Alzheimer’s Disease in Marginalized Communities:

Racism’s Direct Relationship With Neurodegeneration 

 

Image Credit: NewScientist.com 

Alzheimer’s disease is a rapidly growing topic in medical research, with funding surges noted in the past couple of years.  What has perhaps remained the most elusive component of Alzheimer’s is the heritability of the disease, and the genetic variation by which the disease manifests itself.  A study conducted by Kaczorowski et. al. estimated the heritable component to comprise between 50% and 80% of the disease’s progression in humans (Kaczorowski et. al. 2019).  This study from 2019, delving into the genetics of Alzheimer’s, was wildly successful in producing novel AD mouse models to help study and, with further research, better identify the diverse genetic mechanisms that contribute to the disease.

Despite the major advancements made in research and clinical assessments of the disease, there remains a disconnect between Alzheimer’s and the racial implications of the disease.  In 2018, the CDC noted that Alzheimer’s rates differ across racial groups, with African Americans possessing the highest prevalence at 13.8% in the age cohort of 65 years and older.  Though several studies have similarly attested that the genetic mechanisms of Alzheimer’s also differ by race, not much progress has been made in determining exactly why this is.  The NCBI published a systematic review in 2019 with aims to increase participation and retention rates for communities who are often underrepresented in research to help expand knowledge bases of diseases, like Alzheimer’s, in marginalized communities (Gilmore-Bykovskyi et. al. 2019).  However, more answers may be found in why these populations, specifically Black communities, are underrepresented in research in the first place. 

It is no secret that the history of racial discrimination is extensive, with lasting effects that permeate the modern era.  But the conversation of systematic racism must be extended thoroughly to disciplines of research and medicine if adequate treatment options are to be actualized with equity in the population.  Additionally, researchers must recognize the history their discipline has in perpetuating racist ideology and gruesomely racist practices, such as in the infamous Tuskegee Experiment, and how such perceptions may be internalized by marginalized communities.  Alzheimer's is just one example of a disease with racial bias; perhaps, the several diseases exhibiting differential expressions across racial dimensions may be linked.  A study published by the NCBI in 2017 performed an analysis of telomere lengths in African American males in relationship to internalized racism and low socioeconomic status, concluding that the telomere lengths are undeniably shortened by the unique stresses of racist treatment and racialized distributions of wealth that disparately affect the Black community (Chae et. al. 2017).  Though shorter telomere lengths induce a variety of problems, two of the most notable are diseases implicated in chronic aging, namely Alzheimer’s and related dementias, and earlier mortality overall.  Alzheimer’s and racism cannot be separated from one another, and future AD research must implement integrated approaches in order to best treat populations who are suffering from the disease the most brutally and at the highest rates.

Such findings as those published by the NCBI may seem to carry an overwhelmingly afro-pessimist message, but addressing that there is an issue to begin with is a step towards progress.  Yet, the truth still remains: medicine and society operate in an intertwined relationship and, if proper precautions are not taken, they can reinforce the systemic racism that lurks in their foundations.  To ensure AD research does not fall into such a racialized feedback loop, further explorations must not only take a deeper look at the differences in expression of Alzheimer’s across racial demographics, but also aim to elaborate on how racism directly plays a role in Alzheimer’s and other degenerative diseases through telomere shortening.  Additionally, research must promptly begin investigating whether such changes to telomere length at the cellular level are genetically or epigenetically translatable to offspring.  Such findings will drastically impact how potential treatments, for Alzheimer’s or other racially disparate diseases, may impact marginalized communities.  But, perhaps the largest takeaway from AD research as it stands is that racism, though a social construct, has created very real and lasting medical problems at the biological level that are far more complex than the more commonly discussed issues with diversity in and accessibility to medical care.  Until racism, in blatant, systemic, or hidden forms, is retributed and eradicated entirely at a sociological level, research must be extra vigilant of how racism interacts both directly and indirectly with the phenomena of study at hand, again, Alzheimer’s being just one example among many diseases with racial implications.  

To provide a more afro-futuristic outlook of Alzheimer’s research, the work of Kaczorowski deserves another glance.  It is important to note that her team was able to create AD mouse models with the genetic diversity that more closely resembles human expression of the disease than ever before, which is a huge feat not only for AD research at large, but may also allow for a better understanding of divergences in cases of Alzheimer’s across racial demographics, with the potential for precision medicine in treatments down the line (Kaczorowski et. al. 2019).  Another study in 2019, as reported by NPR, performed a cross-cultural study in which lower levels of tau protein were linked to a variant APOE4 gene in African Americans; however, this genetic variant, when expressed in white individuals, can triple the risk for Alzheimer’s development (Hamilton 2019).  The feats of this research, therefore, is two fold.  First, it was able to successfully engage a racially diverse group of participants, which is often lacking in AD research.  Second, it was able to uncover a potential biological source of deviance in racial expressions of Alzheimer’s which, when cross-analyzed with the works of the NCBI, Kaczorowski, and research endeavors in the future, may be able to uncover the genetic mechanisms underlying Alzheimer’s in racially distinct groups.  Kaczorowski, in presenting her work in AD research, described the tau proteins and amyloid plaques, the hallmark biomarkers for Alzheimer’s, as a match, and the degree to which the fire spreads, the degree to which the disease is manifested, is robustly determined by interactions between genes.  Perhaps further research endeavors should embody the same metaphor.  Alzheimer’s is just the match, just the starting point for research, and other disciplines, such as the sociology of race, need to be addressed in order to extinguish the fire.

References: 

CDC. (2018). U.S. burden of Alzheimer’s disease, related dementias to double by 2060. Retrieved from https://www.cdc.gov/media/releases/2018/p0920-alzheimers-burden-double-2060.html

Chae, D. H., Nuru-Jeter, A. M., Adler, N. E., Brody, G. H., Lin, J., Blackburn, E. H., & Epel, E. S. (2014). Discrimination, racial bias, and telomere length in African-American men. American journal of preventive medicine, 46(2), 103–111. https://doi.org/10.1016/j.amepre.2013.10.020

Gilmore-Bykovskyi, A. L., Jin, Y., Gleason, C., Flowers-Benton, S., Block, L. M., Dilworth-Anderson, P., Barnes, L. L., Shah, M. N., & Zuelsdorff, M. (2019). Recruitment and retention of underrepresented populations in Alzheimer's disease research: A systematic review. Alzheimer's & dementia (New York, N. Y.), 5, 751–770. https://doi.org/10.1016/j.trci.2019.09.018

Hamilton, J. (2019, January 7). Alzheimer's Disease May Develop Differently In African-Americans, Study Suggests. In NPR. Retrieved from https://www.npr.org/sections/health-shots/2019/01/07/682036486/study-suggests-alzheimer-s-disease-may-work-differently-in-african-americans

Kaczorowski, K. M. (2021, February 16). Systems genetics of normal cognitive aging and Alzheimer’s disease. Paper presented at the meeting of Loyola University Chicago Neuroscience Department.

Neuner, S. M., Heuer, S. E., Huentelman, M. J., O'Connell, K. M., & Kaczorowski, C. C. (2019, February 6). Harnessing genetic complexity to enhance translatability of Alzheimer's disease mouse models: A path towards precision medicine. Neuron, 399-411. doi:https://doi.org/10.1016/j.neuron.2018.11.040