Alzheimer’s disease is often talked about using large numbers. Millions of people around the world are affected, and the number continues to grow every year.
The cost to families and health systems is enormous. But for those living with the disease and their loved ones, Alzheimer’s is not about statistics. It is deeply personal. It slowly takes away memories, personality, and the sense of who someone is.
One scientist, Nicholas Tonks from Cold Spring Harbor Laboratory, understands this pain firsthand. His own mother lived with Alzheimer’s, and he describes the experience as a long and gradual loss, where the person you love fades away little by little.
For many years, researchers have tried to understand what causes Alzheimer’s disease and how to slow it down. One of the most widely discussed features of the disease is the buildup of a substance in the brain often called plaque. This plaque is made from a small protein fragment known as amyloid-beta.
Amyloid-beta is naturally produced in the brain, but in Alzheimer’s disease, it builds up and sticks together. Over time, these clumps interfere with how brain cells communicate and survive, contributing to memory loss and thinking problems.
In new research, Professor Tonks and his team, including graduate student Yuxin Cen and postdoctoral researcher Steven Ribeiro Alves, have discovered a promising new way to help the brain deal with this harmful buildup.
Their study, published in a leading scientific journal, shows that blocking a protein called PTP1B can improve learning and memory in mice with symptoms similar to Alzheimer’s disease.
PTP1B is an enzyme that Tonks first identified in the late 1980s. Since then, he has spent decades studying how it affects health and disease. In this latest work, the researchers found that PTP1B interferes with another protein called SYK. SYK plays an important role in controlling microglia, which are immune cells in the brain.
These cells act like cleaners, removing waste, damaged cells, and harmful substances such as amyloid-beta.
In the early stages of Alzheimer’s disease, microglia try to clear away amyloid-beta. But as the disease progresses, they become tired and less effective. They struggle to keep up with the growing amount of plaque. The researchers found that PTP1B makes this problem worse by blocking signals that help microglia do their job properly.
When PTP1B was inhibited in the mouse model, microglia worked better and were able to clear more amyloid-beta from the brain. As a result, the mice showed improvements in learning and memory.
This discovery is especially interesting because Alzheimer’s disease is not only linked to amyloid-beta. Conditions such as obesity and type 2 diabetes are also known to increase the risk of developing Alzheimer’s.
These conditions are becoming more common worldwide, and many scientists believe they play a role in the rising number of Alzheimer’s cases. PTP1B is already known to be involved in obesity and diabetes, which makes it an attractive target for treatment. By blocking PTP1B, it may be possible to address several risk factors at once.
Current Alzheimer’s treatments mainly focus on removing amyloid-beta from the brain. While some of these drugs have been approved, their benefits are often limited, and many patients see only modest improvements. The researchers suggest that targeting PTP1B could offer a broader approach.
Instead of focusing on just one part of the disease, PTP1B inhibitors may improve immune function in the brain, support better clearance of harmful proteins, and possibly influence metabolic problems linked to Alzheimer’s.
Professor Tonks and his team are now working with a biotechnology company to develop PTP1B inhibitors for several diseases, including Alzheimer’s. He believes the future of Alzheimer’s treatment will likely involve combining different therapies.
Existing drugs could be used together with new treatments that target PTP1B. The aim is not necessarily to cure the disease, but to slow its progression and help people maintain a better quality of life for longer.
When reviewing these findings, the study stands out because it connects several important pieces of Alzheimer’s disease. It links brain immune cells, plaque buildup, and metabolic health into a single pathway that can be targeted with one type of treatment.
While the results are still based on animal studies and more research is needed before testing in humans, the work provides a strong scientific foundation. It suggests that helping the brain’s own cleaning system work better may be a powerful way to fight Alzheimer’s.
This research offers cautious but real hope that future treatments could be more effective and help families hold on to their loved ones for longer.
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The study is published in PNAS.
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