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A new brain discovery could slow memory loss and protect against Alzheimer’s disease

Scientists have identified a unique group of immune cells in the brain that appear to protect against Alzheimer’s disease. These specialised microglia help reduce inflammation and block the spread of toxic proteins linked to memory loss. Here’s why it offers fresh hope for therapies that could slow or even prevent Alzheimer’s
November 10, 2025 / 11:47 IST
Scientists have found protective brain cells that may slow or prevent Alzheimer’s. Learn how microglia could help shield memory and brain health. (Image: Pexels)

Alzheimer’s is a dreadful  illness that slowly steals memory, thinking, and personality. A new discovery from an international team of researchers suggests it might just be possible that the brain cells could prevent the disease from spreading.

In a recent study published in Nature, scientists from the Icahn School of Medicine at Mount Sinai, working with colleagues in Germany and the US, have found that the brain’s immune cells — known as microglia — aren’t just bystanders in Alzheimer’s disease. Some of them may actually be its protectors.

Microglia have long been seen as double agents, and while they can clear away harmful waste, they can also spark inflammation that worsens brain damage. But this new research has identified a special subset of microglia that behave differently, they calm inflammation, slow the spread of toxic proteins, and appear to shield the brain from decline.

Using a mix of mouse models and human brain tissue, the scientists found that these protective microglia have lower levels of a molecule called PU.1 and higher levels of a receptor called CD28. Together, these changes help them control inflammation and block the build-up of the sticky amyloid plaques and tangled tau proteins that characterise Alzheimer’s.

Also Read: All about of Alzheimer's disease: Stages, risk factors, and management strategies

“Microglia are not simply destructive responders in Alzheimer’s disease, they can become the brain’s protectors,” explains Professor Anne Schaefer, a neuroscientist at Mount Sinai and senior author of the study. “This shows just how flexible these cells are, and how international teamwork can push science forward.” The team discovered that when CD28 was removed from these microglia, the brain’s inflammation worsened and more plaques formed. This confirmed that CD28 is crucial for keeping the cells in their protective mode.

It’s remarkable to see that molecules long known for their roles in the immune system also control microglial behaviour in the brain, says Dr Alexander Tarakhovsky of The Rockefeller University, another co-author. “It opens new doors for developing immune-based treatments for Alzheimer’s.”

The research builds on earlier genetic studies by Dr Alison Goate, also from Mount Sinai, who had found that people with naturally lower levels of PU.1 tend to have a reduced risk of developing Alzheimer’s. “These results explain why that genetic link exists,” she adds. “It’s a direct clue to how we might slow or prevent the disease.”

This discovery gives scientists a clearer picture of how the brain’s immune system might be harnessed to fight Alzheimer’s. Instead of targeting symptoms, future therapies could focus on boosting these protective microglia to maintain memory and brain health.

Here are 5 things you need to know about this discovery: 

  • Alzheimer’s slowly steals memory and thinking: It affects millions worldwide, gradually changing personality, memory, and daily life.
  • Special brain cells called microglia can protect the brain: Scientists discovered a subset of these immune cells that don’t just clean up waste—they also calm inflammation and stop toxic proteins from spreading.
  • Key molecules keep microglia protective: Protective microglia have lower levels of PU.1 and higher levels of CD28, which help control inflammation and block harmful amyloid plaques and tau tangles.
  • Removing CD28 makes the brain more vulnerable: Experiments showed that without CD28, inflammation increases and Alzheimer’s-related plaques grow faster, confirming its protective role.
  • This could lead to new treatments: Instead of just managing symptoms, future therapies might focus on boosting these protective microglia to slow or even prevent Alzheimer’s.

Also Read: Top 3 symptoms of early stage Alzheimer’s and dementia, shared by a neuroscientist

While it’s still early days, the findings mark an exciting shift in how scientists understand Alzheimer’s, not just as a story of brain loss, but also one of the brain’s own defences stepping up to protect itself.

FAQs on Alzheimer's disease:

1. What is Alzheimer's disease?

Alzheimer's disease is a progressive neurological disorder that causes brain cells to degenerate and die, leading to memory loss, cognitive decline, and personality changes.

2. What are the early symptoms of Alzheimer's disease?

Early symptoms include difficulty remembering recent events, confusion about time and place, trouble completing familiar tasks, and changes in mood or behaviour.

3. How is Alzheimer's disease diagnosed?

Diagnosis typically involves a combination of medical history, physical and neurological exams, mental status tests, and imaging tests to rule out other conditions.

4. What are the risk factors for Alzheimer's disease?

Risk factors include age, family history, genetics, head injuries, cardiovascular disease, and lifestyle factors like diet, exercise, and smoking.

5. Can Alzheimer's disease be prevented or cured?

Currently, there is no cure for Alzheimer's disease, but some treatments can help manage symptoms. Research is ongoing to find ways to prevent, slow down, or stop the disease.

Disclaimer: This article, including health and fitness advice, only provides generic information. Don’t treat it as a substitute for qualified medical opinion. Always consult a specialist for specific health diagnosis.

Namita S Kalla is a senior journalist who writes about different aspects of modern life that include lifestyle, health, fashion, beauty, and entertainment.
first published: Nov 10, 2025 11:45 am

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