Bahnbrechendes Medikament, das in Tiermodellen den kognitiven Rückgang bei der Alzheimer-Krankheit umkehren kann: Im Gegensatz zu aktuellen Medikamenten, die Beta-Amyloid-Plaques im Gehirn entfernen, programmiert ein neues experimentelles Medikament das neuronale Epigenom neu, indem es die Genexpression korrigiert, die zum Fortschreiten der Krankheit beiträgt.

Researchers design a **pioneering drug capable of reversing cognitive decline in Alzheimer’s disease in animal models**

A team from the Institute of Neurosciences of the University of Barcelona (UBneuro) has designed and validated in animal models an innovative compound with a pioneering mechanism of action for the treatment of Alzheimer’s disease. **Unlike current drugs, which mainly remove beta-amyloid plaques that accumulate in the brain, this new experimental drug reprogrammes the neuronal epigenome by correcting alterations in gene expression that contribute to the progression of the disease**. The results of this study, published in Molecular Therapy, open the door to an epigenetic-based therapeutic strategy to fight Alzheimer’s disease.

The drugs currently approved to treat Alzheimer’s, such as lecanemab and donanemab, are monoclonal antibodies that work by removing beta-amyloid protein plaques from the brain. “Although they represent a breakthrough, their efficacy is limited, as they only slow cognitive decline by 27% to 35%, have several side effects and only address the part of the pathology caused by beta-amyloid accumulation,” the researchers explain.

In contrast, FLAV-27 works in a completely different way: it is the first inhibitor in its class to affect the G9a enzyme, which is essential in the epigenetic regulation of the brain because it helps to silence genes that are fundamental for neuronal development, synaptic plasticity and memory consolidation.

To inhibit G9a, the new drug prevents access by the natural molecule S-adenosylmethionine (SAM), which the enzyme needs to modify DNA. It thus slows down the epigenetic dysregulation, characteristic of Alzheimer’s disease, and allows neurons to regain normal function.

For those interested, here’s the link to the peer reviewed journal article:

https://www.cell.com/molecular-therapy-family/molecular-therapy/fulltext/S1525-0016(25)01061-5