Anti-aging drug combo damages myelin in mouse brains

A widely studied anti-aging treatment triggered significant brain damage in mice, according to new research from the University of Connecticut. The drug combination dasatinib plus quercetin caused myelin loss and changes resembling those seen in multiple sclerosis. The findings raise questions about its use in longevity studies and off-label therapies.

Researchers at the University of Connecticut tested the dasatinib-quercetin combination on both young and old mice. They found that the treatment reduced protective myelin layers around nerve fibers in the brain, with younger animals showing greater damage than older ones. The corpus callosum also deteriorated in treated mice, producing effects similar to those described as chemo brain in humans undergoing chemotherapy.

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Scientist in lab studying mouse with DNA and brain inflammation overlays representing Alzheimer’s drug research.
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Experimental drug reduced DNA damage and inflammation in an Alzheimer’s mouse model, King’s College London says

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Scientists at King’s College London report that an experimental compound, KCL-286, repaired markers of DNA damage and lowered brain inflammation in a mouse model of Alzheimer’s disease. The team says the drug—originally developed for spinal cord injury—has already completed Phase 1 safety and tolerability testing in humans, which could speed plans for further clinical studies.

Researchers at Texas A&M University have developed a nasal spray that appears to reverse aspects of brain aging after just two doses. The treatment reduced inflammation and restored memory function in models for months afterward. The findings were published in the Journal of Extracellular Vesicles.

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A 2023 study found that falling levels of the protein Menin in the hypothalamus drive multiple signs of aging in mice. Restoring the protein or supplementing with the amino acid D-serine improved memory and other measures.

Scientists at the University of Southern California have found experimental compounds that may reduce harmful brain inflammation associated with Alzheimer’s disease. The work focuses on the enzyme cPLA2 and people who carry the high-risk APOE4 gene.

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Researchers have identified declining levels of phosphatidylcholine as a key driver of age-related mitochondrial dysfunction. The discovery, made at the Leibniz Institute on Aging in Germany, shows that boosting this lipid can restore youthful mitochondrial function in laboratory models.

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