It was a gamechanger for my type 2 diabetic patients when GLP-1 meds like Ozempic, plus another treatment which I’ll go through shortly, burst onto the scene. We were able to get a lot of these patients off insulin and blood pressure meds, their weight came down, and their energy levels skyrocketed.
Then I started prescribing them to my overweight patients and the results were just as dramatic.
Now these two medication classes seem poised to offer yet another huge benefit. This time it’s for those at risk for dementia.
Table of Contents
Dementia
Let’s start with an obvious question: Who is at risk? Many more than you might think. A recent analysis updated older estimates—and they’re much higher than we thought. The analysis projects that 42% of Americans over 55 will eventually develop dementia [1].
And this isn’t confined to the U.S. Globally, the WHO reports that dementia is the 7th leading cause of death and a major cause of disability among older people [2].
In other words, dementia is incredibly common. With an aging population and the prevalence of risk factors like high blood pressure, it promises to get worse. That’s why the possibility that common diabetes meds can lower our chances of getting dementia is a big deal.
So what’s the connection here? How is a treatment for diabetes linked to dementia?
We’ve had evidence for a while that people with type 2 diabetes are at greater risk of decline in their mental functioning [3]. That’s because the main problems generated by type 2 diabetes are also causal drivers of dementia. Take, for example, the presence of chronic inflammation. This accelerates the build-up of plaque inside the arteries. As a result, people with type 2 diabetes have 2 to 4 times the risk of developing heart-related diseases [3].
As plaque accumulates, it restricts blood flow. This can lead to brain cells not getting enough oxygen. The resulting damage starts to impair brain function. This process is one of the major drivers of dementia. This form is called vascular dementia [4].
The other most common form of dementia is Alzheimer’s disease. It also involves damage to brain cells, but through a different mechanism—accumulation of broken proteins around and inside neurons. This interferes with neuron communication, creates inflammation, and can lead to cell death [5].
Despite years of research, we still aren’t sure exactly why Alzheimer’s develops the way it does. But we do know it shares several mechanisms with type 2 diabetes. Both involve insulin resistance, oxidative stress, and heightened inflammation [5].
So with type 2 diabetes sharing key dynamics with both forms of dementia, it makes sense that a treatment for type 2 diabetes could help with dementia, too.
When it comes to diabetes treatments, there are two in particular getting the most attention. The first is GLP-1 agonists like semaglutide, known under brand names like Ozempic and Wegovy. These medications mimic a hormone that regulates insulin and were designed to keep blood sugar levels within a healthy range [6].
They also turned out to be powerful aides to weight loss. They slow how quickly food moves through the stomach, increasing feelings of fullness. They also act on brain receptors that control appetite [6].
There are several potential benefits here when it comes to dementia risks. GLP-1 agonists increase insulin sensitivity and help reduce inflammation, preventing artery plaque buildup. They can also cross the blood-brain barrier and exhibit anti-inflammatory and antioxidant effects in the brain [5].
The second type of medication is called SGLT2 inhibitors. Here’s how they work: your kidneys filter your blood, removing glucose along with waste. Normally, a protein called SGLT2 reabsorbs the glucose back into the bloodstream. SGLT2 inhibitors block that process, so the glucose gets excreted in the urine instead—resulting in lower blood sugar levels [7].
But there’s emerging evidence SGLT2 inhibitors might also protect brain health. They improve small-vessel circulation in the brain and have anti-inflammatory and antioxidant effects [8].
Clinical Evidence on These Meds and Dementia Risk
Both GLP-1 agonists and SGLT2 inhibitors are effective treatments for type 2 diabetes that show promise for addressing dementia causes. But what does the clinical evidence show?
Let’s start with GLP-1 agonists. An early study in 2015 tested liraglutide in mice with early-stage Alzheimer’s. After four months, liraglutide delayed or partially halted memory decline [9].
Then researchers looked at humans. In one study, 38 participants with Alzheimer’s were split into treatment and placebo groups for 26 weeks. Liraglutide treatment preserved the brain’s ability to use glucose—a function that typically declines with Alzheimer’s [10].
