Environmental, Sociocultural, Behavioral, and Biological Factors Associated with Cognitive Decline, Alzheimer’s Disease, and Other Types of Dementia in Black Americans

Abstract

Purpose of Review

This narrative review summarizes environmental, sociocultural, behavioral, and biological factors associated with cognitive decline and dementia in Black Americans.

Recent Findings

Variations in environmental factors (education, toxins) contribute to poor cognition in Blacks. Historical context, early-life educational experiences, and environmental exposures should be considered for addressing late-life cognitive disparities. Sociocultural (stress, discrimination, social networks, social activity, loneliness) and behavioral (depression, coping, health behaviors) factors can have positive and negative implications for cognitive aging. Given these factors are not consistently shown to play a role in maintaining cognition in Blacks, further examination is needed. Cardiometabolic conditions increase the risk of cognitive issues and are more common in Blacks; thus, examination of biological mechanisms (inflammation, vascular changes, etc.) warrants further study.

Summary

Future studies should explore the impact of education and segregation and identify mechanisms linking stress and discrimination to cognitive outcomes. Further, culturally tailored programs focused on preventative behaviors are needed to enhance health outcomes and reduce disparities.

Introduction

Cognitive decline and Alzheimer’s disease and other related dementias (ADRD) in the aging US population are major public health concerns. [1]. However, the burden of these neurodegenerative health conditions is not equally distributed. Older US Blacks, in particular, are disproportionally burdened compared to non-Hispanic White populations [1]. On average, older US Blacks experience a faster rate of cognitive decline, have lower cognitive test scores [2], and are twice as likely to develop Alzheimer’s or other dementias when compared to Whites [1]. Prior studies show that genetic risk factors (e.g., APOE genotype) may account for some of the higher risks of dementia and decline in older Black adults compared to Whites [3]; yet we know there are other contributing factors that may help fully explain these cognitive and ADRD disparities [4••, 5]. Given the aging population of Black Americans is expected to grow over the next few decades (increasing from 9% in 2014 to 12% in 2060 [6]), there is an urgent need to critically explore factors contributing to the high rates of cognitive decline and ADRD among US Blacks.

The National Institute on Aging (NIA) Health Disparities Research Framework [7] was developed to guide research on aging-related health disparities. This framework identifies priority populations at risk for disparities in aging based on fundamental factors such as race, ethnicity, gender, and age and highlights four levels of analysis to guide aging-focused health disparities research. These four levels of analysis include environmental, sociocultural, behavioral, and biological factors. The environmental level of influence represents structural factors related to a person’s physical and political environment. Examples include geography (neighborhood), federal and local policies, socioeconomic conditions, and health care. The sociocultural level of influence represents cultural, social, and psychological factors that are shaped by group-based cultural values, norms, ethnic traditions, and social networks. Factors at this level impact an individual’s self-concept, social identity, and perceptions of bias (i.e., individuals may perceive restricted access to quality health care as institutional racism and view this hardship as discrimination). The behavioral level is characterized by psychological processes and individual attitudes and behaviors. Factors within this level include coping (e.g., active coping, problem-solving skills, cognitive reframing), psychosocial risk and resilience factors (e.g., optimism, pessimism, and sense of control), and individual health behaviors (e.g., smoking, alcohol/drug use, nutrition, physical activity). Lastly, the biological level of influence prioritizes biological processes that help explain mechanisms for observed differences in disease incidence and outcomes. Examples within this level encompass factors associated with physiological (e.g., co-morbidities, HPA overload, inflammation), genetic (e.g., DNA damage via telomere attrition), and cellular processes (e.g., disrupted intercellular function and communication via mitochondrial dysfunction and cellular senescence) [7].

The purpose of this narrative review is to summarize established and emerging factors within the past 5 years associated with cognitive decline and ADRD among Black Americans. Using the NIA Health Disparities Research Framework as a guide, we organize the factors examined according to their corresponding level of influence. Specifically, our review was designed to address the central question of whether environmental, sociocultural, behavioral, and biological factors contribute to cognitive outcomes and ADRD in Black Americans. Results provide a comprehensive synthesis of the potential factors contributing to the high prevalence of cognitive decline and dementia in Black Americans [4••].

