Alzheimer’s disease is becoming more widespread, yet there are no treatments that can delay or stop the progression of the disease, and developing new drugs is a long, expensive, and complicated process.

A study by researchers at Sweden’s Karolinska Institutet and published in the journal Neurology shows that a diabetes drug’s mechanisms can also help protect against Alzheimer’s disease. The findings suggest that the drug’s target protein could be a promising therapy option for Alzheimer’s disease.

Alzheimer’s disease is becoming more widespread, yet there are no treatments that can delay or stop the progression of the disease, and developing new drugs is a long, expensive, and complicated process.

So, an alternative strategy would be to find already-approved drugs that work against the disease and find new ways to use them. Diabetes medicines have been proposed as potential possibilities, but research testing diabetes drugs for Alzheimer’s disease have yielded inconclusive results so far.

In this study, scientists from the Karolinska Institutet used genetic methods to learn more about this.

“Genetic variants within or nearby the genes that encode a drug’s target proteins can cause physiological changes similar to the effects of the drug,” explains Bowen Tang. “We utilize such variants to test the repurposing potential of already approved drugs.”

The first step that the researchers took was to look for genetic variants that have the same pharmacological effect as diabetic medications, specifically a reduction in blood glucose levels. Data from the UK Biobank register, which has information on over 300,000 people, was used to reach that conclusion.

The analysis found changes in two genes that together code for the target protein of a class of diabetes drugs called sulphonylureas. The researchers proved that these variations are linked to increased insulin release, a decreased risk of type 2 diabetes, and a higher BMI, all of which are consistent with the drug’s effects.

The researchers next looked at the relationship between the genetic variants discovered and the risk of Alzheimer’s disease. They accomplished it by analyzing data from over 24,000 individuals with Alzheimer’s disease and 55,000 healthy people. They discovered that sulphonylurea gene variations were associated with a decreased incidence of Alzheimer’s disease.

The findings of the study “suggest that the target protein of sulphonylureas, the KATP channel, may be a therapeutic target for the treatment and prevention of Alzheimer’s disease,” adds Sara Hägg. “This protein is expressed in the pancreas, but also in the brain, and further studies are needed to fully understand the underlying biology.”

Mendelian randomisation is a type of analysis used in the study that leverages knowledge of genetic variants in individuals as a kind of natural randomization, similar to a randomised clinical trial. Individuals who are born with particular protective variations that mimic the impact of medicine can thus be examined for their link to disease.

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