Diabetes Is Associated with Global and Regional Hypometabolism among Elderly Persons: The Mayo Clinic Study of Aging (P07.137)

OBJECTIVE: To investigate cross-sectional associations of diabetes with amyloid accumulation measured using 11C-Pittsburgh Compound B (PIB) and with brain hypometabolism measured using 18F-fluorodeoxyglucose (FDG) positron emission tomography. BACKGROUND: Type 2 diabetes is associated with brain atrophy, mild cognitive impairment, Alzheimer9s disease (AD), and vascular dementia, possibly through vascular mechanisms. Some neuropathological studies have suggested greater plaque pathology in diabetics. Associations with in vivo markers of amyloid accumulation and hypometabolism are not established. DESIGN/METHODS: We studied a population-based cohort of Olmsted County, MN residents across diagnostic categories (cognitively normal, mild cognitive impairment, dementia). PET images were acquired using a PET/CT scanner. FDG-PET images were obtained 1 hour after the PIB scan; diabetic subjects had normal glucose levels. MRI was performed at 3T with a 3D-MPRAGE sequence. Global and region of interest measures were obtained. Diabetes was determined using the Rochester Epidemiology Project medical records-linkage system. RESULTS: Among 760 participants (median age 79 years), FDG ratio was lower in diabetics (n=160) than in non-diabetics (n = 601) for global FDG (1.575 vs. 1.620; p = 0.003), and in posterior cingulate/precuneus (1.752 vs. 1.812, p CONCLUSIONS: Diabetes was associated with lower FDG ratios globally and in regions that are among those thought to be key in AD. Our findings suggest that diabetes has a non-vascular role in the pathogenesis of AD. Supported by: U01 AG006786, P50 AG016574, K01 AG028573, K01 MH68351, R01 AG034676, AG011378, K01 MH68351, R01 AG040042, R01 AG034676, Robert H. and Clarice Smith and Abigail Van Buren Alzheimer9s Disease Research Program. Center for Individualized Medicine of Mayo Clinic, Minnesota Partnership for Biotechnology and Medical Genomics, GE Health Care, The Elsie and Marvin Dekelboum Family Foundation. Disclosure: Dr. Roberts has received research support from Abbott Laboratories. Dr. Mielke has nothing to disclose. Dr. Cha has nothing to disclose. Dr. Pankratz received financial support for research activities from Abbott Laboratories. Dr. Knopman has received personal compensation for activities with Eli Lilly & Company. Dr. Knopman has received personal compensation in an editorial capacity for Neurology. Dr. Knopman has received research support from TauRx. Dr. Geda has nothing to disclose. Dr. Boeve has received research support from Cephalon, Inc.; Allon Therapeutics; and GE Healthcare. Dr. Kantarci has received compensation from Takeda Global Research & Development Center for serving as an advisory board member for research support. Dr. Rocca has nothing to disclose. Dr. Jack has received personal compensation for activities with Janssen, Eisai Inc., General Electric, Johnson & Johnson, and Eli Lilly & Company. Dr. Jack has received research support from Pfizer Inc, Allon, and Baxter. Dr. Jack has received research support from Allon and Baxter. Dr. Petersen has received personal compensation for activities with Pfizer, Inc., Janssen Alzheimer9s Immunotherapy, Elan Pharmaceuticals, GE Healthcare, and Novartis. Dr. Lowe received personal compensation for consulting from Bayer Pharmaceuticals. Dr. Lowe received research grants from GE Health Care, Siemens Molecular Imaging, and AVID Radiopharmaceuticals, Inc.