Dementia is one of the most feared health conditions of our time. It slowly takes away memory, thinking ability, and independence, affecting not only those diagnosed but also their families and caregivers.
Today, more than 50 million people around the world are living with Alzheimer’s disease or related forms of dementia, and that number continues to rise as populations age. Despite decades of research, effective treatments remain very limited.
Most existing therapies focus on brain cells themselves, such as reducing protein build-up or inflammation. However, scientists are now discovering that problems with blood flow in the brain may play a much larger role than previously thought.
A new study from researchers at the University of Vermont’s Robert Larner, M.D. College of Medicine offers fresh hope. The research suggests that restoring a missing natural molecule in the blood vessels of the brain could improve blood flow and reduce symptoms linked to dementia.
The findings were published in the journal Proceedings of the National Academy of Sciences and are based on detailed laboratory studies that explored how brain blood vessels work and what goes wrong in disease.
The brain is an energy-hungry organ. Although it makes up only a small percentage of body weight, it uses a large share of the body’s oxygen and nutrients. To function properly, it depends on a steady and carefully controlled flow of blood.
Even small disruptions in this blood supply can affect memory, attention, and thinking over time. Many scientists now believe that long-term problems with brain blood flow may help drive dementia, especially in conditions like Alzheimer’s disease.
The University of Vermont research team focused on a protein called Piezo1. This protein sits on the surface of cells that line blood vessels. Its job is to sense the physical force created when blood flows past.
When blood moves through vessels, it creates gentle friction, and Piezo1 acts like a sensor that responds to this pressure. Under healthy conditions, this helps blood vessels adjust their size so the brain gets the right amount of blood at the right time.
However, the researchers found that Piezo1 can become overactive in certain brain diseases. When this happens, blood vessels do not respond normally, and blood flow to the brain becomes disturbed.
Previous studies had already shown that changes in the Piezo1 gene can affect how blood vessels behave. This new work goes further by showing that Alzheimer’s disease and related dementias are linked to unusually high Piezo1 activity in brain blood vessels.
The key discovery came when the scientists examined a natural substance called PIP2. PIP2 is a type of fat-like molecule found in cell membranes throughout the body.
Although it may sound unimportant, PIP2 plays a vital role in how cells communicate and how proteins in cell membranes behave. In healthy brain blood vessels, PIP2 helps keep Piezo1 activity under control.
The researchers discovered that PIP2 acts as a natural brake on Piezo1. When PIP2 levels drop, Piezo1 becomes too active. This overactivity disrupts normal blood flow in the brain.
In their experiments, the scientists found that restoring PIP2 levels calmed Piezo1 down and allowed blood vessels to function normally again. As a result, brain blood flow improved.
To test this idea, the team added PIP2 back into the circulatory system in their experimental models. The results were striking. Blood flow in the brain returned to healthier patterns, suggesting that replacing this missing molecule could correct an important underlying problem in dementia-related blood vessel dysfunction.
While the study was conducted in preclinical models, it provides a strong biological explanation for how blood flow problems arise and how they might be fixed.
The lead researcher, Dr. Osama Harraz, described the findings as a major step forward. He explained that understanding the basic biology of how brain blood vessels fail allows scientists to think more clearly about new treatments.
Instead of only targeting damaged brain cells after harm has already occurred, this approach aims to restore healthy blood flow and protect the brain earlier in the disease process.
Looking ahead, the research team plans to study exactly how PIP2 controls Piezo1. They want to know whether PIP2 physically attaches to Piezo1 or whether it works by changing the structure of the cell membrane around it. They also aim to understand why PIP2 levels drop in diseases like Alzheimer’s and whether this loss can be prevented or reversed.
From an analytical point of view, this study is important because it shifts attention toward the blood vessels of the brain, an area that has often been overlooked in dementia research. The findings suggest that vascular problems are not just side effects of dementia but may be active drivers of the disease.
By identifying a specific molecule and a clear mechanism, the research provides a realistic target for future drug development.
While much more work is needed before this approach can be tested in humans, the study offers a promising and logical path toward therapies that restore brain blood flow and potentially slow cognitive decline rather than simply treating symptoms after damage has occurred.
If you care about dementia, please read studies about low choline intake linked to higher dementia risk, and how eating nuts can affect your cognitive ability.
For more information about brain health, please see recent studies that blueberry supplements may prevent cognitive decline, and results showing higher magnesium intake could help benefit brain health.
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