity is tightly interwoven with sociopolitical factors, such as systemic racism, discriminatory policies, and access to care, which are linked to biophysiologic changes, such as neuroendocrine dysregulation, cellular aging, and elevated inflammatory cytokines.10 These biological responses to social factors can contribute to premature morbidity and are not unique to minority populations but are more prevalent owing to the higher burden of psychosocial stress across the life span. Race, particularly in the United States, is associated with markedly different life experiences as well as social and economic opportunities that affect health. Painful legacies of overt racism, abuse, and trauma continue to negatively affect minority communities. VIEWPOINT