(MENAFN) Researchers from the Weill Cornell Medicine center identified that free radicals produced at a particular location in non-neuronal brain cells, termed astrocytes, may drive dementia progression.

The scientific breakthrough published Tuesday in the Nature Metabolism journal revealed that blocking this specific location reduces brain inflammation and shields neurons from damage.

The finding could pave the way for novel therapies targeting neurodegenerative conditions, including frontotemporal dementia and Alzheimer's disease.

"We can now target specific mechanisms and go after the exact sites that are relevant for disease," said Dr. Anna Orr, co-leader of the research, emphasizing the "translational potential" of the discovery.

Investigators concentrated on mitochondria—metabolic structures within cells that produce energy from nutrients and, during this process, emit molecules designated as reactive oxygen species (ROS).

At minimal concentrations, ROS fulfill a crucial function in cellular operations, but they become destructive when generated excessively or at inappropriate times.

Scientists identified multiple small molecules designated S3QELs, or "sequels" that could possess therapeutic value for inhibiting ROS.

Experiments on mice with dementia demonstrated that S3QELs diminished brain inflammation and detrimental alterations in the tau protein, even when administered during advanced disease stages.

Investigators reported that extended treatment with S3QEL prolonged survival in the mice, proved well-tolerated and generated no apparent adverse effects.

The research team intends to advance the development of S3QEL compounds.

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