Researchers at the University of Arkansas for Medical Sciences (UAMS) have made a big breakthrough in the fight against Alzheimer’s disease.
Led by the esteemed Sue Griffin, Ph.D., the team has discovered a new drug that may prevent Alzheimer’s in people who carry the genetic marker linked to a higher risk of developing the disease.
Published in Communications Biology, this exciting development offers hope to millions worldwide.
Alzheimer’s disease affects a vast number of people, with approximately 50–65% of those diagnosed having inherited the Alzheimer’s gene, Apolipoprotein E4 (APOEε4), from their parents.
The risk of developing Alzheimer’s increases with the number of APOEε4 copies a person has. About 25% of the population carries one copy of APOEε4, tripling their risk of Alzheimer’s.
Meanwhile, 2–3% have two copies, making them 12–15 times more likely to develop the disease.
The research team’s discovery revolves around the negative impact of APOEε4 on the brain’s ability to dispose of waste, a process known as lysosomal autophagy.
This dysfunction leads to the accumulation of plaques and tangles in the brain, which are characteristic of Alzheimer’s disease.
Griffin’s team, pioneers in highlighting the role of APOEε4 in disrupting autophagy, have now identified both a druggable target and a promising drug candidate, CBA2, that could block the harmful effects of APOEε4.
The team emphasizes the novelty and potential impact of this discovery.
Unlike most Alzheimer’s research, which has largely focused on removing brain plaques and tangles after they form, the work is pioneering in that it seeks to prevent these hallmarks of the disease from developing in the first place.
This prevention-focused approach could be a game-changer, especially considering the limited success of current treatments aimed at reversing the disease’s progression.
The drug candidate, CBA2, is set to undergo larger-scale preclinical research.
The ultimate goal is for individuals with one or two copies of APOEε4 to take this drug regularly throughout their lives, dramatically lowering their chances of developing Alzheimer’s disease.
The foundation of this discovery was laid in 2017 when UAMS constructed the first full-length structure of the APOEε4 protein.
This achievement was made possible through bioinformatics and computational modeling. It was this detailed understanding of APOEε4’s structure that enabled the identification of a specific site on the protein that could be targeted by drugs.
This breakthrough could transform the approach to Alzheimer’s prevention and bring immense relief and hope to millions at risk of the disease.
As research progresses, the day when Alzheimer’s can be prevented before it ever takes hold seems increasingly within reach.
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The research findings can be found in Communications Biology.
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