Scientists from Auburn University have discovered a fundamental principle of how brain cells remain connected, and their discovery could change how we understand Alzheimer’s disease. Published in Cell reportsThis groundbreaking study reveals that neurons-de cells that use us simple physics to maintain their connections, and that these processes change in the patients of Alzheimer’s.
For decades, scientists have wondered how brain cells keep in touch with each other, even when they do not send signals. Dr. Michael W. Gramlich and his team from Auburn University have now given an answer, with the help of Physics to explain this process for the first time.
We have discovered that neurons use a kind of natural power based on entropy – such as an invisible glue – to keep their connections strong. And when this process stops working correctly, this can be an early sign of Alzheimer’s disease. “
Dr. Michael W. Gramlich, Auburn University
Why this matters
Imagine a city where all traffic lights are always working, so that cars continue to move efficiently. Imagine what happens when some of those lights take out malfunction cars, the traffic slows down and chaos arises. This is similar to what happens in the brain when neurons do not maintain their connections in the early stages of AD. Neurons remain connected in a healthy brain with the help of specific molecular rules, even when they are at rest. But with Alzheimer’s disease, these connections begin to break down, leading to memory loss and cognitive decline.
Dr.’s team Gramlich discovered that neurons maintain a specific density of objects, called Vesicles, to maintain these crucial connections. With the help of advanced microscopes and computer models, they discovered that the closer these blisters are, the stronger the connection between neurons. The results also suggest that neurons use vesicle density as a way to also increase or reduce the connections.
A breakthrough in understanding Alzheimer’s disease
One of the most exciting findings in this study is that changes in these neuronal compounds can be an early warning signal of Alzheimer’s disease. The research team discovered that in the brain that is affected by Alzheimer’s disease, the density of blisters has changed considerably, causing the brain’s ability to communicate. Although previous research teams have focused on the biological basis for Alzheimer’s disease, this study shows that the use of fundamental physics in combination with biology can offer a new path to solve the problem of Alzheimer’s disease.
“This discovery gives us a new way to think about Alzheimer’s disease,” said Dr. Gramlich. “If we can find ways to restore these connections, we may be able to delay or even prevent part of the damage caused by the disease.”
A team effort with permanent impact
This study was the result of a cooperation effort at Auburn University, with contributions from Dr. Miranda rode and graduated student Paxton Wilson, together with three students. Their work not only promotes our understanding of brain function, but also opens the door for new treatments that can help millions of people worldwide.
The findings of this study may have far -reaching implications that may influence future treatments for neurodegenerative diseases. By discovering how neurons maintain their connections, scientists now have a new target for therapies aimed at keeping the brain healthy as we get older.
This work builds on the earlier successful studies of cooperation into the underlying molecular and physical processes that lead to the disease and dementia of Alzheimer’s. The research of Auburn University makes waves in the scientific community, which again proves that advanced discoveries can come from unexpected places. This breakthrough in neuroscience could change how we combat Alzheimer’s disease and protect brain function for coming generations.
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Journal Reference:
Wilson, P., et al .. (2025). Presynaptic recycling pool density regulates spontaneous synaptic vesicle exocytosis speed and is registered in the presence of β-amyloid. Cell reports. doi.org/10.1016/j.celrep.2025.115410.