Methods

A literature search was conducted using five electronic databases—PubMed, CINAHL, Scopus, PsychINFO, and Google Scholar—to identify relevant articles published between 2017 and 2022 for inclusion in this narrative review. Using the Boolean search strategy, search procedures included various combinations of terms in three key areas: (1) study population, (2) outcome of interest, and (3) level of analysis. Search terms for the study population included “African American,” “Black adults,” “US Black,” and “Black American.” Search terms for the outcome of interest included “cognition,” “cognitive decline,” “mild cognitive impairment,” “Alzheimer’s disease,” and “dementia.” Search terms for the level of analysis, as illustrated in Table 1, were informed by the authors’ existing knowledge of risk and protective factors for cognitive decline and ADRD and varied according to the level of influence based on the NIA’s Health Disparities Research Framework. To identify additional literature, we also hand-searched the reference lists of relevant articles previously known to the authors and those retrieved during the initial literature search. Searches were performed between October and December 2022.

Table 1.

Terms used during electronic search procedures for the corresponding level of influence

Level of analysis	Search terms
Environmental	Education Residential or school segregation Environment exposures Toxins Particulate matter
Sociocultural	Perceived stress or stress, stressful life events Discrimination, genderism, racism Social resources or social support
Behavioral	Depression or depressive symptoms Coping or coping resources Prevention Health behaviors Lifestyle factors Diet Exercise or physical activity
Biological	Cardiometabolic disease Heart disease Type 2 diabetes Blood pressure Inflammation

Using a hierarchical approach, articles were selected for inclusion based on the publication date and methodological quality of the study design (i.e., level of scientific rigor). Specifically, the highest priority for inclusion was given to peer-reviewed studies published within the last 5 years and those reporting outcomes from meta-analyses, systematic reviews, narrative reviews, and randomized controlled trials (RCTs). When articles with these types of study designs were not available or when the publication date was greater than 5 years old, we included studies with less rigorous study designs (i.e., observational cohorts, cross-sectional data) and those with older publication dates. Collectively, these search and article retrieval procedures ensured that the information presented in this review is based upon the most recent and rigorous science available.

Findings

Potential factors associated with cognitive decline, Alzheimer’s disease, and other dementias among older Black Americans by level of analysis according to NIA’s Health Disparities Framework are summarized in Table 2. Each of these factors is further described in the text below.

Table 2.

Potential factors associated with cognitive decline, Alzheimer’s disease, and other dementias among older African-Americans by level of analysis^*

Level of analysis
Environmental	Sociocultural	Behavioral	Biological
Education Residential and school segregation Exposure to environmental toxins	Cumulative stress exposure Stressful life events Perceived stress Discrimination# Social network size Social activity engagement Loneliness	Depressive symptoms Coping: John Henryism Other health behaviors	Cardiometabolic risk factors Inflammation

Fundamental factors (race, ethnicity, gender, age, disability status, sexual and gender identities)

^*Adapted from the National Institute on Aging’s Health Disparities Research Framework[7]

^#The original NIA framework listed discrimination as a behavioral level factor and discusses its influence as a sociocultural construct. For the purposes of this review, we categorized discrimination as a sociocultural factor

Environmental

Education

Higher levels of formal education are inversely associated with risk for cognitive decline and ADRD [8]. Black Americans, on average, have lower education levels than their White counterparts, which likely contributes to their high rates of cognitive decline and ADRD [1]. These disparities in education can largely be attributed to America’s history of segregation, particularly policies and practices promoting residential and school segregation prior to the passage of the Civil Rights Act of 1964 (e.g., “Jim Crow” laws) [1, 9].

