Relationship among cerebral Aβ burden, cognitive function and diabetes

Abstract Background Diabetes mellitus (DM) increases the risk of brain atrophy and dementia. We aimed to reveal whether DM could affect cognitive function and the pattern of amyloid retention in cognitively impaired patients. Also we tried to show whether the existence of DM could cause subcortical structural abnormalities with cognitive dysfunction. Method We included consecutive 56 controls and 145 cognitively impaired people (CI, 50 MCI and 95 mild to moderate Alzheimer’s disease (AD) patients). All participants of this cross‐sectional study underwent blood tests, detailed neuropsychological evaluations, 3D T1‐weighted MRI at 3‐Tesla and 18 F‐FBB‐PET. We estimated the cerebral Aβ burden quantitatively using volume‐of‐interest analysis and segmented the volumes of six subcortical structures, using FMRIBs integrated registration and segmentation tool Multiple linear regression analysis adjusted for age and gender was performed to evaluate the relationship among cerebral Aβ burden, cognitive function and diabetes. Result All subcortical structures, except for the globus pallidus, were smaller in CI compared with controls on adjusting for age and gender. CI with DM was associated with the lower volumes of caudate nucleus and putamen than CI without DM patients. Although there was no significant difference of MMSE score within two groups, the performance of frontal‐executive and memory functions was negatively correlated with subcortical structural volume loss in CI with DM. There was no difference between cerebral Aβ burden using composite SUVR and MMSE score in CI patients. However we found higher amyloid retention in CI with DM patients. Conclusion The co‐morbidity of DM in AD patients might cause more specific subcortical volume loss beyond diffuse cerebral atrophy and the resultant cortical‐subcortical dysfunction could make cognitive dysfunction worse, especially frontal‐executive and memory functions. Also, CI with DM patients showed higher cerebral amyloid retention, which might be the accelerating factor of cognitive deterioration.