MRI Correlation of Odor Identification Deficit as a Biomarker for Alzheimer’s Disease. (P2.171)
OBJECTIVE: To refine odor identification deficit (OID) as a biomarker for an amnestic disorder (Alzheimer’s disease (AD) and amnestic Mild Cognitive Impairment (aMCI)) by correlating it with global and tissue specific brain volume measures.
BACKGROUND: OID has been associated with AD and aMCI with an ROC AUC of 0.82 for identifying an amnestic disorder. Volumetric correlation of OID in amnestic disorders has not been reported yet.
METHODS: Cross-sectional study of normal controls (N=27) and amnestic disorder (AD(N=35) and aMCI (N=15)) was performed by measuring OID by the University of Pennsylvania Smell Identification Test (UPSIT) and normalized volumes of gray matter (GM), white matter, brain parenchyma, lateral ventricle and neocortex using T1-weighted MRI as determined by the SIENAX software algorithm. Smell identification measures included the total UPSIT; the top 10 smells by logistic regression and the previously proposed 10-item subset by Tabert. Smeller/non-smeller status was assigned with a cut off of 7 (less than or equal to 7,non-smeller; greater than 7,smeller) based on the top 10-item based on logistic regression. Volumes were compared between smellers and non-smellers within the groups with age and sex as covariates (ANCOVA).
RESULTS: GM and neocortex volumes were lower among non-smellers as compared to smellers within each group. Specifically, in the amnestic group OID was associated with GM (p=0.033) and neocortex volume loss (p=0.017). In the AD group the relationship of neocortex volume loss and smell identification scores are consistent between all OID measures.
CONCLUSION: Olfactory deficit is associated with lower neocortical and GM volumes suggesting that OID is an indicator of neurodegeneration. The consistent association of all OID measures with neocortical and GM volumes loss suggests the utility of the short version. Longitudinal studies are needed to delineate the relationship between decline in smell sensation, cognition and cerebral atrophy.
Study Supported by: NIA/K23/AG036852
MH/NIMH/R25/MH071544 Disclosure: Dr. Rafique has nothing to disclose. Dr. Hagemeier has nothing to disclose. Dr. Woodward has nothing to disclose. Dr. Bergsland has nothing to disclose. Dr. Benedict has received personal compensation for activities with Actelion, Biogen Idec, Bayer, and Novartis as a consultant. Dr. Zivadinov has received personal compensation for activities with Teva Neuroscience, Biogen Idec, EMD Serono, Novartis, Claret Medical Inc., and Genzyme Corporation as a speaker and/or consultant. Dr. Szigeti has nothing to disclose.