Several recent studies have highlighted the detrimental effects residential and school segregation have on the cognitive health of Black Americans in later life. Lamar et al. [10] found that older Blacks (N = 497; mean age = 73.5 years) born and residing in the Southern U.S. until age 12 had lower baseline levels of global and domain-specific cognitive function (excluding episodic memory), but did not experience changes in cognition over time. Further, segregated school status significantly modified the association of residence at age 12 on levels of cognition. Blacks residing in the South attending a legally desegregated (integrated) school had lower baseline cognition (global, semantic, and working memory) than their Northern counterparts attending a legally desegregated or segregated school as well as their Southern counterparts attending a legally segregated school [10]. On the contrary, Peterson [11] found an opposite segregation experience effect (N = 699), such that Blacks (mean age = 68.5 years) who only attended desegregated (integrated) schools (N = 435) or those who transitioned to a desegregated school between grades 1 and 5 (N = 50) had better cognition (semantic memory) compared to those who never attended an integrated school (N = 111). They also found that participants who transitioned to a desegregated school between 1st and 5th grades had the highest executive function scores vs. those that never attended a desegregated school. Although they found no significant differences in cognition among those who transitioned between 6 and 8th or 9th and 12th grades, they did observe negative point estimates for those who integrated between 6 and 8th grade compared to those who never attended a desegregated school [11]. Both authors argue that these findings may be explained by the psychosocial stress experienced by individuals and communities during the school integration processes. It is clear that there are variations in school segregation experience—one form of structural racism—and cognitive health in Blacks. This is critical as “structural racism influences environmental factors such as where people can live, the quality of schools in their communities, and exposure to harmful toxicants and pollutants” (p.27) [1]. Understanding the mechanisms by which early-life residence and school segregation status contribute to differences in cognition (e.g., via exposure to environmental toxins, and psychosocial stress pathways) will be necessary for elucidating the disproportionate ADRD burden in Black Americans.

Environmental Exposures

Environmental exposures, including air pollution (i.e., nitrogen oxides, fine particulate matter, and ozone) and certain chemicals/compounds (i.e., pesticides, fertilizers, and solvents/degreasers), are associated with an elevated risk for cognitive decline and ADRD [12–15]. Previous research has shown that Black Americans are more likely to be exposed to these environmental toxins than their White counterparts [16–18]. Similar to education disparities in Blacks, residential segregation, perpetual economic and political disenfran-chisement of segregated neighborhoods, and discriminatory housing policies (e.g., “redlining”) contribute to higher rates of exposure to environmental toxins [9]. Despite evidence indicating environmental exposure to select toxins increases the risk for cognitive decline and ADRD and that US Blacks are more likely to be exposed to these toxins, few studies have empirically examined the unique role these toxins have on cognitive decline and ADRD risk in US Blacks. Our review of the literature found only two studies examining such relationships [19, 20]. Using data from the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study, Loop and colleagues [20] examined associations between air pollution and incidence cognitive impairment. Results showed no compelling relationship between exposure to fine particulate matter and risk for cognitive impairment [20]. More recently, Younan et al. [19] examined if exposure to fine particulate matter differentially increased ADRD risk in Black vs. White women using data from the Women’s Health Initiative Memory Study (N = 6,485). Results showed that Black women had a higher exposure rate to fine particulate matter and this exposure was linked to a greater risk of developing ADRD in Black women compared to White women, suggesting that not only are Black women more likely to be exposed to air pollutants associated with increased risk of ADRD, but once they are exposed, they are more susceptible to adverse cognitive outcomes [19]. The limited research on this topic underscores the need for future research to explore the distinct role environmental toxins have on risk for cognitive decline and ADRD among US Blacks.

Sociocultural

Stress Exposure

Blacks are disproportionately exposed to stress across their life course [21, 22••], report more stressful life experiences (e.g., financial insecurity, legal issues, divorce, death of a child, being fired from a job) [21, 23, 24], more perceived stress [25], and greater discrimination (i.e., everyday and major lifetime) [26] than Whites.

