Alzheimer’s disease is one of the most common causes of dementia worldwide. It slowly damages memory, thinking ability, and everyday functioning. As the disease progresses, people may struggle to remember recent events, recognize familiar faces, or carry out simple tasks.
Scientists have spent decades trying to understand exactly how Alzheimer’s begins and why it gets worse over time. A major feature of the disease is the buildup of sticky protein clumps in the brain called amyloid plaques. These plaques are believed to damage brain cells and contribute to the loss of memory and other cognitive abilities.
For many years, researchers believed that certain immune cells in the brain, called microglia, mainly helped protect the brain by removing harmful materials, including amyloid plaques. Microglia act as the brain’s cleaning and defense system. They constantly scan the brain for damage, infection, or waste products.
When they detect something harmful, they try to remove it and restore normal conditions. Because of this protective role, many scientists have focused on ways to stimulate microglia so they can clear plaques more effectively in people with Alzheimer’s disease.
However, a new study led by researchers from VIB and KU Leuven in Belgium suggests that the story may be more complicated. The research team discovered that microglia may actually contribute to the formation of amyloid plaques in the early stages of Alzheimer’s disease.
Their findings challenge the long-standing belief that these cells only help remove plaques. The study was published in the scientific journal Proceedings of the National Academy of Sciences.
The scientists found that microglia can transform small, soluble pieces of a protein called amyloid-beta into larger structures known as fibrils. Amyloid-beta is a protein fragment that naturally forms in the brain.
In healthy conditions, it is usually cleared away before it can accumulate. However, in Alzheimer’s disease, amyloid-beta can clump together and form plaques between nerve cells.
In their experiments, the researchers observed that microglia can reshape soluble amyloid-beta, particularly a form called Aβ42, into long fibers that act as “seeds.” Seeding is an important process in many diseases involving protein clumps.
It means that once one protein aggregate forms, it can trigger the formation of many more aggregates. This process can rapidly increase the amount of harmful protein structures in the brain.
According to Professor Joost Schymkowitz, co-senior author of the study at the VIB-KU Leuven Center for Neuroscience, scientists previously thought that amyloid plaques formed naturally through chemical processes in the brain. However, the new findings suggest that microglia may actively help create these plaques while trying to respond to the problem.
Professor Frederic Rousseau, another co-senior author of the study, explained that the amyloid produced by microglia looks very similar to the plaques found in the brains of people with Alzheimer’s disease.
Using special laboratory tests called seeding assays, the researchers showed that the protein aggregates generated by microglia behave much like those observed in patients. They also trigger biological responses in cells that resemble those seen during the disease.
This discovery may help explain why amyloid plaques appear in certain patterns in the brain and why the disease spreads over time. If microglia contribute to the seeding process, they could unintentionally accelerate plaque formation while attempting to protect brain tissue.
The study also provides scientists with a new and more realistic model for studying Alzheimer’s disease. In the past, researchers often created amyloid plaques in laboratory containers by allowing proteins to clump together naturally.
However, scientists later noticed that plaques formed in patients’ brains looked different from those produced in the lab. The new findings suggest that including microglia in experiments may produce amyloid structures that more closely resemble those seen in real patients.
This improved model could help researchers better understand the early stages of Alzheimer’s disease. By studying how microglia influence plaque formation, scientists may be able to design treatments that target the disease more effectively.
The discovery may also affect how future Alzheimer’s therapies are developed. Several experimental treatments aim to activate microglia so they can remove amyloid plaques more efficiently. However, if microglia sometimes contribute to plaque formation, especially early in the disease, scientists may need to rethink these strategies.
Instead of simply stimulating microglia, future treatments might focus on controlling their activity more carefully. For example, therapies could be designed to encourage microglia to remove harmful proteins while preventing them from triggering the seeding process that leads to plaque growth.
Alzheimer’s disease currently affects nearly 55 million people worldwide, and this number is expected to increase as populations age. Understanding how amyloid plaques form and spread in the brain is one of the most important challenges in neuroscience.
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.
The research findings were published in the journal Proceedings of the National Academy of Sciences.
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