Alzheimer’s disease is a serious condition that affects the brain, mostly in older people. It causes memory loss, confusion, and changes in behavior.
One of the key problems in Alzheimer’s is the buildup of a protein called tau inside brain cells. Normally, tau helps keep the structure of nerve cells stable, like a frame holding everything in place.
But in Alzheimer’s, tau proteins lose their normal shape and start sticking together, forming long twisted structures called fibrils. These fibrils block the transport system inside nerve cells, which eventually leads to the death of these cells and memory loss.
Scientists have been trying for years to understand exactly how these tau fibrils form. A new study from researchers at Tokyo Metropolitan University offers a fresh look at the process. Instead of looking at the final stage when fibrils have already formed, the team focused on what happens at the very beginning.
The researchers were led by Professor Rei Kurita. They used ideas from a different area of science—polymer physics—to better understand what’s going on. Polymers are long chains of repeating parts, and scientists have studied how these chains come together to form solid crystals.
They noticed that polymers don’t turn into crystals all at once. First, they form soft, temporary clusters. Only after that do they become solid and well-organized. The team thought something similar might be happening with tau proteins.
To test this idea, they studied tau proteins floating in a solution. They found that tau does not turn into fibrils immediately. Instead, it first forms loose groups of proteins, which are very tiny—only a few nanometers across. These early clusters are not solid or stable. They’re soft and reversible, meaning they can come apart easily.
Using special tools like X-ray scattering and fluorescent dyes, the team confirmed these tiny clusters really existed. Then, they tried changing the solution to see if they could stop the clusters from forming.
By adjusting the salt levels and adding a substance called heparin, they were able to prevent the clusters. When the clusters didn’t form, the tau fibrils didn’t form either.
The researchers believe that the salt reduces the strength of the interaction between tau proteins and heparin. This makes it harder for the proteins to come together and form those early clusters. Since the fibrils grow from these clusters, stopping them early could be the key to preventing Alzheimer’s damage.
This discovery could open a new path for treating Alzheimer’s. Instead of trying to break down the large fibrils after they’ve formed, new treatments could focus on blocking the first step—these soft, tiny clusters. It might be a gentler and more effective way to stop the disease before it causes too much damage.
This idea might also help with other diseases that involve protein buildup in the brain, such as Parkinson’s disease. These findings could shift how scientists think about treating brain disorders caused by protein clumping.
To sum up, the study shows that tau fibrils don’t appear all at once. They grow from smaller, soft clusters of proteins. By stopping these early clusters, we might stop the disease from getting worse. It’s a new and hopeful direction for future Alzheimer’s research.
If you care about Alzheimer’s, please read studies about Vitamin D deficiency linked to Alzheimer’s, vascular dementia, and Oral cannabis extract may help reduce Alzheimer’s symptoms.
For more information about brain health, please see recent studies about Vitamin B9 deficiency linked to higher dementia risk, and results showing flavonoid-rich foods could improve survival in Parkinson’s disease.
The study is published in Neuroscience Research.
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