Recent work has examined whether cumulative stress exposure across the life course explains Black–White (B–W) disparities in cognitive function. Chen and colleagues [22••] using a cross-sectional sample (N = 5947; 5262 White and 685 Black) found that cumulative stress exposures—as measured by 10 domains of stressors (i.e., childhood stress, stressful life events in adulthood, financial stress, work psychological stress, work physical stress, work–family conflicts, neighborhood disorder, relationship stress, perceived inequality, and discrimination)—eliminated 8.4% and 13.2% of the B–W disparity in executive function (verbal fluency, inductive reasoning, processing speed, working memory, and attention-switching tasks) and episodic memory (immediate and delayed recall), respectively [22••]. Likewise, longitudinal studies have further found that stressful life events explain a proportion of B–W cognitive disparities. For example, using a small sample of Blacks with a parental history of AD (N = 1241; 1191 White and 50 Black), Zuelsdorff et al. [21] found that lifetime stressful events (e.g., failing out of school, parental alcohol abuse, involuntary unemployment, death of a child) explained 6.9% of the B–W disparity in executive function (processing speed and flexibility and working memory). More importantly, Blacks reported significantly more stressful life events (nearly 84% higher) than Whites [21].

High levels of stress exposure have distinct health implications since abilities that normally decline with age (in terms of brain speed and flexibility in performing certain tasks) are accelerated by the number of stressful life events experienced. For example, in a longitudinal sample of participants enrolled in the Wisconsin Registry from Alzheimer’s Prevention (N = 1320; 1232 White and 82 Black), each stressful life event added about 1.5 years to normal brain aging in White participants, but in Blacks, each event aged the brain an extra 4 years [23]. Black participants in this study also reported significantly more stressful experiences in their lifetime than non-Hispanic Whites and this exacerbated stress was particularly associated with slower processing speed and flexibility and working memory (executive dysfunction) [23]. Nevertheless, most studies of stress exposure and cognitive function have been conducted in older Whites [27] or compared Blacks to Whites [21, 22••, 23], and only rarely have these associations been examined in Blacks. Yet, stress exposure has been shown to uniquely contribute to negative cognitive outcomes and dementia risk in later life in Blacks [25, 28, 29]. For instance, studies using full samples of Black Americans (N = 467) have shown that higher perceived stress (4-item Perceived Stress Scale; PSS) is associated with declines in global cognition, episodic memory, and visuospatial abilities, independent of demographics, vascular factors, and depressive symptoms [28]. Another study using a larger Black sample (N = 579) found that higher levels of perceived stress (14-item PSS) predicted more subjective memory complaints, controlling for age, gender, and education [29]. A third study, using a majority Black sample (N = 4081; 65.7%), showed that greater perceived stress (6-item PSS) was predictive of worse global cognition at baseline and a greater rate of cognitive decline over nearly 7 years of follow-up, adjusting for sociodemographic (age, sex, race/ethnicity, education), vascular (systolic blood pressure, BMI, chronic medical conditions, use of antihypertensives), health behaviors (smoking), and psychosocial (depression, neuroticism, social engagement, social network size, cognitively stimulating tasks) factors. Additionally, sensitivity analyses of each cognitive domain in this study revealed similar findings in that increasing levels of stress were related to lower baseline global, episodic memory (immediate and delayed recall), and executive function (processing speed) as well as longitudinal declines in both global and episodic memory, adjusting for model covariates [25].

