Scientists are working hard to find better ways to treat Alzheimer’s disease, one of the most common causes of memory loss and dementia around the world. A new study from researchers at the University of Barcelona has reported an exciting discovery.
The team has designed a new experimental drug that works very differently from current Alzheimer’s treatments. Instead of simply removing harmful protein plaques in the brain, the drug appears to help brain cells return to a healthier state by correcting problems in gene activity. The research was published in the scientific journal Molecular Therapy.
Alzheimer’s disease affects millions of people worldwide. It slowly damages the brain and leads to problems with memory, thinking, and behavior. Over time, patients may struggle to remember familiar people, perform daily tasks, or communicate clearly. The disease places a heavy emotional and financial burden on families and healthcare systems.
For many years, scientists believed that a substance called beta‑amyloid was the main cause of Alzheimer’s disease. Beta‑amyloid forms sticky plaques that build up between nerve cells in the brain. Many modern Alzheimer’s drugs, such as lecanemab and donanemab, aim to remove these plaques.
While these drugs are an important step forward, their benefits are limited. Studies show that they slow the worsening of memory and thinking problems by about 27 to 35 percent. They can also cause side effects, and they mainly target only one part of the disease process.
Because of these limitations, scientists are searching for new approaches that target deeper causes of the disease.
The new compound developed by the University of Barcelona team is called FLAV‑27. According to the researchers, this drug does not focus only on beta‑amyloid plaques. Instead, it acts on a process known as epigenetic regulation in brain cells.
Epigenetics refers to chemical changes that control how genes are turned on or off without changing the DNA itself. These changes help determine which genes are active in a cell at any given time. In the brain, epigenetic regulation is important for processes such as learning, memory, and communication between nerve cells.
In Alzheimer’s disease, scientists believe that this gene regulation system becomes disrupted. Some important genes that help neurons stay healthy become less active, while harmful processes may become more active. This imbalance can contribute to the progression of the disease.
The FLAV‑27 compound targets an enzyme called G9a. This enzyme plays an important role in controlling gene activity in the brain. When G9a becomes too active, it can silence genes that are needed for healthy brain function, including genes involved in memory formation and the strengthening of connections between neurons.
The new drug blocks the activity of the G9a enzyme. It does this by preventing another molecule, called S‑adenosylmethionine, from interacting with the enzyme. This slows down harmful epigenetic changes and allows neurons to regain healthier patterns of gene activity.
The scientists tested FLAV‑27 in several laboratory models of Alzheimer’s disease. The experiments included cell studies, research in small organisms such as the worm C. elegans, and studies in mice with forms of Alzheimer’s disease.
The results were encouraging. The treatment reduced key signs of Alzheimer’s disease in the brain, including the buildup of beta‑amyloid and a harmful form of tau protein known as phosphorylated tau. These proteins are known to damage nerve cells and disrupt communication between them.
More importantly, the treated animals also showed improvements in behavior and brain function. In mouse models of Alzheimer’s disease, the researchers observed better short‑term memory, long‑term memory, spatial memory, and social behavior. Brain examinations also showed healthier structures in the connections between neurons, called synapses.
These findings suggest that the drug not only affects biological markers of the disease but may also restore some cognitive abilities.
Another important discovery from the study was the identification of biological markers that could help doctors track how well the treatment works.
The researchers found that certain molecules, including an epigenetic marker called H3K9me2, the protein SMOC1, and a form of tau protein known as p‑tau181, were higher in both the brain and blood when Alzheimer’s disease was present.
When animals were treated with FLAV‑27, the levels of these markers returned closer to normal. This suggests that simple blood tests might eventually help doctors monitor the effectiveness of the treatment in patients.
The ability to measure treatment effects through blood tests could make future clinical trials easier and help doctors identify which patients are most likely to benefit from the therapy.
Although these results are promising, the drug is still in the early stages of development. FLAV‑27 has so far been tested only in laboratory and animal studies. Before it can be used in humans, researchers must complete additional safety studies and regulatory testing.
The next steps include further preclinical studies in different animal species, developing a pharmaceutical form of the drug, and preparing documents needed to apply for approval to begin clinical trials.
A biotechnology company called Flavii Therapeutics, a spin‑off from the University of Barcelona founded in 2025, has obtained the exclusive license to develop FLAV‑27. The company will oversee the remaining research and clinical development needed to test the drug in people.
Overall, the study provides an important new perspective on Alzheimer’s disease. Instead of focusing only on removing harmful proteins, this approach targets deeper biological mechanisms that control how brain cells function.
If future studies confirm these results in humans, epigenetic therapies like FLAV‑27 could represent a new generation of treatments that slow or even modify the disease itself rather than only easing symptoms.
However, it is important to remember that many experimental treatments that work in animals do not always succeed in human trials. The road from laboratory discovery to approved medicine can take many years and involves careful testing to ensure safety and effectiveness.
Even so, the findings highlight a promising direction for Alzheimer’s research. By studying how gene activity changes in the brain, scientists may discover new ways to restore healthy brain function and slow the progression of this devastating disease.
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.
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