Scientists develop game-changing Alzheimer’s drug that reverses brain damage

A scientific breakthrough from Spain may soon bring new hope to people living with Alzheimer’s disease. Researchers have developed a drug candidate that doesn’t target brain plaques like most current treatments. Instead, it aims to stop the brain inflammation that may be driving the disease in the first place.

Alzheimer’s is the top cause of dementia worldwide. More than 800,000 people in Spain alone live with the condition. There is no cure. Current drugs help only modestly—and mainly in early stages. But new evidence suggests inflammation in the brain may be more than a symptom. It could be one of the main engines of disease progression.

A team at the University of Barcelona believes it may have found a way to shut that engine down. The researchers created a new molecule that targets inflammation directly, offering a fresh approach to treatment. Their work centers on a key enzyme that affects how the brain controls inflammation.

This enzyme, known as soluble epoxide hydrolase (sEH), breaks down protective compounds called EETs. These molecules help calm inflammation and guard nerve cells. When sEH levels are high, those helpful compounds vanish, and harmful ones take their place. In both Alzheimer’s patients and mouse models, sEH levels were abnormally high in the hippocampus—the brain’s memory hub.

By blocking sEH, the brain retains more of its natural anti-inflammatory tools. That could be a game-changer. Alzheimer’s is messy—it doesn’t have just one cause. The disease involves plaques, tangles, cell loss, and an overactive immune response. A drug that lowers inflammation could tackle several of these issues at once.

This thinking led the team to develop a new compound called UB-SCG-74. The journey began with an earlier molecule, UB-SCG-51, which crossed the blood-brain barrier and blocked sEH efficiently. In mice with Alzheimer’s, the drug did more than reduce inflammation. It slowed nerve cell death, cut toxic proteins, and boosted brain performance.

Still, there was room to improve. The new version, UB-SCG-74, absorbs better in the body and sticks around longer. These upgrades make it a stronger candidate for future clinical trials. The research team believes this compound could be a key step toward a much-needed treatment that addresses the disease’s root causes—not just its symptoms.

UB-SCG-74 was tested in 5XFAD mice—animals that quickly develop symptoms similar to human Alzheimer’s. The treated mice showed better memory, stronger synaptic plasticity (the ability of brain cells to communicate), and fewer signs of brain damage. Even more exciting, these benefits lasted for a full month after the treatment ended. That long-lasting impact hints that the drug might not just mask symptoms, but actually change the disease’s course.

UB-SCG-74 outperformed both donepezil, a commonly used Alzheimer’s drug, and ibuprofen, a known anti-inflammatory. No signs of toxicity were found in safety tests, which supports moving the compound toward preclinical development.

For decades, scientists have focused on clearing amyloid plaques from the brain as a way to treat Alzheimer’s. But that strategy has often failed. In the past ten years, many plaque-targeting drugs have not shown enough benefit to make it to patients.

The team behind UB-SCG-74 believes that tackling brain inflammation could be a more powerful way to protect the brain. "Strategies that have been tried unsuccessfully over the past ten years have specifically targeted beta-amyloid accumulation and plaque formation in the brain, but there is evidence that neuroinflammation is a major cause of Alzheimer’s disease,” the study authors wrote.

The new compound works by restoring the balance of inflammatory molecules. It not only lowers harmful cytokines but also raises levels of molecules that reduce inflammation. This wide-reaching impact on many pathways at once may explain why the treatment helped preserve neurons and protect brain function.

Mercè Pallàs, one of the lead researchers and a scientist at the University of Barcelona and CIBERNED, says that this anti-inflammatory action is tied to improved blood flow in the brain as well.

EETs play a role in keeping blood vessels healthy, so stopping sEH allows the brain to maintain better circulation. That could offer protection against strokes or oxygen loss, which often worsen Alzheimer’s symptoms.

Mice treated with UB-SCG-74 didn’t just perform better on memory tasks. Their brain cells also looked healthier under the microscope. Dendrites—the tiny branches that allow neurons to connect—were preserved. The structure of neural networks remained intact. These findings point to more than temporary relief. They suggest the drug may be able to stop or even reverse damage in the brain.

Santiago Vázquez, another lead author from the University of Barcelona, says this result is crucial. “This could help preserve neuronal function and reduce neuronal death associated with Alzheimer’s disease,” he noted. The fact that these effects lasted even after treatment stopped suggests that the drug changes how the disease unfolds, not just how it feels.

Despite the strong results in mice, much work remains before this compound can be used in humans. Drug development is a slow and careful process. Researchers must complete further lab tests, followed by clinical trials involving real patients. These trials will need to confirm both the safety and the effectiveness of the drug in people with Alzheimer’s.

The University of Barcelona has licensed the patent for UB-SCG-74 to a U.S. pharmaceutical company, which will lead the next steps in development. Pallàs and Vázquez are working with the company as consultants. Their goal is to ensure the project stays focused on fighting neuroinflammation and moving the drug forward.

They aren’t alone in this work. Scientists from the Institute of Biomedical Research of Barcelona, the August Pi i Sunyer Biomedical Research Institute, the Centre for Biomedical Research Network (CIBERNED), and the University of Bonn are also part of the research effort. The study was published in ACS Pharmacology & Translational Science.

This seven-year project shows how rethinking Alzheimer’s could open new doors. Instead of trying to remove plaques after they form, it may be more effective to protect the brain before they cause too much harm. That’s where sEH inhibitors like UB-SCG-74 could make a difference.

Blocking this enzyme helps keep inflammation in check, supports blood flow, prevents nerve cell death, and improves memory—all at the same time. This broad, multitarget approach could become a new standard in treating Alzheimer’s, especially since past single-target strategies have fallen short.

If future trials confirm these benefits in humans, this treatment might not just slow the disease—it could change the way it develops entirely. That kind of shift would bring much-needed hope to families affected by dementia and move medicine a step closer to one day curing Alzheimer’s disease.

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

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