Correlates of Perceived Stress

Evidence further suggests there are specific correlates of perceived stress in Black Americans. For example, Glover et al. [30] examined the factors that impact perceptions of stress. She found that Black Americans 60 and older (N = 722) report unique antecedents of perceived stress, including environmental (larger life space), sociocultural (larger social network), behavioral (more depressive symptoms), and biological (higher cognition) correlates [30]. Some correlates (higher global cognition) were associated with lower levels of perceived stress, while others (more depressive symptoms and memory complaints) were associated with higher levels of stress [30]. Similar findings have been reported by Byrd et al. [31] in a longitudinal study of Black Americans 51 and older (N = 450; 51–96 years), whereby greater baseline depressive symptoms were related to higher levels of perceived stress at 33-month follow-up, controlling for baseline perceived stress level, age, sex, education, and chronic health conditions. The depression–stress association further varied by age group such that the impact of baseline depression on changes in perceived stress was greatest in Blacks in their 60s versus those in their 50s (b = 0.267, p = 0.001) [31]. These findings document the important role of depressive symptoms and cognitive health in shaping perceptions of stress and the bi-directional relationship between these constructs in Blacks, particularly those 60 years and older.

In addition, research indicates that perceived stress (sociocultural) and depressive symptoms (behavioral) may partially explain the longevity advantage in Black Americans. Whitfield and colleagues [32], for instance, examined within-group cohort differences in health and psychosocial factors that lead to exceptional longevity among older Black Americans. They found that there are changes in the characteristics of those who make it to later life. Specifically, they show the variances for memory (alpha span test) and other health indicators (lung function as measured by average peak expiratory flow) increased in older (80–99 years) vs. younger age groups (60–79 years) [32]. However, the differences in the variances by age group for memory were no longer significant after accounting for perceived stress and depressive symptoms. The authors argue that this resistance to age-related variability may indicate that after Black Americans surpass their life expectancy (in their 70s), the pressures that increase their likelihood of memory problems are due in part to stress and depressive symptoms [32]. These changes in variability with advanced age underscore the importance of examining both sociocultural (perceived stress) and behavioral (depression) factors that explain exceptional survivorship in Black Americans.

Discrimination

Sociocultural (perceived stress) and behavioral (depression) factors appear to influence both memory outcomes and ADRD risk, as well as exceptional longevity in Black Americans. Yet, studies examining the effects of other sociocultural studies examining the effects of other sociocultural (discrimination, social networks, social activity engagement, and loneliness) factors on cognition report inconsistent findings. Some studies, for instance, have demonstrated a significant association between higher levels of discrimination and better cognition in Black Americans [33–35], while others have not [36–38]. Using data from the Health and Retirement Study, Sutin and colleagues [33] found that Black participants who reported more everyday racial discrimination had better cognitive health. Similar findings for major lifetime discrimination have been reported using data from a multiethnic cohort of Kaiser Permanente members 65 years and older [35]. Additionally, Pugh et al. [34] found that everyday discrimination (not due to race, age, or gender) was related to improved baseline global cognition and working memory and better performance on semantic memory over time in a sample of 617 Black adults. On the other hand, Barnes et al. [36] found that 407 older Black Americans (mean age = 72.9 years) experiencing more everyday discrimination performed worse on cognitive tasks, particularly episodic memory, and processing speed. However, this relationship was no longer significant after adjusting for depressive symptoms [36]. Similarly, using a large cohort of Black women aged 55 years and older (N = 17,320), Coogan and colleagues [38] reported that experiences of both daily and institutional racism were associated with decreased subjective cognitive function (SCF). Specifically, women in the highest quartile of daily racism (e.g., poorer service in stores) had 2.75 times the risk of poor SCF as women in the lowest quartile. Women reporting institutional racism in five to six domains (i.e., discriminated against in employment, housing, police encounters, judicial system, education, and obtaining health care due to their race) had 2.66 times the risk of poor SCF as those who reported no such experiences. Similar to Barnes [36], a substantial proportion of the adverse effects of daily and institutional racism on SCF appeared to be mediated by depression as well as insomnia [38]. Overall, results suggest that there is an association between discrimination and cognitive function, but the exact nature of this association in Black Americans remains unclear.