Though exciting, the study was small. That’s why a 2020 analysis of the REWIND trial was so important. It included nearly 10,000 people with diabetes and lasted over 5 years [11]. Two cognitive function tests were used at the start and throughout. They found that dulaglutide, a GLP-1 agonist, reduced the risk of cognitive decline by 14% [11].
Then came a major 2025 study. Researchers examined 9 years of health records from almost 100,000 type 2 diabetes patients without prior dementia. They compared those taking GLP-1 agonists to others. The result? A 33% lower risk of dementia among GLP-1 agonist users [12].
What about SGLT2 inhibitors? A 2024 meta-analysis looked at three observational studies and found SGLT2 inhibitors were associated with a 38% lower risk of dementia [13]. But results varied widely. One study showed no reduction at all [13].
However, the 2025 study mentioned earlier also looked at SGLT2 inhibitors. Users had a 43% lower risk of dementia than those using other diabetes medications [12].
There wasn’t much difference between GLP-1 agonists and SGLT2 inhibitors in terms of dementia risk reduction. Both were strongly associated with lower risk [12].
It seems the greatest cognitive benefits are seen when treatment begins early—especially in those with prediabetes or early-stage type 2 diabetes [14]. One study also found that people with heart disease or cerebrovascular disease experienced the most benefit [15].
But it’s important to note: almost all the research so far has been in populations with type 2 diabetes. We don’t yet know if these meds can help slow or prevent dementia more broadly.
Fortunately, trials are underway. The Evoke and Evoke+ studies are testing semaglutide over three years in those with early-stage Alzheimer’s. Results are expected in 2026 [16].
In the meantime, SGLT2 inhibitors have shown other benefits, too. They help treat liver disease and heart failure [7], and reduce blood pressure [17].
That’s actually the reason I personally take an SGLT2 inhibitor. Along with the potassium in MicroVitamin+ Powder, it helps me keep my blood pressure at optimal levels. But just because I take a medication or supplement doesn’t mean you need to, too.
Another intriguing result: SGLT2 inhibitors might extend lifespan. In a mouse study, canagliflozin extended median survival by 14%—but only in males [18].
Conclusion
There’s growing, compelling evidence that GLP-1 agonists and SGLT2 inhibitors—both originally designed for managing type 2 diabetes—can also reduce the risk of dementia. With more research underway, particularly in non-diabetic populations, we may soon have more answers about their broader potential.
In the meantime, managing blood sugar, reducing inflammation, and protecting vascular health continue to be key strategies—not just for metabolic health, but for brain health as well.
References
1. https://www.nature.com/articles/s41591-024-03340-9
2. https://www.who.int/news-room/fact-sheets/detail/dementia
3. https://pmc.ncbi.nlm.nih.gov/articles/PMC8659196/
4. https://www.ncbi.nlm.nih.gov/books/NBK430817/
5. https://www.mdpi.com/2813-2564/4/1/2
6. https://www.ncbi.nlm.nih.gov/books/NBK551568/
7. https://www.ncbi.nlm.nih.gov/books/NBK576405/
8. https://pmc.ncbi.nlm.nih.gov/articles/PMC11351143/
9. https://pmc.ncbi.nlm.nih.gov/articles/PMC4878312/
10. https://pmc.ncbi.nlm.nih.gov/articles/PMC4877513/
11. https://pubmed.ncbi.nlm.nih.gov/32562683/
12. https://jamanetwork.com/journals/jamaneurology/article-abstract/2831976
13. https://pmc.ncbi.nlm.nih.gov/articles/PMC10363181/
14. https://journals.sagepub.com/doi/10.1177/25424823251342182
15. https://pmc.ncbi.nlm.nih.gov/articles/PMC12125485/
16. https://pubmed.ncbi.nlm.nih.gov/39780249/
17. https://cardiab.biomedcentral.com/articles/10.1186/s12933-020-01071-
