BackgroundShort‐chain fatty acids are exclusively produced by gut microbiota and are reduced in feces of patients with Parkinson's disease (PD). The objective of this study was to conduct a case–control study on peripheral concentration of short‐chain fatty acids based on evidence of pathologic changes in the blood–brain barrier in PD and the possible role of short‐chain fatty acids in blood–brain barrier permeability.MethodsThe plasma short‐chain fatty acid concentration was measured in 38 PD and 33 normal controls using gas chromatography. The clinical characteristics of patients with PD and controls were evaluated, and dietary information was obtained using a food frequency questionnaire. Short‐chain fatty acid concentrations were further compared after adjusting for age, sex, and significant food frequency questionnaire items.ResultsThe concentrations of acetate, propionate, and butyrate did not differ between patients with PD and controls in unadjusted comparison. Dietary intakes of fibers, carbohydrates, lipids (total and fatty acids), and proteins did not differ between groups. After correction of covariates, acetic acid concentration was higher in patients with PD than in controls (116.47 ± 16.83 vs 108.20 ± 18.37 μmol/L; P = 0.010). In correlation analyses, acetic acid concentration was positively correlated (R = 0.374, P = 0.021) with age, propionic acid concentration was negatively correlated with UPDRS part III score (R = −0.376, P = 0.020) and use of entacapone (R = −0.325, P = 0.047), and butyric acid concentration was correlated with monoamine oxidase inhibitor use (R = 0.382, P = 0.018) and anticholinergic use (R = −0.385, P = 0.024).ConclusionsPlasma short‐chain fatty acids were paradoxically increased in PD and were associated with disease severity and antiparkinsonian medications. Further studies are warranted to elucidate the relationships of gut dysbiosis and inflammation with plasma short‐chain fatty acids. © 2020 International Parkinson and Movement Disorder Society

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Using our methodology, the precise and continuous monitoring of freezing events with unconstrained sensing can assist patients in managing their chronic disease in daily life effectively.

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Objective It is unclear whether the decline in dopamine transporters (DAT) differs among idiopathic rapid eye movement sleep behavior disorder (iRBD) patients with different levels of olfactory impairment. This study aimed to characterize DAT changes in relation to nonmotor features in iRBD patients by olfactory loss. Methods This prospective cohort study consisted of three age-matched groups: 30 polysomnography-confirmed iRBD patients, 30 drug-naïve Parkinson’s disease patients, and 19 healthy controls without olfactory impairment. The iRBD group was divided into two groups based on olfactory testing results. Participants were evaluated for reported prodromal markers and then underwent 18 F-FP-CIT positron emission tomography and 3T MRI. Tracer uptakes were analyzed in the caudate, anterior and posterior putamen, substantia nigra, and raphe nuclei. Results Olfactory impairment was defined in 38.5% of iRBD patients. Mild parkinsonian signs and cognitive functions were not different between the two iRBD subgroups; however, additional prodromal features, constipation, and urinary and sexual dysfunctions were found in iRBD patients with olfactory impairment but not in those without. Tracer uptake showed significant group differences in all brain regions, except the raphe nuclei. The iRBD patients with olfactory impairment had uptake reductions in the anterior and posterior putamen, caudate, and substantia nigra ( p < 0.016 in all, adjusted for age), which ranged from 0.6 to 0.8 of age-normative values. In contrast, those without olfactory impairment had insignificant changes in all regions ranging above 0.8. Conclusion There was a clear distinction in DAT loss and nonmotor profiles by olfactory status in iRBD.

To evaluate the diagnostic value of putaminal abnormality on 3-T magnetic resonance imaging (MRI) for differentiating early parkinsonism-predominant multiple system atrophy (MSA-p) from Parkinson disease (PD) based on long-term clinical follow-up data. Totals of 23 clinical MSA-p (6 possible and 17 suspicious) and 50 PD patients were included. Subjects submitted to 3-T MRI at baseline and were followed up to substantiate the initial diagnosis. MRI findings were compared between MSA-p and PD patients based on the final diagnosis. Putaminal abnormalities were recorded as presence of atrophy, signal hypointensity, and abnormal disruption of the hyperintense lateral rim of the putamen. The sum scores for putaminal abnormality were calculated from the presence of each item. During the follow-up over 3 years, the diagnosis of MSA-p was supported in 17 patients (14 probable and 3 possible) and the diagnosis of PD was stable in all 50 patients. Putaminal abnormalities were more frequent in MSA-p (n = 17) than in PD (n = 50). A sum score of >1 on 3-T MRI had sensitivity, specificity, and positive- and negative-predictive values of 70.6, 93, 77.4, and 90.3%, respectively, for differentiating MSA-p from PD. Fourteen of the initial 23 clinical MSA-p patients had a sum score of >1, and in all but two, the diagnosis became supported during the follow-up, whereas the diagnosis of five of the nine patients with a sum score of ≤1 remained uncertain. Putaminal abnormality on 3-T MRI can be a specific diagnostic marker for early stage MSA-p.