Researchers discover new protein that protects the brain against Alzheimer’s disease

A new study from St. Jude Children’s Research Hospital and published in the journal, Nature Structural & Molecular Biology, offers a fresh path in the battle against Alzheimer’s disease. For the first time, scientists have shown that a protein called midkine may protect the brain by stopping harmful changes that lead to memory loss. While midkine has been linked to Alzheimer’s before, this study shows clear evidence that the protein plays an active role in slowing the disease.

Alzheimer’s disease affects millions of people worldwide and has long puzzled researchers. It’s marked by clumps of a sticky substance called amyloid beta that build up in the brain. These clumps—or “assemblies”—disrupt brain cells and cause them to die, leading to memory loss, confusion, and changes in behavior. The new research reveals that midkine may act as a shield, preventing these harmful clumps from forming in the first place.

Midkine is a small growth factor protein. It’s most active during early human development but also plays a role in healing and cell growth later in life. In cancer, it’s often found in high amounts and is used as a biomarker. In the past, scientists noticed that people with Alzheimer’s disease also had more midkine in their brains. But no one knew why—or what it meant.

Dr. Junmin Peng, who led the study at St. Jude’s Departments of Structural Biology and Developmental Neurobiology, wanted to dig deeper. “We know that correlation is not causative,” he explained. “So we wanted to demonstrate convincingly that real interactions are occurring between the two proteins.”

Using a mix of advanced lab tools—including electron microscopy, circular dichroism, fluorescence sensors, and nuclear magnetic resonance (NMR)—his team studied how midkine interacts with amyloid beta. What they found was surprising: midkine doesn’t just show up near amyloid beta; it actively prevents it from sticking together.

This discovery is crucial. It suggests that the protein isn’t simply a byproduct of Alzheimer’s—it could be part of the body’s natural defense system.

To test this idea, the scientists used a special fluorescent dye called thioflavin T. This dye lights up when it detects amyloid beta clumps. When midkine was added, the brightness dropped, suggesting fewer clumps were forming. It didn’t stop there. Using NMR, the team saw that midkine disrupted two specific steps in the buildup process: elongation and secondary nucleation.

Elongation is when the sticky protein chains get longer. Secondary nucleation is when small clumps trigger more clumps to form nearby. Both processes are essential for the disease to progress. Midkine interrupted both.

“Once the amyloid beta assemblies grow, the signal becomes weaker and broader until it disappears because the technique can only analyze small molecules,” Peng said. “But when we add in midkine, the signal returns, showing that it inhibits the large assemblies.”

To go further, the researchers created a mouse model of Alzheimer’s disease. These mice were designed to have higher levels of amyloid beta, mimicking the human version of the disease. Then, the scientists removed the midkine gene from some of the mice.

The result? The mice without midkine had even more amyloid beta clumps than the ones with it. This proved midkine has a protective effect in a living brain, not just in lab dishes.

The team’s discovery doesn’t just help explain part of the disease—it opens up new options for how to treat it. While most Alzheimer’s drugs focus on clearing amyloid beta after it forms, this approach is different. It suggests we may be able to stop the problem before it begins.

“We want to continue to understand how this protein binds to amyloid beta so we can design small molecules to do the same thing,” said Peng. “With this work, we hope to provide strategies for future treatment.”

Drug developers might be able to design compounds that mimic midkine’s action, or even create synthetic versions of midkine that work better in the body. Since midkine is a naturally occurring protein, therapies based on it might also avoid some of the side effects that have troubled other Alzheimer’s treatments.

It also raises the question: could midkine levels be boosted naturally? If researchers can find ways to safely increase midkine in the brain, that may delay the onset of the disease or make it less severe.

This study adds a new piece to the Alzheimer’s puzzle. For years, the field has focused on how to clear amyloid beta from the brain once it’s formed. But this research from St. Jude points toward a new strategy—preventing the buildup in the first place.

What makes this finding even more interesting is how midkine behaves in other diseases. It’s been studied for its role in cancer and inflammation, and now it seems to have a part to play in the brain as well. Understanding one protein in different health conditions could help scientists find shared pathways and targets.

Importantly, this study also shows how science builds on itself. The link between midkine and Alzheimer’s had been seen before—but it took new tools and careful experiments to figure out what that link actually meant. Thanks to this work, researchers now have a new direction to explore in the search for better treatments.

Alzheimer’s remains a complex and devastating disease, but this breakthrough gives hope. By learning how midkine works, future treatments could be developed that slow or even stop the disease’s progress. That could one day change the lives of millions of people.

Note: The article above provided above by The Brighter Side of News.

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