People who take a drug used to lower blood sugar levels in type 2 diabetes have less amyloid-beta in their brains, a biomarker of Alzheimer's disease, than people who do not take the drug. The study was published in Neurology.
Type 2 diabetes happens when the body no longer efficiently uses insulin to regulate blood sugar levels. Dipeptidyl peptidase-4 inhibitors, also known as gliptins, can be prescribed to patients to help control blood sugar levels when other diabetes drugs do not work.
For the study, the researchers followed 282 people at an average age of 76 for six years. All had been diagnosed with either pre-clinical, early, or probable Alzheimer's disease. Among them, 70 had diabetes, and were being treated by gliptins, 71 had diabetes but were not being treated with the drugs, and 141 did not have diabetes.
All had scored similarly on cognitive tests at the start of the study, and each participant took a thinking and memory test called the Mini-Mental State Exam (MMSE) every 12 months for an average of 2.5 years.
In the end, the researchers saw that patients with diabetes taking gliptins had an average annual decline of 0.87 MMSE points. Meanwhile, those with diabetes who did not take the drugs had an annual decline of 1.65 points, and those without diabetes had a decline of 1.48 points.
After adjusting for other factors, the researchers found that the cognitive abilities of those on gliptins declined 0.77 MMSE points more slowly per year than those not on the drug. Brain scans also revealed that those on gliptins had lower average amounts of amyloid plaques in their brains compared to both other groups.
"Our results showing less amyloid in the brains of people taking these medications and less cognitive decline, when compared to people without diabetes raises the possibility that these medications may also be beneficial for people without diabetes who have thinking and memory problems," said Phil Hyu Lee, one of the study's authors.
"More research is needed to demonstrate whether these drugs may have neuroprotective properties in all people," he added.
The researchers note that their study was limited as it did not track amyloid-beta levels over time, nor did it show cause and effect.
Sources: Neurology, Science Daily
