Can this neurodegenerative disorder can be fixed anytime soon?

By Hira Sundar

Imagine a world where you can’t trust even yourself — where everything is not as it seems — so you stay hypervigilant to combat the stress that torments your unsleeping mind.

Imagine a world, dark and dim, where all you know is that you’ll never be the same. 

Imagine a world where nothing is for certain, where your own mind betrays you in a twisted cycle of never ending confusion and pain. 

These symptoms are what plagued the lives of over 5.8 million Americans in 2018 alone, in a deadly, wide-reaching condition called Alzheimer’s disease. Discovered by Alois Alzheimer, this neurodegenerative disease causes a buildup, or aggregation, of proteins in the brain, leading to symptoms such as memory loss, aggression, personality changes and confusion. 

Junior Roma Ankolekar knows this all too well — after all, her very own grandmother contracted Alzheimer’s disease when Ankolekar was just 8 years old.

“I didn’t really understand,” Ankolekar said. “They told me she was sick, but they didn’t really tell me exactly what had happened. ”

For Roma and many other families, the disease was something unknown that ravaged their lives, step by step — one symptom at a time, until it suddenly ballooned into dementia, a neurodegenerative disorder. 

“Every year there would be a dramatic change,” Ankoleakar said. “One year, [my grandmother] would not be able to read to herself anymore, and slowly as the disease progressed, she forgot who we were basically.”

Alzheimer’s disease has been studied for years, yet a cure seems as unattainable as ever. And with America’s Baby Boomers hitting the threshold age — about 65 — for dementia, a cure is imperative to help maintain our aging population. 

But first — a little background. Alzheimer’s disease is a chronic neurodegenerative disease that affects people aged mainly 65 years and above, causing symptoms such as aggression, agitation irritability, decline in vocabulary, personality changes and delusions. It starts off with a minuscule change — a tiny tweak in the gene APOE-e4

However this microscopic change has a mammoth effect on the rest of our body. A protein named Amyloid-beta stops working, and because of it, our myelin sheaths — bundles of fat surrounding our neurons — are ripped apart. The result is disastrous, as neurons cannot communicate with each other. Eventually, the brain ends up disjointed, separate, broken fragments, unable to do anything, stagnating until the disease finally takes its victims life. 

 On top of this disaster, another misfolded protein caused by the mutation of gene P301, tau, clamps to itself in a velcro-like pattern, building long, tendril-like fibers called neurofibrillary tangles. These tangles are “water-tight” — impossible to pry apart.The combination of these two prions wreak havoc on the brain, destroying sensory and memory neurons in the entorhinal cortex and hippocampus, two major ganglions that control memory and other cognitive abilities. 

Scientists can’t figure out how to stop this aggregation of prions from happening. They’ve been trying everything from fixing the root mutation in APOE-e4 that caused all of this, to even utilizing common herbs we use to try and alleviate the symptoms of Alzheimers. But nothing is working — Alzheimers will not go down without a fight. 

“Every day researchers and scientists come up with newer and newer inventions, ” Ankoleakar said. “They found this specific biomarker which shows signs of dementia and the next week it was disproven.” 

In fact, this very issue happened to her grandmother. “[The treatment] wasn’t that advanced,” Ankolekar said. “So her with depression — she was getting treatment for depression and her symptoms were getting worse and worse.”

A lack of treatment means a lack of safety, and when it comes to human lives, that’s something we simply cannot afford.

 “We [need to] have better research to come up with better treatment options,” former Phlebotomist Samantha Skolnik said. “Currently right now it’s pretty bleak if you have Alzhimers, and you are going to lose everything you know and love. Until we understand what’s causing [Alzheimer’s disease], the idea of stopping it or curing is crazy.”

But there’s still hope, as MVHS students are teaming up to help remedy the destruction the disease has wreaked upon their families. Senior Ashley Yeh has worked on a science project in MVHS’s STEM class that just might offer more insight into this ongoing battle to end Alzheimers. 

Her project involves injecting the electron carrier NADPH into the common fruit fly, Drosophila Melanogaster, which surprisingly has a pattern of cognitive decline similar to humans. Her experiment involves a negative geotaxis assay, a simple but ingenious test to measure the cognitive decline in flies. 

It starts off with some flies, already prepared by being fed NADPH, and a bottle. Drosophila Melanogaster have an ability to resist the gravity of the Earth, meaning a predisposition to flit upwards when given the opportunity. Yeh measured the time it took for them to fly upwards when given NADPH and without NADPH. She then compared these two scores to see if NADPH actually did help alleviate Alzheimers. 

“I saw that if you had a certain amount of the molecule NADPH,” Yeh said. ”It does have a positive effect on drosophila”

It’s projects like these — simple in execution but ingenious in thought — that can further research. Outside of STEM research, people can  still contribute by donating to research facilities and serving patients in medical facilities.  

“ If you can be more knowledgeable and more understanding, that is the best way to contribute,” Skolnick said. “Above and beyond that is of course financial contributions to increasing research. One of the ways to do that is when it comes up on ballot measures, it has the ability to vote in more money towards the disease that could be a way to do it if you don’t have money yourself.”

Though some MVHS students are not of voting age, urging parents or guardians to contribute can also play an important role in fighting the disease. It’s not impossible, but it’ll be a long journey till we cure Alzhiemer’s. However, with everyone’s contributions, the process will be much quicker. 

Header image: “Alzheimer’s Disease International” by Simone Mascagni is licensed under CC BY-NC-ND 4.0

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