Diabetes related to lower brain metabolism, but not amyloid plaque

Type two diabetes definitively leads to neuronal injury, but the jury is still out whether it contributes to the buildup of beta-amyloid in the brain associated with Alzheimer’s disease, according to a study published March 20 by the Journal of Nuclear Medicine.

Rosebud O. Roberts, MBChB, a researcher at the Mayo Clinic in Rochester, Minn., and colleagues evaluated how dysfunctional signaling of insulin in diabetes patients affected brain function by reviewing diabetes patients within the population-based Mayo Clinic Study of Aging. All patients included in this study underwent both FDG and amyloid PET scans to assess brain metabolism and amyloid deposition.

The study included data on 749 patients with a median age of 79 and no diagnosis of dementia. Of these, 20 percent were diabetic and 81 percent deemed cognitively normal. Results showed that FDG hypometabolism in Alzheimer’s disease-related regions of interest was more common in the diabetes sub-population than in nondiabetes patients, about 48 percent vs. 29 percent, respectively.

There was an elevated odds ratio for FDG hypometabolism and abnormal Alzheimer’s signature in diabetic individuals. This analysis included adjustments for age, sex and education as well as cognitive status, apolipoprotein e4 allele and glycemic level. However C-11 Pittsburgh compound B (PiB) studies showed no significant increase in amyloid deposition between diabetes and non-diabetics.

“It is possible that diabetes may have greater effects on neuronal injury and brain atrophy than on amyloid accumulation in elderly persons,” wrote Roberts et al. “The null association may also be due to interactions of timing of onset of vascular pathology with amyloid deposition in diabetic individuals. By contrast, subjects with diabetes and C-11 PiB deposition occurring independently at earlier ages may progress more rapidly from MCI [mild cognitive impairment] to dementia and may be less likely to be captured in our cohort because we did not initially enroll demented subjects to imaging studies.”

Additional longitudinal studies are needed to understanding the true impact of diabetes on Alzheimer’s pathology.