GAINESVILLE, FLORIDA — A study published on June 9, 2026, in Nature Metabolism found an association between glucosamine use and Alzheimer's disease progression and mortality. The research, conducted by a University of Florida team, used artificial intelligence to analyze deidentified electronic health records from UF Health. These records were collected between 2012 and 2024.
The analysis focused on patients diagnosed with Alzheimer's disease and related dementias or mild cognitive impairment. Glucosamine use was associated with a 25 percent higher likelihood of progression from mild cognitive impairment to dementia after adjusting for age, sex, and demographic factors. Among patients with established Alzheimer's disease and related dementias, glucosamine use was linked to a 25 percent increase in mortality risk. Glucosamine use did not show a corresponding increase in mortality risk in the mild cognitive impairment patient group.
Approximately 7 million people in the United States live with Alzheimer's disease, and millions more have related forms of dementia. Eight percent of patients in the studied groups reported taking glucosamine. This included 1,896 individuals with Alzheimer's and related dementias, and 2,750 individuals with mild cognitive impairment. Glucosamine is a naturally occurring sugar-related molecule that can cross the blood-brain barrier. Commercial glucosamine supplements are typically manufactured from shellfish shells or corn.
Ramon Sun, Ph.D., director of the Center for Advanced Spatial Biomolecule Research and associate director for innovation at UF's McKnight Brain Institute, commented on the findings. "A lot of these people actively take an over-the-counter supplement that could be making their disease progression worse," Sun said. "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."
The researchers examined human brain specimens and genetically modified mouse models using advanced spatial analysis imaging technology, which Sun said "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." In mouse models, glucosamine administration increased the attachment of sugar residues to proteins in cells, and glucosamine-treated mice exhibited worsened deficits in social memory recognition. Chemically inhibiting this sugar attachment process improved memory function in the mouse models. Human brain specimens from the UF Neuromedicine Brain and Tissue Bank showed increased sugar attachment compared to control specimens. The researchers propose that altered metabolic processes involving protein sugar-tagging pathways may contribute to disease progression.
Matt Gentry, Ph.D., chair of UF's Department of Biochemistry and Molecular Biology, said, "The electronic health record data are very provocative. While it's an association and not proof of causality, it does raise an important clinical question that now deserves much more attention." He added, "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. 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."