Misfolded and aggregated α-synuclein is a neuropathological hallmark of Parkinson’s disease (PD). Thus, α-synuclein aggregates are regarded as a biomarker for the development of diagnostic assays. Quantification of α-synuclein aggregates in body fluids is challenging, and requires highly sensitive and specific assays. Recent studies suggest that α-synuclein aggregates may be shed into stool. We used surface-based fluorescence intensity distribution analysis (sFIDA) to detect and quantify single particles of α-synuclein aggregates in stool of 94 PD patients, 72 isolated rapid eye movement sleep behavior disorder (iRBD) patients, and 51 healthy controls. We measured significantly elevated concentrations of α-synuclein aggregates in stool of iRBD patients versus those of controls (p = 0.024) or PD patients (p < 0.001). Our results show that α-synuclein aggregates are excreted in stool and can be measured using the sFIDA assay, which could support the diagnosis of prodromal synucleinopathies.

No abstract

This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

Impulsivity is a multidimensional, cross-diagnostic behavioural construct that has been described in various psychiatric disorders including obsessive-compulsive disorder (OCD) and Tourette syndrome (TS). Different interpretations of results in the past have raised the question of heightened impulsivity as an explanatory model for self-described impulsive behaviour, especially in OCD. Our study included 16 patients with OCD, 14 patients with TS, and 28 healthy control subjects (HC). Self-assessed impulsivity was examined by the Barratt Impulsiveness Scale-11 (BIS-11), and the behavioural test used was the immediate and delayed memory task (IMT/DMT). Significantly heightened self-assessed impulsivity of the patient collective compared to HC could be observed in in only one dimension: lack of attention (χ2 (2) = 24.910, p < 0.001). Post-hoc tests were performed using Bonferroni adjusted alpha levels of 0.0167 per test (0.05/3) and revealed significantly higher scores in patients with OCD (M = 19.57, SD = 2.82), z = 4.292, p < 0.001 as with TS (M = 19.38, SD = 3.62), z = 3.832, p < 0.001 compared to HC (M = 13.78, SD = 3.18). In patients with OCD, correlations between the dimension of obsessive thoughts with a lack of attention in the form of first-order factor cognitive instability could be shown (n = 14, p = 0.024, rs = 0.599) while in patients with TS, tic symptomatology correlated significantly with second-order factor attentional impulsivity (n = 12, p = 0.027, rs = 0.635). In behavioural testing, no significant group differences could be observed either in impulsive behaviour (IMT: χ2 (2) = 4.709, p = 0.824; DMT: χ2 (2) = 0.126, p = 0.939) or in sustained attention (IMT: χ2 (2) = 0.388, p = 0.095; DMT: χ2 (2) = 0.663, p = 0.718). Heightened impulsivity as an explanatory model for the observed lack of attention, especially in patients with OCD, should be questioned and interpretation biases considered in the future. The necessity of a multidimensional approach to the research of impulsivity is underscored by our results.