Alzheimer’s disease is a progressive neurodegenerative disorder characterized by compromised memory, thinking, and behavioral patterns. It is believed that Alzheimer’s is a result of aggregations of beta-amyloid protein fragments between neurons as well as neurofibrillary tangles inside neurons that result from accumulations of tau protein. These protein accumulations grow to effectively disrupt communication and signaling between neurons (“What happens to the brain in Alzheimer’s disease?,” 2017). The nature of these biological markers surrounding Alzheimer’s often leads to symptoms of cognitive impairment to appear much later in one’s life than the true start of the disease. Current research still cannot explain what conclusively causes these harmful protein aggregations; however, the biggest risk for Alzheimer’s has been linked to aging.
While the discussion surrounding this disease has generally been restricted to genetic and biological associations, recent data suggests communities of color are disproportionately impacted in the risk of developing and obtaining a diagnosis for Alzheimer’s. Compared to white individuals, African Americans are twice more likely to develop Alzheimer’s, and Hispanics are one and one-half times more likely to have Alzheimer’s (Alzheimer’s Association, 2020). Despite the higher prevalence rate of Alzheimer’s, these respective groups are still less likely to be given a timely diagnosis in earlier stages which inevitably restricts potential treatment options contingent on early intervention. It is reported for the age of initial symptoms to be, on average, 6.8 years earlier in Hispanic individuals than the average age of initial symptoms in white individuals (Alzheimer’s Prevention Initiative, 2012). With an earlier onset of initial symptoms and a delayed awareness of the proper diagnosis, one can see how the gap of accessing correct treatment may worsen the prognosis of the Alzheimer’s condition. The racial and ethnic disparities that are seen in Alzheimer’s data may suggest how socioeconomic factors play into the development of this disease in certain groups.
Socioeconomic factors have been linked to neurocognitive disorders and cognitive function as individuals with more access to educational and occupational resources are more likely to have normal cognitive function throughout adulthood. It is typically seen that higher educational resources are quite beneficial for memory-based function in elders which ties back to the prevalence of Alzheimer’s disease between different groups of varying socioeconomic backgrounds (Racial and Ethnic Disparities in Alzheimer’s Disease: A Literature Review, 2014). Research conducted by Amy Kind, a physician-scientist in the Division of Geriatrics and Gerontology of the University of Wisconsin, focused on analyzing the prevalence of Alzheimer’s biomarkers and baseline cognition in terms of a socioeconomic context. Kind pooled her cohort of participants, late-to-middle-aged adults with a parental history of Alzheimer’s, from the Wisconsin Registry for Alzheimer’s Prevention (WRAP) study. Through the American Community Survey and Census data, neighborhood and socioeconomic quantifications were created to compile a metric, Area Deprivation Index (ADI) which accounts for poverty, education, housing, and employment indicators to predict health-disparity related outcomes (Kind et al., 2017, p.195). All participants were thereby ranked into deciles of neighborhood disadvantage using ADI and measured for their baseline cognitive function and levels of Aβ42 and Ptau181 in their cerebrospinal fluid. Results had shown those living in more disadvantaged neighborhoods were associated with a lower baseline of cognitive outcome and function in areas of memory and speed despite being controlled for age and education. Although Aβ42 levels did not vary considerably within the different neighborhood deciles, it was noted that those in the most disadvantaged neighborhoods measured disproportionately higher levels of phosphorylated tau in their cerebrospinal fluid with an average of 11.61 P-tau units higher than those in the lesser disadvantaged neighborhoods (Kind et al., 2017, p.196). With these observed differences in biomarker levels and cognitive performance, one may say that socioeconomic and neighborhood disadvantage may be correlated to a higher risk of developing Alzheimer’s.
For the majority of Alzheimer’s research, there has been a dominant bias of acquiring information and data from largely white participants which unfortunately has created a lack of understanding of how this disease can first appear or develop in different groups of people. A 2019 study conducted by John C. Morris, a neurologist and professor at Washington University in St. Louis, measured the differences in Alzheimer’s disease manifestations in African American and white individuals. 1,255 participants of ages 43 or more, based in the St. Louis area, volunteered in studies conducted at Knight Alzheimer Disease Research Center. This cohort aimed to be a representative sample proportional to the different backgrounds within St. Louis. Biological data was extracted from the participants through different testing such as PET scans, MRI scans, or spinal taps to detect and measure amyloid protein buildup, levels of Alzheimer’s biomarkers, and signs of brain shrinkage or damage (Bhandari, 2019). Although PET and MRI scans did not show significant differences between African American and white individuals, it has been seen African Americans who exhibited mild to very mild signs of Alzheimer’s measured lower than threshold levels of expected tau. As stated previously, tau protein accumulations inside neurons create disruptions in how neurons communicate. Larger tau levels signify a greater likelihood of cognitive decline. Therefore, normal and high levels of tau may have been previously misrepresented and could have caused misdiagnoses in African Americans (Bhandari, 2019).
Socioeconomic and racial inequalities continue to create disparities in the prevalence of diseases such as Alzheimer’s. In future research, hopefully, such neurodegenerative disorders can be analyzed carefully into both biological and social factors to create a more health-equitable future.
Alzheimer’s Association. (2020, March). Race, Ethnicity, and Alzheimer’s. Alzheimer’s Disease & Dementia Help. https://www.alz.org/aaic/downloads2020/2020_Race_and_Ethnicity_Fact_Sheet.pdf
Alzheimer’s Prevention Initiative. (2012). Alzheimer’s Disease Facts and Figures. Alzheimer’s Prevention Registry. https://www.endalznow.org/storage/documents/Cor/alzheimers%20disease%20facts_figures_factsheet_updated_aug.pdf
Bhandari, T. (2019, January 21). Racial differences in Alzheimer’s disease unveiled. Washington University School of Medicine in St. Louis. https://medicine.wustl.edu/news/racial-differences-in-alzheimers-disease-unveiled/
Kind, A. J., Bendlin, B. B., Kim, A. J., Koscik, R. L., Buckingham, W. R., Gleason, C. E., Blennow, K., Zetterberg, H., Carlsson, C. M., & Johnson, S. C. (2017). Neighborhood socioeconomic contextual disadvantage, baseline cognition and Alzheimer’s disease BIOMARKERS in the Wisconsin registry for Alzheimer’s prevention (Wrap) study. Alzheimer’s & Dementia, 13(75), 195-196. https://doi.org/10.1016/j.jalz.2017.07.054
Racial and Ethnic Disparities in Alzheimer’s Disease: A Literature Review. (2014, January 31). Racial and ethnic disparities in Alzheimer’s disease: A literature review. ASPE. https://aspe.hhs.gov/reports/racial-ethnic-disparities-alzheimers-disease-literature-review-0
What happens to the brain in Alzheimer’s disease? (2017, May 16). National Institute on Aging. https://www.nia.nih.gov/health/what-happens-brain-alzheimers-disease