New research published in PLOS reports an association between the use of antidiabetic medication and evidence of fewer clinical markers of Alzheimer’s disease (AD). A growing body of evidence has associated dementia, cognitive decline, and impairment with prediabetes and clinical type 2 diabetes mellitus (T2DM) diagnosis. It is hypothesized that the accumulation of amyloid-beta and abnormal tau proteins may be related to brain insulin-receptor signaling pathways (IRSPs).

The research, led by Vahram Haroutunian, PhD, a professor of psychiatry and neuroscience at the Icahn School of Medicine at Mount Sinai in New York City, and his team, analyzed the brain tissue of patients diagnosed with both diabetes and AD. Specifically, the scientists examined the IRSP and endothelial cell markers in the parahippocampal gyri of controls (n = 30), individuals with AD (n = 19), and those with both T2DM and AD who had been treated with antidiabetic medications (insulin and/or oral agents; n = 34). This research was built upon previous studies conducted by Dr. Haroutunian and colleagues that demonstrated that patients who were treated for diabetes (whether insulin or oral antidiabetic medication) had less abnormal brain pathology.  

The main analyses were performed on the expression of specific genes, with the primary goal of  determining the extent to which IRSP and endothelial cells were abnormal in patients with AD when compared with controls. According to the authors, “About half of diabetics develop dementia, and that roughly doubles the cost of caring for each demented diabetic patient, especially since their cognitive decline makes it impossible for the patient to participate in the monitoring and modulation of his/her diabetic status. Given the dual epidemics of T2D and dementia in the most rapidly growing segment of our population, there is enormous importance in elucidating the basis for cognitive impairment in T2D so that potentially meaningful interventions can be evaluated.”
 
 « Click here to return to Diabetes Update.

​