Social Networks, Social Activity Engagement, and Loneliness

Other sociocultural factors such as social networks, social activity engagement, and loneliness have also shown a mixed effect on cognition in Black Americans. For example, an influential study by Barnes et al. [39] with a predominately Black sample (N = 6102; 62.1%) found that individuals with a larger number of social networks (as measured by the number of children, relatives, and friends seen at least once a month) and more frequent social engagement (as measured by a greater frequency of participation in social activities) had higher baseline cognition scores (composite of global, episodic memory, and processing speed) and experienced significantly less cognitive decline over 5.3 years of follow-up. These findings were similar for older Blacks and Whites, with one exception: the magnitude of the association between more frequent social engagement and reduced cognitive decline was stronger in Whites than Blacks, suggesting a weaker effect of social activity engagement but a protective effect of social network size on cognition in Blacks [39]. Building upon this work, Pugh and colleagues [34] also examined the influence of social network size, engagement in social activities as well as loneliness as predictors of cognitive function and decline (measured by a composite of global, episodic, working, and sematic memory, perceptual orientation, and processing speed) in a full sample of older Black adults (N = 617). They found that the size of one’s social network (number of children, family, and friends seen at least once a month) generally did not predict cognitive function or decline. However, they did report that having a larger social network was associated with more cognitive decline over time (i.e., slower processing speed), suggesting a potentially harmful effect of social network size. The authors also found, similar to Barnes (2004), that increased social activity (how often in the past year have participants engaged in common activities that involve social interaction, e.g., going on day trips or overnight trips) was associated with better global and domain-specific cognitive function (working and semantic memory) as well as improved performance over time (global, episodic memory, perceptual orientation, and processing speed), suggesting a protective effect of social activity engagement [34]. Collectively, these findings suggest that there is a nuanced/complex relationship between social networks, engagement in social activities, and cognition in older Blacks.

In a recent systematic review of 39 studies (3 RCTs, 34 observational studies [including 32 longitudinal] and 2 twin studies, including 189 pairs of participants) [40] that examined these factors in older adults (50 + years), larger social networks and increased social activity were both associated with improved global cognition. Of these, engagement in social activity was more consistently associated with better global cognition (global or composite measures of cognitive function). The weaker association of social networks with cognition may be because this relationship is largely dependent on social network composition (vs. social network size) [41]. One study (N = 548; 170 White, 225 Black, 153 Caribbean Hispanic) found that social network size and composition (i.e., the proportion of family vs. friends in one’s network) were significantly associated with cognition in older Black Americans but not among non-Hispanic Whites or Caribbean Hispanics. In particular, Black Americans with larger networks comprised of a greater proportion of friends reported better global cognition than those with large networks comprised mostly of family and those with small networks, regardless of composition [41]. These findings highlight the importance of examining social network characteristics, including size and composition, as well as other sociocultural factors and cognitive aging in Black Americans.

Pugh and colleagues [34] further examined whether loneliness predicts cognitive function and decline. They report conflicting findings in that higher levels of loneliness were associated with worse global cognition and semantic memory at baseline but were also linked to better semantic memory performance over time [34]. Overall, social network size, social activity, and loneliness have consistently been noted as predictors of cognitive decline in older adults, particularly racially and ethnically diverse groups [4••, 41]. Yet, the findings are incongruent in Black Americans.

Behavioral

Coping Style

Coping style [42] has also emerged as a potential factor influencing cognition. Yet, its unique role remains unclear. For example, John Henryism, an active coping scale developed specifically for Black Americans that reflects a “strong personality predisposition” to actively cope with psychosocial and environmental stressors such as systematic racism and discrimination by expending high levels of effort that may result in negative health consequences, has been associated with lower levels of global and domain-specific (semantic memory, working memory, and visuospatial ability) cognitive function in older Black adults, but not with rate of cognitive decline [42]. The lack of an association between John Henryism and the rate of cognitive decline may suggest that there are other possible sociocultural (perceived stress) and biological (underlying health conditions) factors more strongly correlated with decline [42], making the relative contribution of coping style harder to detect [25, 28, 29]. Given that the mechanisms by which John Henryism is related to the level of global cognition in Blacks are unknown, future studies should further explore this relationship as well as other sociocultural, behavioral, and biological markers of the underlying disease, which lead to cognitive decline.

