Olfactory Dysfunction and Neuroimaging Biomarkers Among Cognitively Normal Individuals (S35.006)

OBJECTIVE: To assess the cross-sectional association between olfactory function and imaging biomarkers of brain pathology in the population-based Mayo Clinic Study of Aging (MCSA). BACKGROUND: Olfactory impairment may be an important clinical marker of cognitive decline and Alzheimer’s disease (AD) dementia. Thus, olfaction may also be associated with brain imaging biomarkers for Alzheimer’s disease (AD) pathology. However, this association has not been studied extensively in cognitively normal elders. DESIGN/METHODS: Participants were enrolled in the MCSA and were cognitively normal (CN) at the time of olfactory testing by the Brief Smell Identification Test (B-SIT) and imaging using magnetic resonance imaging (MRI) (n=951), 11C-Pittsburgh compound B (11C-PiB) (n=306), 18fluorodeoxyglucose (18F-FDG) (n=305) positron emission tomography (PET). Olfactory function categories were defined as: anosmia (B-SIT score <6), microsmia (men 6-10, women 6-10.25), and normosmia (men 10.25-12; women 10.5-12). The association of olfactory function with imaging biomarkers was examined using logistic regression models adjusted for age, sex and education. RESULTS: Among 951 CN participants (mean age 79.52 years; 52.5[percnt] men), 111 (11.67[percnt]) had anosmia. Individuals with anosmia were 2.7 times more likely to have an abnormal amyloid PET (Odds Ratio [OR]: 2.75; 95[percnt] confidence interval [CI], 1.13-6.71; vs. normosmia [reference group]), 2 times more likely to have an abnormal AD signature MRI cortical thickness (OR: 2.21; 95[percnt] CI 1.26-3.89), and were 2.5 times more likely to have an abnormal hippocampal volume (OR: 2.48; 95[percnt]CI: 1.22, 5.01). CONCLUSIONS: Severe olfactory dysfunction was associated with brain pathology among CN individuals. Longitudinal follow-up should provide more definitive information on the association of smell dysfunction and brain pathology. Study Supported by: National Institutes of Health grants U01 AG006786, K01 AG028573, P50 AG016574, R01 AG011378, R01 AG041851 and was made possible by the Rochester Epidemiology Project (R01 AG034676). Disclosure: Dr. Vassilaki has nothing to disclose. Dr. Mielke has received personal compensation for activities with Lysosomal Therapeutics, Incorporated. Dr. Christianson has nothing to disclose. Dr. Geda has nothing to disclose. Dr. Kremers has nothing to disclose. Dr. Alhurani has nothing to disclose. Dr. Machulda has nothing to disclose. Dr. Knopman has received personal compensation for activities with Lundbeck Pharmaceuticals. Dr. Knopman has received personal compensation in an editorial capacity for Neurology. Dr. Knopman has received research support from Lilly Pharmaceuticals and Ta Dr. Ronald Petersen received personal compensation from Pfizer, Inc., Janssen Alzheimer9s Immunotherapy. Merck, inc. Roche, Inc. Genentech, Inc. Biogen, Inc. Eli Lilly and Co. as a consultant or speaker. Dr. Lowe has received personal compensation for activities with Bayer Pharmaceuticals as a consultant. Dr. Jack has received personal compensation for activities with Janssen Research & Development, LLC by providing consulting services. Dr. Jack has received research support from the National Institutes of Health (R01-AG011378, RO1-AG041851, RO1-AG037551. Dr. Roberts has nothing to disclose.