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Facial emotion recognition (FER) is a crucial component of social cognition and is essential in social‐interpersonal behaviour regulation. Although FER impairment is well‐established in advanced PD, data about FER at the time of diagnosis and its relationship with social behavioural problems in daily life are lacking. The aim was to examine FER at the time of PD diagnosis compared to a matched healthy control (HC) group and to associate FER with indices of social behavioural problems. In total, 142 de novo, treatment‐naïve PD patients and 142 HC were included. FER was assessed by the Ekman 60 faces test (EFT). Behavioural problems in PD patients were assessed using the Dysexecutive Questionnaire (DEX‐self and DEX‐proxy) and the Apathy Evaluation Scale (AES‐self). PD patients had significantly lower EFT‐total scores (p =.001) compared to HC, with worse recognition of Disgust (p =.001) and Sadness (p =.016). Correlational analyses yielded significant correlations between AES‐self and both EFT‐total (rs =.28) and Fear (rs =.22). Significant negative correlations were found between DEX‐proxy and both EFT‐total (rs = −.28) and Anger (rs = −.26). Analyses of DEX‐subscales showed that proxy ratings were significantly higher than patient‐ratings for the Social Conventions subscale (p =.047). This DEX‐proxy subscale had the strongest correlation with EFT‐total (rs = −.29). Results show that de novo PD patients already show impaired FER compared to HC. In addition, lower FER is linked to self‐reported apathy and proxy‐reported social‐behavioural problems, especially concerning social conventions. These findings validate the importance of the inclusion of social cognition measures in the neuropsychological assessment even in early PD. [ABSTRACT FROM AUTHOR]

Background: Parkinson's Disease (PD) is a heterogeneous, progressive neurodegenerative disorder which is characterized by a variety of motor and non-motor symptoms. To date, no disease modifying treatment for PD exists. Here, the study protocol of the Dutch Parkinson Cohort (DUPARC) is described. DUPARC is a longitudinal cohort study aimed at deeply phenotyping de novo PD patients who are treatment-naïve at baseline, to discover and validate biomarkers for PD progression, subtypes and pathophysiology.Methods/design: DUPARC is a prospective cohort study in which 150 de novo PD subjects will be recruited through a collaborative network of PD treating neurologists in the northern part of the Netherlands (Parkinson Platform Northern Netherlands, PPNN). Participants will receive follow-up assessments after 1 year and 3 years, with the intention of an extended follow-up with 3 year intervals. Subjects are extensively characterized to primarily assess objectives within three major domains of PD: cognition, gastrointestinal function and vision. This includes brain magnetic resonance imaging (MRI); brain cholinergic PET-imaging with fluoroethoxybenzovesamicol (FEOBV-PET); brain dopaminergic PET-imaging with fluorodopa (FDOPA-PET); detailed neuropsychological assessments, covering all cognitive domains; gut microbiome composition; intestinal wall permeability; optical coherence tomography (OCT); genotyping; motor and non-motor symptoms; overall clinical status and lifestyle factors, including a dietary assessment; storage of blood and feces for additional analyses of inflammation and metabolic parameters. Since the start of the inclusion, at the end of 2017, over 100 PD subjects with a confirmed dopaminergic deficit on FDOPA-PET have been included.Discussion: DUPARC is the first study to combine data within, but not limited to, the non-motor domains of cognition, gastrointestinal function and vision in PD subjects over time. As a de novo PD cohort, with treatment naïve subjects at baseline, DUPARC provides a unique opportunity for biomarker discovery and validation without the possible confounding influences of dopaminergic medication.Trial Registration: NCT04180865; registered retrospectively, November 28th 2019. [ABSTRACT FROM AUTHOR]

Background: In the newly proposed research criteria for Alzheimer’s disease (AD), patients are defined as having memory dysfunction in addition to either hippocampal atrophy or an abnormal cerebrospinal fluid (CSF) profile. This study applies the criteria in a memory clinic population, using clinical criteria as the reference criterion. Methods: 138 AD patients, 145 nondemented subjects, 78 patients with other dementias and 91 patients with mild cognitive impairment (MCI) were included. Dichotomized medial temporal lobe atrophy (MTA) score on MRI and dichotomized CSF profiles (based on beta-amyloid1–42, tau and phosphorylated tau at threonine 181 levels) were used in combination with an episodic memory test to assess sensitivity, specificity and likelihood ratios (LR) of the newly proposed criteria and their components separately. Results: We found specificities of 95 and 49% for comparison with nondemented subjects and other demented patients, respectively, with a sensitivity of 86% for AD. Specificity was highest (100 and 77%, respectively, LR+ = 48) when both MTA score and CSF profile were abnormal in addition to the episodic memory test, at the cost of a low sensitivity (48%). Conclusion: The newly proposed research criteria for AD yield a good specificity for comparison with nondemented subjects. When the type of dementia is clinically doubted, however, at least two supportive features should be considered (i.e. abnormal MTA score and CSF profile) in addition to memory impairment as core diagnostic criterion. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Different cerebrospinal fluid (CSF) amyloid-beta 1-42 (Aβ1-42), total Tau (Tau) and Tau phosphorylated at threonine 181 (P-Tau) levels are reported, but currently there is a lack of quality control programmes. The aim of this study was to compare the measurements of these CSF biomarkers, between and within centres. Methods: Three CSF-pool sampleswere distributed to 13 laboratories in 2004 and thesame sampleswere again distributed to 18 laboratories in 2008. In 2004 six laboratories measured Aβ1-42, Tau and P-Tau and seven laboratories measured one or two of these marker(s) by enzyme-linked immunosorbent assays (ELISAs). In 2008, 12 laboratories measured all three markers, three laboratories measured one or two marker(s) by ELISAs and three laboratories measured the markers by Luminex. Results: In 2004, the ELISA intercentre coefficients of variance (interCV) were 31%, 21% and 13% for Aβ1-42, Tau and P-Tau, respectively. Thesewere 37%, 16% and 15%, respectively, in 2008. When we restricted the analysis to the Innotest® (N = 13) for Aβ1-42, lower interCV were calculated (22%). The centres that participated in both years (N = 9) showed interCVs of 21%, 15% and 9% and intra-centre coefficients (intraCV) of variance of 25%,18% and 7% in 2008. Conclusions: The highest variability was found for Aβ1-42. The variabilities for Tau and P-Tau were lower in both years. The centres that participated in both years showed a high intraCV comparable to their interCV, indicating that there is not only a high variation between but also within centres. Besides a uniform standardization of (pre)analytical procedures, the same assay should be used to decrease the inter/intracentre variation. [ABSTRACT FROM AUTHOR]