Health Behaviors

Numerous health behaviors are associated with reduced risk for cognitive decline and ADRD. Not smoking [43, 44], light-to-moderate alcohol intake [45, 46], consuming a healthy diet, such as the Mediterranean or Dietary Approaches to Stop Hypertension (DASH) diet [47, 48], engaging in regular moderate-to-vigorous leisure-time physical activity [49–51], getting adequate sleep (i.e., between 5 and 9 h/night) [48, 52–54], and adherence to medications prescribed for cardiometabolic diseases (i.e., statins, anti-hypertensive medications) [55, 56] are associated with reducing risk for ADRD across diverse populations, including among Blacks [4••, 5, 49, 50, 55, 57]. Engaging in two or more of these healthy lifestyle behaviors further decreases the risk for cognitive decline and ADRD, independent of race/ethnicity [5, 57–60], with some evidence indicating a dose–response relationship, particularly for ADRD prevention [57]. For example, recent findings from the Southern Community Cohort Study (N = 17,209) [57], which is comprised of approximately two-thirds Blacks, showed that never smoking, low-to-moderate alcohol intake, eating a healthy diet (based on a healthy eating index), meeting national physical activity guidelines, and sleeping between 7 and 9 h per night were lifestyle factors independently associated with reducing the risk for ADRD, with no differential effects between Whites and Blacks. Engaging in two or more of these health behaviors showed evidence of a dose–response relationship, with participants engaging in all five behaviors demonstrating a 36% reduced risk for developing ADRD [57]. The robust evidence for lifestyle behaviors reducing risk for cognitive decline and ADRD, coupled with extant data showing that Blacks are less likely to engage in many of these health behaviors when compared to Whites [61–64], underscores the potential link health behaviors have on the disproportionate burden of ADRD among Black Americans.

Biological

Cardiometabolic Risk Factors and Inflammation

Cardiometabolic risk factors are associated with an increased risk for cognitive decline and ADRD [65, 66]. Hypertension, cardiovascular disease, diabetes, obesity, high levels of low-density lipoprotein (LDL) cholesterol, and low levels of high-density lipoprotein (HDL) cholesterol are all linked to higher rates of cognitive decline and ADRD [67, 68]. Midlife hypertension, in particular, has some of the strongest evidence for increasing risk for cognitive decline and ADRD [68]. Individuals with two or more of these conditions (i.e., multi-morbidity), which is more common in Blacks than Whites [69, 70], further damage the blood vessels and increase the risk of cognitive decline and ADRD [71, 72]. Specifically, two or more of these conditions are linked to poorer memory (verbal) performance [73] and significant declines in processing speed among Blacks [74••, 75]. The high prevalence of these conditions among Blacks, as illustrated in Table 3, is hypothesized to partially explain the higher levels of cognitive decline and ADRD experienced by them [76, 77].

Table 3.

Prevalence of cardiometabolic risk factors and diseases among non-Hispanic African Americans and non-Hispanic Whites, stratified by sex [64]

Cardiometabolic health condition	Non-Hispanic African-Americans		Non-Hispanic Whites
	Males	Females	Males	Females
Hypertensiona	58.3	57.6	51.0	40.5
Cardiovascular Diseasesb	60.1	58.8	53.6	42.1
Diabetesc	16.8	16.5	14.9	10.4
Obesityd	38.2	55.2	40.7	38.7
Elevated LDLe	29.3	24.3	26.0	29.6
Low levels of HDLf	17.0	7.9	26.3	7.7

^aSystolic blood pressure ≥ 130 mmHg or diastolic blood pressure ≥ 80 mmHg

^bIncludes coronary heart disease, heart failure, stroke, and hypertension

^cIncludes both diagnosed and undiagnosed diabetes, with type 2 accounting for 90–95% of all cases

