Kelvin L Chou1, Nicolaas I Bohnen. 1. Department of Neurology, University of Michigan, Ann Arbor, MI, USA. klchou@med.umich.edu
Abstract
BACKGROUND: Previous studies have shown selective deficits of odor identification in both Parkinson's disease (PD) and Alzheimer's disease (AD). Brief, selective AD smell screening tests have been developed to identify subjects at risk of AD. The disease specificity of such screening tests has not been formally evaluated. OBJECTIVE: To evaluate the performance of an Alzheimer-selective odor identification test in patients with PD and its relationship with cerebral dopamine transporter (DAT) activity. METHODS: PD patients (n=44; Hoehn and Yahr stages I-III; 13f/31m; mean age 59.3+/-10.1) and 44 controls matched for gender and age completed the University of Pennsylvania Smell Identification Test (UPSIT). All patients had PD duration > 1 year and none had evidence of dementia. Using the UPSIT, we calculated performance on the 10 odors previously reported to be selective for AD risk (UPSIT-AD10). A subset of 29 PD patients also underwent brain DAT [(11)C]beta-CFT (2-beta-carbomethoxy-3beta-(4-fluorophenyl) tropane) PET imaging. DAT binding was assessed in the hippocampus, amygdala, ventral and dorsal striatum. RESULTS: UPSIT-AD10 scores were significantly lower in the patient (5.8+/-2.1) compared to the control group (8.6+/-2.4) (t=5.8, P<0.0001). However, UPSIT-AD10 performance in the PD patients did not correlate with striatal or mesolimbic DAT activity. CONCLUSIONS: Hyposmia in PD and AD overlap and supposed Alzheimer-selective smell screening tests may not be specific for AD. However, the supposed AD-selective hyposmia scores in PD did not correlate with cerebral DAT binding and may reflect a non-dopaminergic olfactory mechanism.
BACKGROUND: Previous studies have shown selective deficits of odor identification in both Parkinson's disease (PD) and Alzheimer's disease (AD). Brief, selective AD smell screening tests have been developed to identify subjects at risk of AD. The disease specificity of such screening tests has not been formally evaluated. OBJECTIVE: To evaluate the performance of an Alzheimer-selective odor identification test in patients with PD and its relationship with cerebral dopamine transporter (DAT) activity. METHODS:PDpatients (n=44; Hoehn and Yahr stages I-III; 13f/31m; mean age 59.3+/-10.1) and 44 controls matched for gender and age completed the University of Pennsylvania Smell Identification Test (UPSIT). All patients had PD duration > 1 year and none had evidence of dementia. Using the UPSIT, we calculated performance on the 10 odors previously reported to be selective for AD risk (UPSIT-AD10). A subset of 29 PDpatients also underwent brain DAT [(11)C]beta-CFT (2-beta-carbomethoxy-3beta-(4-fluorophenyl) tropane) PET imaging. DAT binding was assessed in the hippocampus, amygdala, ventral and dorsal striatum. RESULTS: UPSIT-AD10 scores were significantly lower in the patient (5.8+/-2.1) compared to the control group (8.6+/-2.4) (t=5.8, P<0.0001). However, UPSIT-AD10 performance in the PDpatients did not correlate with striatal or mesolimbic DAT activity. CONCLUSIONS:Hyposmia in PD and AD overlap and supposed Alzheimer-selective smell screening tests may not be specific for AD. However, the supposed AD-selective hyposmia scores in PD did not correlate with cerebral DAT binding and may reflect a non-dopaminergic olfactory mechanism.
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