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The Dual Role of Sitagliptin in Improving Cognitive Function and Glycemic Control

Study conducted in mice has shown that sitagliptin might offer beneficial effects in reversing cognitive impairment…

Alzheimer’s disease (AD) is the most common form of dementia. Symptoms progress slowly and worsen over time resulting in interference with common daily activity. There is no known cure of AD, but the use of sitagliptin could slow the worsening of dementia.

In order to assess the role of sitagliptin in reversing cognitive function decline in patients with diabetes and Alzheimer’s disease, researchers at Ulster University conducted an experiment in mice. The goal was to assess whether or not sitagliptin can reverse memory impairment and improve metabolic control in mice.

A high-calorie diet was given, then either sitagliptin or saline was administered to mice over 21 days. Glucose and insulin were used as energy intake.

The study found that sitagliptin improves metabolic control, including glucose tolerance and insulin sensitivity. It also inhibits dipeptifyl peptidase-4 (DPP-4) activity, which improves memory of the mice without affecting anxiety level and hypermoteric activity.

Currently, sitagliptin shows promising results as dual method in managing blood glucose and reducing cognitive decline. Additional clinical trials will be conducted in human to assess the effectiveness in reducing cognitive decline in patients with Alzheimer’s disease.

Professor Victor Gault stated: “Our studies now show that when these mice are treated orally with sitagliptin that this drug reverses their cognitive decline as well as their diabetes.” He also commented: “Ulster University believes these new findings offer enormous potential for drug repurposing and that an already licensed drug could be tested safely in humans to ascertain if the drug also offers beneficial neuroprotective effects in diabetes and Alzheimer’s disease.”

V. Gault. Sitagliptin, a dipeptidyl peptidase-4 inhibitor, improves recognition memory, oxidative stress and hippocampal neurogenesis and upregulates key genes involved in cognitive decline. Diabetes, Obesity and Metabolism, DOI: 10.1111/dom.12432