Abstract
Olfactory dysfunction is a robust and early sign for Parkinson’s disease (PD). Previous studies have revealed its association with dementia and related neural changes in PD. Yet, how olfactory dysfunction affects white matter (WM) microstructure in newly diagnosed and untreated PD remains unclear. Here we comprehensively examined WM features using unbiased whole-brain analyses. 88 newly diagnosed PD patients without dementia (70 with hyposmia and 18 without hyposmia) and 33 healthy controls underwent clinical assessment and diffusion tensor imaging (DTI) scanning. Tract-based special statistics (TBSS), graph-theoretic methods and network-based statistics (NBS) were used to compare regional and network-related WM features between groups. TBSS analysis did not show any differences in fractional anisotropy and mean diffusivity between groups. Compared with controls, PD patients without hyposmia showed a significant decrease in global efficiency, whilst PD patients with hyposmia exhibited significantly reduced global and local efficiency and additionally a disrupted connection between the right medial orbitofrontal cortex and left rectus and had poorer frontal-related cognitive functioning. These results demonstrate that hyposmia-related WM changes in early PD only occur at the network level. The confined disconnectivity between the bilateral olfactory circuitry may serve as a biomarker for olfactory dysfunction in early PD.
Highlights
Mounting evidence has suggested that olfactory dysfunction is an early and consistent non-motor symptom in Parkinson’s disease (PD), affecting 45~90% of PD patients[1]
Post-hoc analysis showed that hypos-PD patients performed worse than healthy controls (HCs) on this test, but no difference was found between the two PD groups and between norms-PD and HC groups
Post-hoc analysis indicated that both HCs and norms-PD patients had higher University of Pennsylvania Smell Identification Test (UPSIT) scores than hypos-PD patients, whilst no significant difference existed between the former two groups
Summary
Mounting evidence has suggested that olfactory dysfunction is an early and consistent non-motor symptom in Parkinson’s disease (PD), affecting 45~90% of PD patients[1]. Patients with hypos-PD showed reduced activation in the bilateral rectus, orbitofrontal cortex (OFC), amygdala and parahippocampus and reduced functional connectivities between the left rectus and prefrontal, temporal, occipital, and limbic areas, compared with healthy controls (HCs)[14]. Structural MRI studies using region-of-interest (ROI) methods have unraveled the neuroanatomical basis of the metabolic and functional changes and have found that olfactory-related atrophy occurred in the primary olfactory cortex (e.g., the piriform and amygdala), and extended to the OFC, temporal, parietal-occipital, and cingulate cortex in PD9,15–17. There are no known studies examining the whole-brain WM network alterations that underlie olfactory dysfunction in PD, especially in early PD. We used DTI to investigate the whole brain to determine whether olfactory dysfunction would compromise WM regional and network properties in early PD. We hypothesised that WM would be altered at the network level, but not regional level, in early PD patients with olfactory dysfunction
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