Is there a link between glucosamine and dementia?

For many older adults, taking glucosamine is part of a daily routine to ease aching joints. But research suggests this familiar supplement deserves closer attention when someone also has problems with memory and thinking.

Scientists at the University of Florida found that glucosamine use was associated with a higher likelihood of mild cognitive impairment progressing to dementia. Published in Nature Metabolism, the study analysed patient records alongside experiments involving mice and donated human brain tissue.

The findings raise questions about whether a supplement taken for one health concern could have unintended effects elsewhere. However, they do not establish that glucosamine causes dementia or worsens it in humans.

Mild cognitive impairment describes memory or thinking difficulties beyond those expected with normal ageing, while everyday independence remains largely intact. Researchers examined health records from 2012 to 2024, comparing patients with recorded glucosamine use and those without.

After accounting for factors including age and sex, they found a 25% higher likelihood of progression to dementia among glucosamine users with mild cognitive impairment. This was an increase relative to non-users, not a finding that 25% of everyone taking the supplement would develop dementia.

Among patients already diagnosed with Alzheimer’s disease or related dementias, glucosamine use was also associated with a 25% higher risk of death during follow-up. The same link was not observed in the mild cognitive impairment group.

Differences in health, lifestyle or other characteristics between users and non-users could have influenced the findings, even after statistical adjustments. Study co-author Matt Gentry, who chairs the university’s department of biochemistry and molecular biology, stressed the need for further investigation.

“While it’s an association and not proof of causality, it does raise an important clinical question that now deserves much more attention,” he said. The team also explored a possible explanation in the laboratory.

Glucosamine occurs naturally in the body and can cross the protective barrier between the bloodstream and the brain. It helps fuel a process that attaches sugar structures to proteins, allowing them to take the right shape, reach the right places and work properly.

These tiny “tags” are part of normal cell function, but the researchers found evidence that this system becomes overactive in Alzheimer’s disease. Donated brain tissue from people with Alzheimer’s showed more of these structures than tissue from people without the disease.

In mice genetically engineered to develop Alzheimer’s-like features, glucosamine worsened their ability to recognise animals they had encountered before. Reducing activity in the sugar-building process, meanwhile, improved memory performance.

Together, these findings suggest that changes in how brain cells process these molecules could contribute to the disease. However, results in mice cannot establish what a supplement will do in people.

So, what does this mean for supplement users?

A brain already affected by disease may respond differently to glucosamine from a healthy one. Human clinical trials are needed before firm conclusions can be drawn about its effects.

For now, the study does not show that everyone taking glucosamine faces an increased dementia risk. Nor does it establish that stopping the supplement will slow cognitive decline.

People with diagnosed cognitive impairment or dementia who take glucosamine can discuss the findings with their doctor or pharmacist when reviewing their medicines and supplements.

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