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Health / Wed, 24 Jun 2026 The Shillong Times

New molecule helps scientists reprogram brain immune cells to fight Alzheimer’s

A newly discovered molecule, OLE, restored the brain’s immune cells to a more protective state in Alzheimer’s disease models. Researchers in Spain and Switzerland have identified an experimental molecule that may help restore the brain’s natural defences against Alzheimer’s disease. The compound, known as OLE, appears to “reprogram” microglia, the brain’s immune cells, allowing them to regain some of their protective abilities. How OLE targets Alzheimer’sOne of the hallmarks of Alzheimer’s disease is the buildup of beta-amyloid plaques in the brain. “In Alzheimer’s disease, these cells become progressively impaired.

A newly discovered molecule, OLE, restored the brain’s immune cells to a more protective state in Alzheimer’s disease models. The treatment reduced the accumulation of toxic plaques and improved memory performance, highlighting its potential as a promising new therapeutic strategy.

Researchers in Spain and Switzerland have identified an experimental molecule that may help restore the brain’s natural defences against Alzheimer’s disease. The compound, known as OLE, appears to “reprogram” microglia, the brain’s immune cells, allowing them to regain some of their protective abilities.

The research was led by Jose Vicente Sanchez Mut of the Institute for Neurosciences (IN), a joint center of the Spanish National Research Council (CSIC) and Miguel Hernandez University of Elche (UMH), together with Johannes Graff of the École Polytechnique Federale de Lausanne (EPFL). Their findings were published in the journal Cell Death and Disease.

According to the study published by Sciencedaily, OLE helps microglia surround and contain beta-amyloid plaques, reducing both their size and their harmful effects. In animal studies, the treatment also led to better performance on memory tests.

How OLE targets Alzheimer’s

One of the hallmarks of Alzheimer’s disease is the buildup of beta-amyloid plaques in the brain. At the same time, microglia, which normally help remove these toxic deposits, gradually become less effective.

As their protective functions decline, they can contribute to damage in brain cells.

Researchers discovered that OLE, a molecule produced by the PM20D1 gene, can restore microglia to a more protective state. Following treatment, the microglia migrated toward beta-amyloid plaques and formed a barrier around them, reducing direct contact between the plaques and surrounding neurons. As a result, the harmful effects of the plaques on brain tissue were significantly diminished.

“One of the most significant findings is that we have identified a molecule capable of restoring microglia’s protective function,” explains Sanchez Mut.

“In Alzheimer’s disease, these cells become progressively impaired. Our results suggest that this process can be reversed, pointing to new therapeutic and research avenues to counteract the disease,” adds the researcher, who leads the Functional Epi-Genomics of Aging and Alzheimer’s Disease laboratory at the IN CSIC-UMH.

To better understand how OLE works, the researchers examined the activity of thousands of individual cells in the brain. Their analysis revealed that microglia were the cells most strongly affected by the treatment.

Following exposure to OLE, microglia activated pathways involved in clearing beta-amyloid and regained their ability to move toward plaques and contain them.

The findings are covered by two European patents, including one owned by the CSIC. The researchers say this strengthens the translational potential of the work and supports future efforts to develop therapeutic applications based on the discovery. (ANI)

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