As the global population ages, dementia rates are surging, and scientists continue the uphill search for treatments that can meaningfully alter its course. But in the absence of a breakthrough cure, researchers are looking closely at existing medications — and a new study suggests that some diabetes drugs may quietly be doing more than just controlling blood sugar.

A study published in JAMA Neurology has added compelling evidence to the idea that glucagon-like peptide-1 receptor agonists (GLP-1RAs), such as Ozempic and Wegovy, and sodium-glucose cotransporter-2 inhibitors (SGLT2is), like Jardiance, could play a protective role against dementia. Drawing from a large cohort of over 92,000 people living with type 2 diabetes in the southeastern United States, researchers found that those using GLP-1RAs had a 33% lower risk of developing dementia. For SGLT2is, the risk dropped by 43%.

These findings point toward a promising avenue for both prevention and broader understanding of how metabolic health intertwines with brain function. While scientists have long recognized that type 2 diabetes increases the risk for dementia, the mechanisms connecting the two have remained murky. Inflammation, oxidative stress, and impaired insulin signaling — shared culprits in both conditions — are now drawing deeper scrutiny.

“We’ve suspected for some time that addressing insulin resistance might benefit the brain,” said Dr. William Kapp, longevity specialist and CEO of Fountain Life. “These drugs appear to be impacting brain health in a way that extends beyond glucose control.”

To conduct the study, researchers sifted through patient data collected from 2007 to 2023 across Florida, Georgia, and Alabama. Participants, all aged 50 or older and diagnosed with type 2 diabetes, were tracked until either the onset of dementia or their death. Diagnoses included a range of conditions, from Alzheimer’s and vascular dementia to Lewy body and frontotemporal dementias.

The study took a rigorous approach, comparing the cognitive outcomes of those on GLP-1RAs or SGLT2is against those using other second-line diabetes medications. The results were statistically significant even after adjusting for a wide range of potential confounding factors.

But how exactly might these medications protect the brain?

For GLP-1RAs, the theories are stacking up. Research has shown they can reduce inflammation in the brain, improve insulin signaling in neural tissue, and even encourage neurogenesis — the birth of new neurons. SGLT2 inhibitors, meanwhile, may enhance blood flow to the brain, reduce oxidative stress, and boost mitochondrial performance.

There’s also early evidence that both drug types may help reduce levels of amyloid-beta and tau, proteins that are closely associated with Alzheimer’s disease pathology.

“These medications do more than regulate sugar,” said Dr. David Strain, an expert in cardiometabolic health at the University of Exeter. “They reduce systemic inflammation and vascular risk — two major players in neurodegeneration.”

However, not all studies have reached the same conclusion. On the same day this research was published, JAMA Neurology also released a meta-analysis of 26 trials involving more than 164,000 people. That paper confirmed the cognitive benefits of GLP-1RAs but found no significant link between SGLT2is and reduced dementia risk.

One possible explanation? Time. Both studies had relatively short follow-up periods — typically less than five years — which may not be enough to fully capture dementia’s long, slow development.

Still, the latest findings add to growing momentum around repurposing diabetes drugs for cognitive protection. And while this research focused only on individuals with type 2 diabetes, it opens a provocative question: could these drugs benefit people without diabetes too?

“There’s potential, especially if the root benefits come from reducing inflammation or improving metabolic health,” Kapp said. “But we have to be cautious. What’s good for one population isn’t necessarily safe or effective for another.”

As with all promising science, the next steps will require long-term studies and careful scrutiny. But for now, the connection between metabolic disease and brain decline has become harder to ignore — and existing medications may soon offer new hope for a condition that has long felt untouchable.