^dBMI ≥ 30 kg/m²

^eLDL ≥ 130 mg/dL

^fHDL < 40 mg/dL

The physiological mechanisms underlying the relationship between cardiometabolic health conditions and cognitive decline and ADRD are not fully known [67]. Emerging evidence suggests that inflammation [78] and vascular changes arising from cardiometabolic health conditions accelerate the pathogenesis of cognitive decline and ADRD [67, 79]. For example, studies have demonstrated a significant association between elevated inflammatory markers (i.e., C-reactive protein [80] and Interleukin 6 [81]) and an increased risk of AD and decline on both global [80–83] and specific cognitive domains (e.g., attention and executive functioning [84]), while others have not [85, 86]. These discrepancies may be partially explained by methodological differences in the assessment of inflammatory biomarkers (i.e., some studies measured inflammation at one, two [81, 84], or more time points [80]) and the different types of cognitive outcomes examined. Moreover, the majority of this research has used highly selected samples such as Japanese-American men [80], Dutch older adults [84], predominantly White participants [81], or compared Blacks and Whites [82, 83, 87].

Moreover, studies that have examined whether race or ethnicity modify the pathogenic association between vascular changes arising from cardiometabolic conditions and risk for cognitive decline or ADRD suggest that this relationship differs by race/ethnicity [88–91]. Some studies, for instance, have shown that hypertension-related declines in cognition may be greater in Blacks than Whites [92, 93]. Yet, the blood pressure (BP) threshold associated with impaired cognitive function in Blacks is currently unknown [94], as most existing evidence compares Blacks and Whites when examining whether race or ethnicity modify the pathogenic pathways linking an increased risk for cognitive decline and ADRD to cardiometabolic conditions, rather than examining these disease-causing pathways specifically among Blacks. Future research should determine what BP threshold (as well as thresholds for other cardiometabolic conditions) is associated with hypertension-related cognitive declines in older Black Americans, given that they are a unique group that may show substantial heterogeneity in their biological risk factors. Such research will allow for a better understanding of physiological mechanisms/vulnerability within this population, including the interplay between inflammation, cardiometabolic vascular changes, cognitive decline, and ADRD pathogenesis.

Conclusion

The purpose of this review was to summarize potential environmental, sociocultural, behavioral, and biological factors contributing to the disproportionally high rates of cognitive decline and ADRD in Black Americans. Findings highlight several opportunities for future research in this area.

First, early-life residence and school segregation are key risk factors for poor cognitive function in late-life. These factors are known to influence and greatly impact quality education attainment and should be considered in future work. Further, greater examination of the contribution of environmental exposures/toxins to cognitive decline and ADRD is needed, as most studies have not examined these associations in Blacks. Second, stress exposure has been shown to uniquely contribute to worse cognitive outcomes and dementia risk in later life in Blacks, yet most studies have been conducted in older Whites or compared Blacks to Whites. Future work should examine these associations within Blacks. Third, while there is a link between network size and composition (particularly large networks with mostly friendships), social activity engagement, loneliness, and cognitive function, the exact nature of these associations remains unclear [40]. Given these sociocultural factors are not consistently shown to play a role in maintaining cognitive functioning in Black Americans, further examination is needed. Similarly, discrimination (sociocultural) and specific coping styles (behavioral) should also be addressed in future work as these constructs have mixed effects on cognition in Black Americans.

Fourth, the development and testing of innovative and culturally tailored approaches to address preventative health behaviors associated with reduced risk of cognitive decline and ADRD are needed. Culturally tailored behavior change programs have a longstanding history of enhancing health outcomes in Black Americans [95–97] and embody a health equity approach for reducing cognitive-related health disparities experienced by them. Lastly, most of the extant inflammation-cognition literature focuses on specific racial/ethnic groups (Japanese-American men, Dutch older adults, Whites), largely neglecting Black Americans. There is a great deal of heterogeneity with respect to biological variation within Blacks, which has implications for cognitive health. Hence, it is important to clarify biological pathways along with all of the other previously cited levels of analyses when considering aging-related health disparities research in Black Americans [7].