New research links Alzheimer’s to metabolic issues, offering hope for early treatment

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Alzheimer’s disease is one of the most well-known and widespread forms of dementia, affecting millions of people around the world, especially older adults. It slowly damages memory, thinking, and behavior, and despite years of intense research, there is still no known cure.

But a new study from Yale-NUS College is offering fresh hope by suggesting a different way to understand and possibly treat the disease.

For a long time, scientists believed that Alzheimer’s was mainly caused by the buildup of a sticky protein called amyloid-beta in the brain. These clumps, or plaques, were thought to disrupt brain function and lead to memory loss. However, treatments targeting this protein have not been very successful. That’s why researchers have been exploring other possibilities.

In this new study, scientists are focusing on a different idea: that Alzheimer’s may be linked to problems with how the body produces and uses energy, especially in the brain.

More specifically, they’re looking at the mitochondria—the part of the cell that acts like a power plant, producing energy for everything the cell does. If the mitochondria don’t work properly, the entire cell suffers.

What makes this research especially interesting is that the scientists found signs of metabolic problems in their study models before any major increase in amyloid-beta levels appeared. This suggests that changes in metabolism might happen earlier than the buildup of plaques—and could even be the real starting point of the disease.

To study this, the research team used a tiny worm called Caenorhabditis elegans. It’s a simple organism, but it shares many biological features with humans, making it a useful model for studying diseases like Alzheimer’s.

One of the most exciting parts of the study was the use of Metformin, a common drug used to treat type 2 diabetes. When the researchers gave Metformin to the worms, it reversed the metabolic problems and even extended their health and lifespan.

This points to the possibility that a drug already being used safely for another condition might help delay or even prevent Alzheimer’s by fixing energy problems in the brain early on.

The findings support the idea that instead of waiting for Alzheimer’s to show up and then trying to treat it, we should focus more on preventing it by keeping our metabolism and mitochondria healthy. This approach could shift the focus of future treatments toward improving overall cell health, especially as we age.

Dr. Jan Gruber, who led the study, explains that this research supports a bigger idea: many diseases we associate with aging, including Alzheimer’s, might actually be caused by the same underlying issues—mainly, how our cells age and how their energy systems weaken over time.

By understanding aging better and keeping our cells healthy longer, we might be able to prevent not just Alzheimer’s but a wide range of age-related diseases.

Published in the journal eLife, this study is an important step toward changing how we view and approach Alzheimer’s disease. It encourages a more holistic view—one that connects brain health to the health of our body’s energy systems and highlights the potential of preventive care over reactive treatment.

In short, this research offers new hope that we may one day be able to stop Alzheimer’s before it starts—by taking care of how our bodies age at a cellular level.

If you care about Alzheimer’s disease, please read studies about the protective power of dietary antioxidants against Alzheimer’s, and eating habits linked to higher Alzheimer’s risk.

For more health information, please see recent studies that oral cannabis extract may help reduce Alzheimer’s symptoms, and Vitamin E may help prevent Parkinson’s disease.

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