Alzheimer’s Disease: Searching for the Cure

Nedilynn Bowser
The Eta Zeta Biology Journal
3 min readOct 27, 2023
Photo by National Cancer Institute on Unsplash

Link to original article

Background

Alzheimer’s disease is as a neurodegenerative disease (NDD) that accounts for 60–80% of dementia cases. Aging and genetics have been recognized as the main factors that increase one’s risk of contracting it. Cognitive decline is a natural part of aging, but the rate of tissue atrophy and alteration of neurotransmitters seen in the brains of Alzheimer’s patients is detrimentally anomalous.

Alzheimer’s disease has been linked to problems with protein synthesis in the brain. Like other NDDs, the symptoms result from toxic effects of misfolded proteins. These “mutant” proteins overwhelm the functional proteins, causing dysfunction within the brain. Unfortunately, this disease has no cure.

Alzheimer’s research is laborious and many components are still unknown. In order to find a cure for Alzheimer’s, a point of attack must first be identified. In this article, researchers explore specific pathways that, once fully understood, could potentially be exploited for Alzheimer’s treatment and prevention.

Summary

In this study, researchers focused on two proteins that seem to be the main source of pathology: Aß and tau. These are amyloid proteins that mutate and clump together to form a toxic complex. Researchers continue to debate whether Aß or tau is the main source of pathology or whether they work in conjunction.

As of now, there is no known method to reverse the damage caused by these rogue proteins. Each patient is treated on a case-by-case basis, which may involve either pharmacological or alternative treatments. The best outcomes require early diagnosis, because disease progression can be slowed if it is caught early. There are two existing drugs for the treatment of AD, but they only manage the symptoms while doing nothing to combat the etiology.

Generally, developing a drug that targets specific proteins is not difficult. However, the non-mutated forms of Aß and tau have essential physiological functions within the body. If these proteins were to be destroyed, it would cause major systemic complications for patients.

This article discusses four unsuccessful drug development methods. Initially, researchers attempted to develop a drug that decreases Aß protein production. Results of this experiment were not promising. They then tried blocking Aß and tau protein aggregation. Finally, they examined the dysfunction in the blood brain barrier caused by Aß protein. Unfortunately, none of these research pathways led to the development of viable treatments.

Although the results of this study did not lead to a cure, the research increased the body of knowledge on how AD develops. As scientists learn more about this disease, they will be able to design new treatments that target specific aspects of its development. Scientists suspect that AD cannot be adequately treated with a single drug. Instead, they believe that a mixture of medications, varying based on an individual’s stage of AD progression, may be the best strategy for controlling this disease. They are on the cusp of discovering such treatment s— they just need to find how all the pieces fit together. ‌

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