1 1 Symposium Chemosensory Receptors Satellite DEVELOPMENT ...

109 Poster Chemosensory Coding and ClinicalCEREBRAL ACTIVATION IN PD DURING OLFACTORYSTIMULATION—AN FMRI STUDYWelge-Lüssen A. 1 , Westermann B. 1 , Wattendorf E. 1 , Uta S. 1 , Peter F. 1 ,Wolfensberger M. 2 , Hummel T. 3 , Bilecen D. 1 1 University HospitalBasel, Basel, Switzerland; 2 Otorhinolaryngology, University HospitalBasel, Basel, Switzerland; 3 University of Dresden, Dresden, Saxony,GermanyObjectives: Olfactory dysfunction is common in patients withParkinson´s disease (PD). The cerebral systems however being involvedin the olfactory disorder in PD are still largely unknown. Methods: In12 PD patients and 16 age-matched healthy controls olfactory functionwas evaluated using psychophysical testing (Sniffin´Sticks test battery)and functional (f)MRI. In both experiments, olfactory stimuli(phenylethylalcohol, PEA) were separately applied to the left and rightnostril using a computer-controlled dynamic olfactometer (OM2S;Burghart, Germany). Statistical analysis of functional images wasperformed using SPM2. Results: In contrast to controls, in PD patients,activation was almost exclusively observed during left-sidedstimulation. In PD left-lateralized activation was observed in theamygdala, the hippocampal formation, and in region of the inferiorparietal lobe. Direct contrasts between both groups revealed reducedactivity in the inferior parietal lobe in PD patients. Conclusions:Olfactory stimulation produced distinct patterns of activation in PDwith a prevalence for left-sided activation. Olfactory stimuli in PDpatients seem not to be sufficient to gain bilateral access to olfactoryprocessing even in the amygdala, a primary olfactory relay. A reducedinterhemispheric exchange could explain the lateralized activity inregions of the inferior parietal lobe in PD patients. SNF 3100-068282110 Poster Chemosensory Coding and ClinicalIMPAIRMENTS IN SOURCE MEMORY FOR OLFACTORYSTIMULI IN PRECLINICAL GENE CARRIERS OFHUNTINGTON´S DISEASEPirogovsky E. 1 , Rice J. 1 , Mekrut A. 1 , Vallejo F. 1 , Brushfield A.M. 1 ,Gilbert P.E. 1 , Murphy C. 1 1 Psychology, San Diego State University, SanDiego, CASource and item memory for olfactory and visual stimuli wereexamined in 10 pre-symptomatic Huntington's disease (HD) genecarriers and 10 controls. During the study phase, a male and a femaleexperimenter (sources) presented odors and objects to the participant inan alternating sequence. To assess item memory, the participant chosebetween a stimulus from the study phase and a novel stimulus. Toassess source memory, the participant identified whether the male orfemale experimenter had previously presented the stimulus. The presentstudy also assessed odor detection in gene carriers and controls. Nosignificant differences were detected between gene carriers and controlsin source memory for visual stimuli. However, source memory forolfactory stimuli was impaired in gene carriers compared to controls.Gene carriers and controls did not differ in item memory for olfactoryor visual stimuli. In odor detection, gene carriers were significantlyimpaired compared to controls. The effect size for the olfactory sourcememory result was notably higher than the effect size for the odorthreshold finding. This suggests an important cognitive component inaddition to the olfactory sensory impairment in gene carriers. Overall,these results suggest that source memory for olfactory stimuli may beparticularly sensitive to neuropathological changes in preclinical stagesof HD. Supported by NIH grant #AG04085 to CM. We thank the UCSDHD Clinical Research Group for their contribution.111 Poster Chemosensory Coding and ClinicalOLFACTORY IDENTIFICATION AS A FUNCTION OF APOE-STATUS IN NON-DEMENTED ADULTS: EVIDENCE FROM APOPULATION-BASED SAMPLEOlofsson J.K. 1 , Nordin S. 1 , Larsson M. 2 , Cruts M. 3 , Adolfsson R. 4 ,Sleegers K. 3 , Van Broeckhoven C. 3 , Nilsson L. 2 1 Psychology, UmeåUniversity, Umeå, Sweden; 2 Psychology, Stockholm University,Stockholm, Sweden; 3 Molecular Genetics, University of Antwerp,Antwerp, Belgium; 4 Clinical sciences and Psychiatry, Umeå University,Umeå, SwedenThe ε-4 allele of the ApoE gene is a well-established risk factor forAlzheimer´s disease (AD). Having one or two ε-4 alleles is associatedwith impairment in cued odor identification, a test that therefore mightindicate AD at a preclinical stage. The present study investigates theApoE gene´s influence on odor identification ability in a largepopulation-based sample (N = 1572) of individuals screened fordementia at 5 years post-test. The sample was divided into a middleaged (45-60) and an elderly (65-80) group. Results show that ApoE ε-4is associated with poor odor identification ability which is morepronounced in elderly males. We also show that homozygotic ε-4carriers (two ε-4 alleles) display poorer odor identification ability thanheterozygotic ε-4 carriers (one ε-4 allele) at older age, but not at middleage. The present findings provide evidence that elderly individuals withhigh and low genetic risk of developing AD can be differentiated on thebasis of olfactory identification ability. Sponsored by the Bank ofSweden Tercentenary Foundation, The Swedish Council for Planningand Coordination of Research, the Swedish Research Council, and theSwedish Council for Working Life and Social Research to L.-G.N.112 Poster Chemosensory Coding and ClinicalLONGITUDINAL EVALUATION OF SMELLIDENTIFICATION DEFICITS IN PATIENTS WITH MILDCOGNITIVE IMPAIRMENTTabert M. 1 , Albers M. 2 , Liu X. 3 , Devanand D. 4 1 New York StatePsychiatric Institute and Psychiatry, Columbia University, New York,NY; 2 Neurology, Columbia University, New York, NY; 3 Biostatistics,Columbia University, New York, NY; 4 Columbia University and the NewYork State Psychiatric Institute, New York, NYPatients with Alzheimer's disease (AD) and Mild CognitiveImpairment (MCI) consistently exhibit smell identification deficitsrelative to healthy control subjects in cross sectional studies. Fewlongitudinal studies have directly examined the evolution of thesedeficits over time in AD or MCI patients relative to elderly controls. Ina prospective study of putative predictors of conversion to AD in MCIpatients, we administered the University of Pennsylvania SmellIdentification test (UPSIT) to 150 MCI patients (40 converters to AD onfollow-up evaluation and 110 non-converters) and 63 group-matchedhealthy controls at baseline (BL), 2-year follow-up, and 4-year followupevaluations. Two- and 4-year test-retest reliability of UPSIT scoresfor the entire sample of controls and patients was high (BL to 2 year, r =0.86; 2-year to 4-year, r = 0.87; and BL to 4-year, r = 0.74). All groupsdemonstrated significant (p < 0.05) declines in mean UPSIT scoresacross successive test intervals. Using ANOVA, a two-way group bytest interval interaction revealed that patients who converted to ADshowed significantly greater decline across test intervals than didhealthy controls or non-converting patients (p < 0.001), even afteradjusting for group differences in age (p = 0.001). These findingsdemonstrate that the UPSIT is sensitive to the evolution of smellidentification deficits over time as a function of normal aging and earlyAlzheimer's disease. Supported by NIA: AG1776128