Abstract

AbstractBackgroundImpaired olfaction has been associated with neurodegenerative diseases and may be a useful tool to aid in diagnosis or track disease progression. We sought to compare olfaction in participants with the clinical diagnoses of idiopathic REM sleep behavior disorder (RBD), dementia with Lewy bodies (DLB), or Alzheimer’s disease dementia (AD).MethodParticipants from the Mayo Clinic Alzheimer’s Disease Research Center database who had a diagnosis of RBD (n=27, 56% male), DLB (n=51, 84% male), or AD (n=83, 47% male), and were given the Brief Smell Identification Test (B‐SIT) were included in this analysis. The B‐SIT score was calculated as the sum of correct responses (12 possible). Scores were categorized as reflecting anosmia (<6), hyposmia (6‐10), and normal olfactory function (>10). All participants underwent clinical and neuropsychological evaluations.ResultGlobal cognition was lower in AD and DLB than RBD (MMSE 21.5 ±4.9 in AD, 23.3 ±4.3 in DLB, 28.8 ± 1.2 in RBD; p <0.001). The mean B‐SIT total score was significantly lower for DLB (4.5 ± 3.1) compared to RBD (7.5 ± 3.0) or AD (7.0 ± 2.7) (p<0.001) using an ANOVA F‐test. Anosmia was present in 76% of DLB, which compared to 32% in RBD, and 32% in AD (p=0.9). Hyposmia was present in 18% of DLB, 47% of RBD, and 52% of AD (p=ns). Of 22 patients with normal olfaction, X% were DLB, X% RBD, and X% AD (p=X). An item analysis illustrated that participants with DLB were less likely to identify Menthol, Clove, Strawberry, Smoke, and Soap than those with RBD and AD. On serial examination, 12 RBD (60%) patients’ B‐SIT score decreased by at least one point at their most recent visit compared to their baseline visit.ConclusionThese findings suggest that impaired olfactory function is frequent in RBD, DLB and AD, with olfaction being worst in DLB in this cohort. Olfaction was declining in most of those with RBD who underwent serial evaluations. Further analyses are needed to determine if any scents are more sensitive to phenotype, progression, and degree of cognitive impairment. Supported by: NIH grants AG016574, NS100620, AG056639, AG015866

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