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Taking the diabetes drug semaglutide by mouth did not help slow down memory loss or thinking problems in people with early Alzheimer's disease.

Study Aim

The main goal of the evoke and evoke+ trials was to find out if taking oral semaglutide (a medicine usually used for diabetes) could safely slow down the worsening of symptoms in people with early-stage Alzheimer's disease. The researchers wanted to see if this drug could help people with mild memory and thinking problems caused by Alzheimer's disease. Simply put: The study wanted to see if a diabetes drug could help slow down early Alzheimer's symptoms.

Study Design

The researchers ran two large, international clinical trials called evoke and evoke+. They included people aged 55 to 85 who had early Alzheimer's disease confirmed by brain scans. Participants were randomly given either semaglutide (up to 14 mg daily) or a fake pill (placebo) for up to three years. The main thing measured was how much their memory and thinking abilities changed over two years, using a test called the Clinical Dementia Rating-Sum of Boxes (CDR-SB). Safety was also closely watched. In total, 3,808 people took part across 40 countries. Simply put: The study gave people with early Alzheimer's either the drug or a fake pill and checked their memory over two years.

Findings

The trials showed that people who took semaglutide did not have slower memory or thinking decline compared to those who took the placebo. The difference between the two groups was very small and not meaningful. Side effects were similar to what is seen when semaglutide is used for other health problems, and there were no new safety concerns. Because the drug did not help, the trials were stopped early. The authors suggest that semaglutide should not be used to treat early Alzheimer's disease based on these results. Simply put: The drug did not help slow down Alzheimer's, and it was about as safe as expected.

Abstract

BACKGROUND: Evidence, including animal, clinical, and real-world studies in individuals with type 2 diabetes and/or obesity, suggests reduced risk of dementia and Alzheimer's disease after GLP-1 receptor agonist exposure. The evoke and evoke+ trials aimed to investigate the efficacy and safety of oral semaglutide in individuals with early Alzheimer's disease. METHODS: evoke and evoke+ were multicentre, randomised, double-blind, placebo-controlled phase 3 trials conducted across 566 sites in 40 countries. The trials assessed the efficacy and safety of oral semaglutide up to 14 mg once daily in participants with amyloid-confirmed Alzheimer's disease, aged 55-85 years, with mild cognitive impairment or mild dementia due to Alzheimer's disease. In evoke+, participants with significant small vessel pathology were included. Participants were randomly assigned (1:1) to once-daily semaglutide 14 mg (flexible dose) or placebo for up to 156 weeks. The primary endpoint was change in Clinical Dementia Rating-Sum of Boxes (CDR-SB) score from baseline to week 104, assessed in all randomised participants. Safety was assessed in all randomised participants and reported for those receiving at least one dose of study drug. These trials were registered at ClinicalTrials.gov (NCT04777396 and NCT04777409); both trials have been discontinued due to negative clinical outcome. FINDINGS: Between May 18, 2021, and Sept 8, 2023, 9981 participants were screened, of whom 3808 were randomly assigned; 1855 in evoke (semaglutide, n=928; placebo, n=927) and 1953 in evoke+ (semaglutide, n=976; placebo, n=977). Mean age was 72·2 years (SD 7·1), and mean CDR-SB score was 3·7 (SD 1·6) at baseline. In evoke+, 54 (2·8%) participants had small vessel pathology. In evoke and evoke+, mean changes in CDR-SB score from baseline to week 104 were 2·3 (SE 0·1) and 2·2 (0·1) with semaglutide, compared with 2·3 (0·1) and 2·1 (0·1) with placebo (estimated difference -0·08 [95% CI -0·35 to 0·20], p=0·57 in evoke and 0·10 [-0·17 to 0·38], p=0·46 in evoke+). Treatment-emergent adverse events were reported in 1729 (91·2%) of 1896 participants receiving semaglutide versus 1613 (84·8%) of 1902 receiving placebo. There were five fatalities considered treatment-related by the investigators (one in the semaglutide group and four in the placebo group). INTERPRETATION: Oral semaglutide was not efficacious in slowing clinical progression in participants with early Alzheimer's disease. Safety and tolerability of semaglutide in early Alzheimer's disease is consistent with studies in other indications. FUNDING: Novo Nordisk.

Referenced In

GLP-1s, Dementia, Alzheimer's, and Type 3 Diabetes

The suite of new GLP-1 agonists (GLP-1RAs) have shown a cascade of fascinating impacts, but the one that I have my eye on is this new idea that GLP-1 drugs may be preventative of brain aging diseases like Alzheimer's and Dementia.

GLP-1 is a naturally produced hormone in the human gut that regulates appetite and insulin secretion. The GLP-1 agonists drugs that have made a splash the last few years like semaglutide (Ozempic/Wegovy), liraglutide (Victoza/Saxenda), and dulaglutide (Trulicity), were originally developed for type 2 diabetes management.

But a 2026 Systematic Review found:

This study contributes to the clinical understanding of GLP-1 RAs and their effect on cognitive dysfunction. Findings from this study indicate GLP-1 RAs as potential therapeutics targeting cognitive function and neurocognitive disorders in persons living with T2DM.

This finding was echoed by a 2025 review which stated:

preclinical evidence has consistently shown the neuroprotective effects of GLP-1RAs, including reduced amyloid and tau pathology, improved synaptic function and enhanced neuronal survival

And a 2025 meta-analysis found that:

(GLP-1RAs) were associated with a statistically significant reduction in dementia

This finding was paired with a null result for the alternative cardio-protective glucose lowering agent sodium-glucose cotransporter-2 inhibitors (SGLT2is), suggesting the the GLP-1RAs are either using a unique pathway or are simply more effective. Contradictorily, a read world study released on the same day found benefits for both GLP-1RAs and SGLT2is; the meta-analysis may have been underpowered to detect SGLTis' benefits.

The link between Alzheimer's or Dementia and Diabetes is well known, with diabetes cited as a major risk factor. This is important to remember when contextualizing these findings as the population for the studies were almost all individuals with Type 2 Diabetes. That means we don't know if these neuroprotective effects can be generalized to people without T2D.

Interestingly as pointed out by the 2025 review, Alzheimer's and Dementia may be thought of as Type 3 Diabetes, as these diseases may be symptoms of underlying insulin dysregulation in the brain and damaged blood vessels. The tie between dementia and cardiovascular health echoes what we've heard in the past, that what's good for the heart is good for the brain. GLP-1 is naturally boosted by exercise and may point to the same correlation we see with exercise and brain health.

Excited to see how these findings pan out over the next few years, GLP-1RAs still require long term trials and reviews against the general population. The results for major trial targeting adults with early onset Alzheimer's released in March 2026 failed to show efficacy of oral semaglutide in reducing Alzheimer's. Note this study was funded by Novo Nordisk.

Oral semaglutide was not efficacious in slowing clinical progression in participants with early Alzheimer's disease.

This could be due to several reasons like the drug being more preventative than capable of reversing symptoms, weaker impacts of older generation GLP-1RAs or effects not being generalized outside of TD2 patients. But this is the strongest clinical result yet and points to the need for more trials before comprehensively marking success.

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