Researchers at the University of Barcelona have designed and tested an experimental compound, FLAV-27, that works on Alzheimer's disease through a mechanism unlike any approved drug: instead of clearing beta-amyloid plaques from the brain, it reprogrammes the epigenome of neurons, correcting the altered patterns of gene expression that help drive the disease forward. The findings, obtained in animal models, were published in the journal Molecular Therapy.
The distinction matters because the current generation of Alzheimer's therapies is built almost entirely around a single pathological target. As Aina Bellver, a researcher at the UB Institute of Neurosciences and first author of the paper, put it, FLAV-27 has the potential to modify the disease process itself because it acts on underlying molecular mechanisms rather than on symptoms or one biomarker alone.
The work was led by professors Christian Griñán and Mercè Pallàs of the Faculty of Pharmacy and Food Sciences, with collaborators from UBneuro, the CIBER Area for Neurodegenerative Diseases, the UB Institute of Biomedicine, the Institute of Nutrition and Food Safety, the August Pi i Sunyer Biomedical Research Institute and other national and international centres.
For patients and families, the practical significance is still some distance away. FLAV-27 has been validated in animals, not in people, and the long road from preclinical results to a usable medicine is well documented in Alzheimer's research. What the study offers now is a proof of principle that the epigenome is a viable therapeutic target - a direction that has had little presence in Alzheimer's drug development to date.