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TOPLINE:

Semaglutide was associated with a 20%-46% reduced risk for Alzheimer’s disease (AD)-related dementia in patients with type 2 diabetes (T2D) compared with other antidiabetic medications, with a particularly strong protective effect against vascular dementia, new research showed.

METHODOLOGY: 

• Researchers examined electronic health records (EHRs) of more than 1.7 million US adults with T2D with or without obesity and with no prior diagnosis of AD or AD-related dementia.
• They compared semaglutide (n = 64,267 users) to seven other antidiabetic medications (n = 1,646,728 users) on the first-time diagnosis of AD-related dementia, as well as the subtypes of vascular dementia, frontotemporal dementia (FTD), and Lewy body dementia, during a 3-year follow-up.
• The other antidiabetic medications included insulin, metformin, DPP-4 inhibitors, SGLT2 inhibitors, sulfonylurea, thiazolidinedione, and first-generation GLP-1 receptor agonists (albiglutide, dulaglutide, exenatide, liraglutide, and lixisenatide).
• Secondary outcomes included prescriptions of dementia-related medications.

TAKEAWAY:

• Semaglutide was associated with a significantly reduced risk for AD-related dementia compared to insulin (hazard ratio [HR], 0.54), metformin (HR, 0.67), and older GLP-1 receptor agonists (HR, 0.80).
• Protection against vascular dementia was also greater for semaglutide compared to insulin (HR, 0.48), metformin (HR, 0.55), and GLP-1 receptor agonists (HR, 0.67). No significant associations were found between the use of semaglutide and the risk for FTD or Lewy body dementia.
• The link between semaglutide and reduced AD-related dementia risk vs insulin, metformin, and GLP-1 receptor agonists was stronger in younger adults (mean age, 51.7 years) compared to older adults (mean age, 70.9 years), with risk reductions ranging from 32% to 56% vs 20% to 39%.
• The use of semaglutide vs other antidiabetic medications was associated with significantly fewer prescriptions of dementia-related medications.

IN PRACTICE:

“There is no cure or effective treatment for dementia, so this new study provides real-world evidence for its potential impact on preventing or slowing dementia development among at high-risk population,” Rong Xu, Case Western Reserve University School of Medicine, Cleveland, said in a press release.

“Future works are needed to establish causal relationships through randomized clinical trials and to characterize the underlying mechanisms,” the investigators wrote.

SOURCE:

This study was led by William Wang, Case Western Reserve University School of Medicine, Cleveland. It was published online on June 24 in the Journal of Alzheimer’s Disease.

LIMITATIONS:

This retrospective, observational, EHR-based study was limited by potential over-, under-, or misdiagnosis; unmeasured confounders; and a short 3-year follow-up period. Diagnosis of AD-related dementia relied on International Classification of Diseases, 10th Revision codes and prescription data, which may have lacked precision. This study also lacked data on medication adherence, cognitive function tracking, and genetic profiles, and could not fully adjust for variation of healthcare use.

DISCLOSURES:

This study was funded by grants from the National Institute on Aging and the National Center for Advancing Translational Sciences. One investigator reported being the editor in chief of the publishing journal but was not involved in the peer-review process. The other investigators reported having no relevant financial conflicts.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.