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A popular supplement used by millions of Americans for joint pain may be linked to faster progression of Alzheimer’s disease, according to new research from the University of Florida (UF). In the study, people with mild cognitive impairment (MCI) who reported taking glucosamine were 25% more likely to develop dementia than those who did not use the supplement.
Published June 9 in Nature Metabolism, the findings also identified a potential biological mechanism that may help explain the association. While researchers caution that the study does not prove glucosamine causes Alzheimer’s disease, they say the results raise important questions about how commonly used supplements may affect disease progression.
For nurses and other healthcare professionals caring for older adults, the findings highlight the importance of assessing supplement use during cognitive health evaluations and patient education.
What the Study Reveals About Glucosamine Dementia Risk
Glucosamine is one of the most commonly used dietary supplements among older adults and is frequently marketed to support joint health and relieve osteoarthritis-related pain.
To investigate whether the supplement could influence Alzheimer’s disease and related dementias (ADRD), researchers analyzed deidentified electronic health records from UF Health collected between 2012 and 2024. Using artificial intelligence, they examined records from patients diagnosed with either ADRD or mild cognitive impairment.
Among the study population, glucosamine use was relatively common. Researchers identified 1,896 patients with ADRD and 2,750 patients with MCI who reported taking the supplement, representing approximately 8% of each group.
After adjusting for factors including age, sex, and demographics, investigators found that glucosamine use was associated with a 25% greater likelihood that patients with MCI would later develop dementia.
The study also found that glucosamine use was associated with a 25% increase in mortality risk among people already diagnosed with ADRD. Researchers did not observe a similar increase among patients with MCI.
Why the Findings Matter
The researchers emphasized that the study demonstrates an association rather than causation. To determine whether glucosamine directly contributes to disease progression, clinical trials will be needed.
“In the United States, there are about 7 million people living with Alzheimer’s and millions more with related dementias such as Lewy body or frontotemporal dementia,” said senior author Ramon Sun, Ph.D., director of the Center for Advanced Spatial Biomolecule Research and associate director for innovation of UF’s McKnight Brain Institute. “A lot of these people actively take an over-the-counter supplement that could be making their disease progression worse.”
For nurses caring for patients with cognitive impairment, the findings underscore the importance of including over-the-counter supplements in medication reconciliation and patient assessments.
A Potential New Target in Alzheimer’s Disease
Researchers identified evidence that a protein and sugar-tagging pathway is excessively active in Alzheimer’s disease, suggesting a potential target for future treatments.
“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.
Using advanced spatial analysis technology, researchers examined thousands of metabolically active molecules to identify pathways that might otherwise have remained hidden.
“This technology allows us to examine thousands and thousands of molecules created when the body breaks down food or drugs and to uncover intricate pathways that otherwise would stay hidden,” Sun said.
What Researchers Found in the Brain
Glucosamine is a naturally occurring sugar-related molecule capable of crossing the blood-brain barrier. Once in the brain, it can contribute to biochemical processes involved in the formation of complex sugar structures on proteins.
“The electronic health record data are very provocative,” said Matt Gentry, Ph.D., chair of UF’s Department of Biochemistry and Molecular Biology and a study co-author. “While it’s an association and not proof of causality, it does raise an important clinical question that now deserves much more attention.”
Mouse studies provided additional support for the hypothesis. Researchers found that glucosamine increased the attachment of sugar molecules to proteins within cells, and mice receiving glucosamine also showed worsening deficits in social memory, the ability to recognize and remember other individuals.
When researchers chemically reduced this sugar-tagging activity, memory performance improved.
The team also analyzed human brain tissue from the UF Neuromedicine Brain and Tissue Bank. Compared with healthy control samples, Alzheimer’s brain tissue showed substantially higher levels of sugar attachment to proteins.
Taken together, these findings suggest that the metabolic abnormality may actively contribute to Alzheimer’s disease progression rather than simply occur as a result of the disease.
“Proteins are the cell’s molecular machines, and many of them need sugar tags added in just the right way to fold correctly, travel to the right place, and do their jobs,” Gentry said. “What we found in Alzheimer’s is that this sugar-tagging system appears to be overactive. The Alzheimer’s brain is adding too many of these sugar structures, and this seems to contribute to the disease rather than protect against it.”
What Nurses Should Know
While researchers stress that the findings do not prove glucosamine causes Alzheimer’s disease, the study raises important questions about how commonly used supplements may affect disease progression. For nurses and other healthcare professionals, it also highlights the importance of discussing supplement use with patients experiencing cognitive decline.
