The patients were either taking sodium-glucose cotransporter-2 (SGLT-2) inhibitors, which work by reducing the amount of glucose the kidneys reabsorb, allowing it to pass out of the body in urine, or dipeptidyl peptidase 4 (DPP-4) inhibitors, also known as gliptins, which work by blocking an enzyme that helps the body increase insulin levels after eating.
During a follow-up period, 1,172 people were newly diagnosed with dementia.
The study found SGLT-2 inhibitors were linked to a 35 per cent lower risk of dementia compared with DPP-4 inhibitors.
The researchers said: “This association was similarly observed for Alzheimer ’s disease and vascular dementia and was also consistent across subgroups.
“We observed a greater association with treatment duration longer than two years.
“These findings underscore the need for future randomised controlled trials.”
Responding to the study Dr Jacqui Hanley, head of research at Alzheimer’s Research UK, called for the findings to be confirmed in “robust clinical trials”.
She said: “It will also be important to investigate the mechanisms behind this apparent effect, as this could give researchers clues for other treatment approaches.
“It is encouraging to see large studies exploring whether drugs that have already been licensed could be repurposed as dementia treatments.”
“Since these drugs have already been shown to be safe for use in people, this could potentially speed up the process of testing them in clinical trials against dementia, as well as making it significantly cheaper.”
Dr Hanley added that the idea of repurposing existing drugs to treat the diseases that cause dementia has huge potential with a third of drugs in clinical trials for Alzheimer’s disease already used for other conditions.
Dr Ivan Koychev, senior clinical researcher for Dementia Platform UK based at the University of Oxford, said: “The results add to existing strong epidemiological evidence for dementia risk reduction through diabetes medications, namely SGLT2-inhibitors and glucagon-like peptide-1 receptor agonists.
“As in the current study, the risk of developing dementia is reduced substantially (30-40 per cent). The mechanism through which these effects take place are unknown but likely relate to either affecting inflammation in the brain, reducing the risk for cerebrovascular events or modulating glucose metabolism in the brain.”
However, he said a caveat is that it is not possible to draw links between cause and effect but the studies do strengthen the case for further clinical trials to take place.
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