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Samyuktha Shanthakumar

Mrs. Ginger McClendon

Prosper Career Independent Study

19 January 2024

Evidence of Learning: First Mentor Meeting of Second Semester

Throughout the first semester of PCIS, I focused my research on neuroscience, primarily

on how the brain makes new neural pathways when a person faces severe injuries to the brain.

My mentor is a cardiovascular researcher who researches pharmaceutical products and diseases

that affect the circulatory system. During our first meeting, I discussed with my mentor that I

would like to create a children’s book or a poster about some neurological phenomena. My

mentor told me that the project I would work on could be based on how endothelial damage

contributes to the development of diseases like Alzheimer’s and Dementia.

The endothelium is a single layer of tightly packed cells that cover the surfaces of organs

and cavities in our body, such as the heart, blood vessels, and lymphatic vessels. If we visualize a

blood vessel as a multilayered tube, the endothelium of a blood vessel would be the innermost

layer of the blood vessel. The endothelium’s functions include controlling the artery’s size,

releasing essential chemicals, and transporting blood and other nutrients throughout the body.

When discussing how endothelial dysfunction contributes to Alzheimer’s, we are referring to the

cerebral endothelial cells that comprise the blood-brain barrier (BBB). The BBB is a diffusion

barrier that covers the innermost layer of the blood vessels in our brains. Its primary function is

to regulate or impede the diffusion of solutes and other compounds from the blood into the

brain’s cerebrospinal fluid. If the endothelial cells of the BBB become dysfunctional or damaged,
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a break will form in the BBB. The damaged BBB, as a result, fails to regulate solute flow and

allows many toxic compounds to enter the cerebrospinal fluid. In the elderly population, the

unregulated flow of toxic compounds causes the neuronal cells to disintegrate. Currently, there is

no definitive answer for what causes endothelial cell dysfunction in the BBB. One hypothesis my

mentor explained to me is an accumulation of copper in endothelial cells that eventually

toxicates the cell and breaks it down. Like many other elements in the body, copper plays a vital

role in helping our body conduct essential functions. However, in excess, this element is toxic to

endothelial cells. Researchers hypothesize that this accumulation of copper is caused by the

interference of the protein amyloid-β. Generally, copper travels through endothelial cells in

various steps and is eventually expelled. However, when an amyloid-β protein interferes, it can

disrupt a step of the process when the copper is traveling and prevent it from exiting the cell,

ultimately causing copper to accumulate. The deposition of copper causes the cells to break

down, causing a leak in the blood-brain barrier. Treatments to prevent endothelial damage caused

by amyloid-β are still being researched.

I can use the knowledge I gained during my first mentor meeting to plan my final project.

As of now, I have an idea to make a poster with information about this topic and present it to

people who are most susceptible to Alzheimer’s and Dementia: the elderly population. As I am

taking the Certified Nurse Assistant course this year, I have made connections with a couple of

nursing homes and assisted living facilities. By speaking with the directors or managers at these

facilities, I could present my research to the seniors there. I am incredibly grateful to my mentor

for informing me about this fascinating hypothesis and study.

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Works Cited

Blood Brain Barrier. Dr Matt & Dr Mike, 2020. Youtube, https://youtu.be/eakL-xHwWL4.

Accessed 20 January 2024.

Kelleher, Rory J., and Roy L. Soiza. “Evidence of endothelial dysfunction in the development of

Alzheimer's disease: Is Alzheimer's a vascular disorder?” American Journal of

Cardiovascular Disease, vol. 3,4, no. 197-226, 2013,

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3819581/. Accessed 1 January 2024.