New research warns that the popular joint supplement glucosamine may accelerate the progression of Alzheimer’s disease in people who already show signs of memory decline.
Study links glucosamine to higher risk of dementia among those with mild cognitive impairment
Scientists at the University of Florida examined de‑identified electronic health records spanning 2012 to 2024. The analysis covered roughly 24,000 patients diagnosed with Alzheimer’s disease or related dementias and more than 41,000 individuals with mild cognitive impairment (MCI).
About eight percent of the MCI group reported using glucosamine supplements. After adjusting for age, sex and demographic factors, the investigators found that supplement users had a 25 percent higher chance of advancing to Alzheimer’s compared with non‑users.
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They also observed a similar increase in mortality risk—again roughly the same proportion—among patients already diagnosed with Alzheimer’s who took glucosamine during the study period.
Lead author Ramon Sun, Ph.D., director of the Center for Advanced Spatial Biomolecule Research, said the findings do not prove causation. “Because this was an observational study based on medical records, it can only identify an association, not a direct cause‑and‑effect relationship,” the report noted.
To explore possible mechanisms, the team turned to genetically engineered mice that develop Alzheimer‑like pathology. In those animals, glucosamine appeared to boost a process called hyperglycosylation, where excess sugar molecules attach to brain proteins. This heightened activity coincided with worsening memory performance, and blocking the pathway led to modest improvement.
Similar hyperglycosylation patterns were identified in human brain tissue from Alzheimer’s patients, suggesting a shared biochemical link. The authors emphasize that the observed risk applies to individuals who already have cognitive impairment; they do not claim glucosamine triggers Alzheimer’s in otherwise healthy adults.
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“Our results suggest that altered metabolism is a significant contributor to Alzheimer’s progression and, in addition, addressing the metabolic defect could be an important complement to approaches focused on Alzheimer’s plaques and tangles,” Sun said in a press release.
Co‑author Matt Gentry, Ph.D., chair of the university’s Department of Biochemistry and Molecular Biology, described the electronic health record data as “provocative.” He added that while the association is clear, “it does raise an important clinical question that now deserves more attention.”
Glucosamine is sold over the counter and widely used by older adults seeking relief from joint pain. Because the supplement is readily available, many take it without consulting a physician. The new findings suggest that patients with MCI or diagnosed Alzheimer’s should discuss glucosamine use with their healthcare providers.
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Earlier studies have produced mixed results, with some indicating lower dementia risk among cognitively healthy glucosamine users. The current analysis, however, highlights a potential danger for a vulnerable subgroup.
Further investigation is needed, including prospective trials that monitor outcomes after discontinuing the supplement. For now, the evidence adds to a growing body of literature linking metabolic disruptions to neurodegenerative disease.
The study appears in Nature Metabolism, and the authors plan to continue probing the biochemical pathways involved.
