Olfactory Dysfunction in Incidental Lewy Body Disease and Parkinson's Disease: An Update

Shemonti Hasan; Charles H Adler; Nan Zhang; Geidy E Serrano; Lucia I Sue; Holly A Shill; Shyamal H Mehta; Thomas G Beach; Erika D Driver-Dunckley

Olfactory Dysfunction in Incidental Lewy Body Disease and Parkinson's Disease: An Update

Innov Clin Neurosci. 2022 Oct-Dec;19(10-12):19-23.

Authors

Shemonti Hasan¹, Charles H Adler¹, Nan Zhang², Geidy E Serrano³, Lucia I Sue³, Holly A Shill⁴, Shyamal H Mehta¹, Thomas G Beach³, Erika D Driver-Dunckley¹

Affiliations

¹ Drs. Hasan, Adler, Mehta, and Driver-Dunckley are with the Parkinson's Disease and Movement Disorders Center, Department of Neurology, Mayo Clinic in Scottsdale, Arizona.
² Ms. Zhang is with the Department of Health Science Research, Section of Biostatistics, Mayo Clinic in Scottsdale, Arizona.
³ Drs. Serrano and Beach and Ms. Sue are with Civin Laboratory for Neuropathology, Banner Sun Health Research Institute in Sun City, Arizona.
⁴ Dr. Shill is with Barrow Neurological Institute in Phoenix, Arizona.

PMID: 36591548
PMCID: PMC9776774

Abstract

Objective: Measuring olfactory dysfunction shows promise as one of a number of nonmotor biomarkers that can be used to detect clinically manifest and prodromal Parkinson's disease (PD) and dementia with Lewy bodies (DLB) and to differentiate these from nonsynucleinopathies. Using a larger sample size than in our previous study, we evaluated the relationship between olfactory dysfunction based on the University of Pennsylvania Smell Identification Test (UPSIT) to the clinicopathological findings in patients with PD (n=41), patients with incidental Lewy body disease (ILBD) (n=47), and controls with no neurodegenerative disease (n=137).

Design: This study was conducted through the Arizona Study of Aging and Neurodegenerative Disease (AZSAND). We selected individuals who had an UPSIT score completed antemortem and were clinicopathologically diagnosed with PD, ILBD, or control. Various measures included density of Lewy type synucleinopathy (aSyn) in the olfactory bulb and tract, as well as connected mesial temporal lobe structures. Cases and controls were analyzed using one-way analysis of variance (ANOVA) with pairwise contrasts.

Results: Compared to controls (mean: 27.8, standard deviation [SD]: 6.0), the mean UPSIT scores were lower for PD (15.8, SD: 6.0, p<0.001) and ILBD (24.1, SD: 8.6, p<0.001). The sensitivity for detecting ILBD from controls, based on a cutoff score of less than 23 (23/47), was 48.9 percent. The specificity for detecting a control was 79.6 percent with a cutoff greater than 23 (109/137).

Conclusion: These findings replicate, with a larger sample size, our previously published findings that individuals with autopsy-confirmed PD and ILBD have significantly lower UPSIT scores compared to controls. These data add to the growing body of evidence supporting early olfactory dysfunction as a prodromal biomarker for the risk of developing PD and ILBD as a prodromal Lewy body disorder.

Keywords: Hyposmia; Parkinson’s disease; incidental Lewy body disease.

Abstract

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