Suchergebnisse

Background: In recent years, a growing body of literature has highlighted the role of wearable and mobile remote measurement technology (RMT) applied to seizure detection in hospital settings, whereas more limited evidence has been produced in the community setting. In clinical practice, seizure assessment typically relies on self-report, which is known to be highly unreliable. Moreover, most people with epilepsy self-identify factors that lead to increased seizure likelihood, including mood, behavior, sleep pattern, and cognitive alterations, all of which are amenable to measurement via multiparametric RMT. Objective: The primary aim of this multicenter prospective cohort study is to assess the usability, feasibility, and acceptability of RMT in the community setting. In addition, this study aims to determine whether multiparametric RMT collected in populations with epilepsy can prospectively estimate variations in seizure occurrence and other outcomes, including seizure frequency, quality of life, and comorbidities. Methods: People with a diagnosis of pharmacoresistant epilepsy will be recruited in London, United Kingdom, and Freiburg, Germany. Participants will be asked to wear a wrist-worn device and download ad hoc apps developed on their smartphones. The apps will be used to collect data related to sleep, physical activity, stress, mood, social interaction, speech patterns, and cognitive function, both passively from existing smartphone sensors (passive remote measurement technology [pRMT]) and actively via questionnaires, tasks, and assessments (active remote measurement technology [aRMT]). Data will be collected continuously for 6 months and streamed to the Remote Assessment of Disease and Relapse-base (RADAR-base) server. Results: The RADAR Central Nervous System project received funding in 2015 from the Innovative Medicines Initiative 2 Joint Undertaking under Grant Agreement No. 115902. This Joint Undertaking receives support from the European Union's Horizon 2020 research and innovation program and European Federation of Pharmaceutical Industries and Associations. Ethical approval was obtained in London from the Bromley Research Ethics Committee (research ethics committee reference: 19/LO/1884) in January 2020. The first participant was enrolled on September 30, 2020. Data will be collected until September 30, 2021. The results are expected to be published at the beginning of 2022. Conclusions: RADAR Epilepsy aims at developing a framework of continuous data collection intended to identify ictal and preictal states through the use of aRMT and pRMT in the real-life environment. The study was specifically designed to evaluate the clinical usefulness of the data collected via new technologies and compliance, technology acceptability, and usability for patients. These are key aspects to successful adoption and implementation of RMT as a new way to measure and manage long-term disorders. International Registered Report Identifier (IRRID): PRR1-10.2196/21840

© 2020 – IOS Press and the authors. ; [Background]: Previous studies suggest that Dickkopf-1 (DKK1), an inhibitor of Wnt signaling, plays a role in amyloid-induced toxicity and hence Alzheimer's disease (AD). However, the effect of DKK1 expression on protein expression, and whether such proteins are altered in disease, is unknown. [Objective]: We aim to test whether DKK1 induced protein signature obtained in vitro were associated with markers of AD pathology as used in the amyloid/tau/neurodegeneration (ATN) framework as well as with clinical outcomes. [Methods]: We first overexpressed DKK1 in HEK293A cells and quantified 1,128 proteins in cell lysates using aptamer capture arrays (SomaScan) to obtain a protein signature induced by DKK1. We then used the same assay to measure the DKK1-signature proteins in human plasma in two large cohorts, EMIF (n = 785) and ANM (n = 677). [Results]: We identified a 100-protein signature induced by DKK1 in vitro. Subsets of proteins, along with age and apolipoprotein E ɛ4 genotype distinguished amyloid pathology (A + T–N–, A+T+N–, A+T–N+, and A+T+N+) from no AD pathology (A–T–N–) with an area under the curve of 0.72, 0.81, 0.88, and 0.85, respectively. Furthermore, we found that some signature proteins (e.g., Complement C3 and albumin) were associated with cognitive score and AD diagnosis in both cohorts. [Conclusions]: Our results add further evidence for a role of DKK regulation of Wnt signaling in AD and suggest that DKK1 induced signature proteins obtained in vitro could reflect theATNframework as well as predict disease severity and progression in vivo. ; This research was conducted as part of the EMIF-AD project which has received support from the Innovative Medicines Initiative Joint Undertaking under EMIF grant agreement n° 115372, resources of which are composed of financial contribution from the European Union's Seventh Framework Programme (FP7/2007-2013) and EFPIA companies' in-kind contribution. The DESCRIPA study was funded by the European Commission within the 5th framework program (QLRT-2001-2455). The EDAR study was funded by the European Commission within the 5th framework program (contract # 37670). The Leuven cohort was funded by the Stichting voor Alzheimer Onderzoek (grant numbers #11020, #13007 and #15005). The Lausanne cohort study was supported by a grant from the Swiss National Research Foundation to JP (SNF 320030_141179). RV is a senior clinical investigator of the Flemish Research Foundation (FWO). JS is currently an employee of UCB, Braine-l'Alleud, Belgium. The San Sebastian GAP study is partially funded by the Department of Health of the Basque Government (allocation 17.0.1.08.12.0000.2.454.01.41142.001.H). We acknowledge the contribution of the personnel of the Genomic Service Facility at the VIB-U Antwerp Center for Molecular Neurology. The research at VIB-CMN is funded in part by the University of Antwerp Research Fund. FB is supported by the NIHR biomedical research centre at UCLH. RD is supported by Health Data Research UK, the National Institute for Health Research (NIHR) Biomedical Research Centre at South London, Maudsley NHS Foundation Trust, King's College London and the NIHR University College London Hospitals Biomedical Research Centre. LS is funded by DPUK through MRC (grant no. MR/L023784/2) and the UK Medical Research Council Award to the University of Oxford (grant no. MC_PC_17215). Also support was received from the NIHR Biomedical Research Centre at Oxford Health NHS Foundation Trust.