A popular joint supplement, glucosamine, has been linked to faster progression of Alzheimer’s disease.

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According to a new, large-scale study by researchers at the University of Florida (UF Health), glucosamine, a dietary supplement widely used to relieve joint pain, is associated with faster progression of Alzheimer’s disease and dementia in people with cognitive problems. The report, published in Nature Metabolism, shows that glucosamine use is associated with a 25% higher likelihood of mild cognitive impairment (MCI) progressing to dementia.

Using artificial intelligence, the researchers analyzed patients’ medical records collected between 2012 and 2024. They found that among patients who already had Alzheimer’s disease or related dementias (ADRD), glucosamine use was also associated with a 25% higher risk of death. No increase in mortality was observed in the group with mild cognitive impairment, suggesting that the supplement may have a stronger adverse effect in people with established dementia.

The study authors also identified a potential biological mechanism underlying this association. It involves the process of attaching sugar structures to proteins, known as “sugar-tagging,” which occurs normally in healthy cells but becomes overactive in the brains of people affected by Alzheimer’s disease. Experiments in genetically modified mice showed that glucosamine further accelerated this process, leading to a marked decline in recognition and memory in the animals. The same pattern was observed in brain tissue samples from people who had died with Alzheimer’s disease.

University of Florida professors Ramon Sun and Matt Gentry emphasize that the study is observational and does not yet prove that glucosamine directly causes dementia to progress. Clinical trials are needed to determine whether the supplement accelerates neurodegenerative processes and whether patients should stop taking it. Nevertheless, the findings underscore the potentially important role of altered metabolism in the development of Alzheimer’s disease.

ScienceDaily

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