ORCID Profile
0000-0003-4512-6945
Current Organisations
Ludwig-Maximilians-Universität München
,
Deutsches Zentrum für Neurodegenerative Erkrankungen
,
University of Wollongong
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Publisher: Informa UK Limited
Date: 04-03-2023
Publisher: Elsevier BV
Date: 10-2022
Publisher: Public Library of Science (PLoS)
Date: 09-01-2018
Publisher: Maad Rayan Publishing Company
Date: 2017
Publisher: Oxford University Press (OUP)
Date: 20-03-2019
DOI: 10.1093/BRAIN/AWZ050
Abstract: Aβ deposition in the basal ganglia is common in autosomal dominant Alzheimer’s disease. Vöglein et al. report an increased severity of motor symptoms in autosomal dominant versus sporadic disease in advanced disease stages. Motor symptoms are more severe in post-codon 200 presenilin 1 mutation carriers and correlate with basal ganglia Aβ.
Publisher: Informa UK Limited
Date: 03-07-2020
Publisher: Wiley
Date: 03-05-2017
DOI: 10.1002/MDS.26987
Publisher: Frontiers Media SA
Date: 11-09-2019
Publisher: Cold Spring Harbor Laboratory
Date: 07-07-2020
DOI: 10.1101/2020.07.07.20148064
Abstract: Care of patients at risk of deterioration on acute medical and surgical wards requires timely identification, increased monitoring and robust escalation procedures. The critical care outreach role brings specialist-trained critical care nurses and physicians into acute wards to facilitate these processes. Performing this role is challenging, as the breadth of information synthesis required is both high and rapidly updating. We propose a novel automated ‘watch-list’ to identify patients at high risk of deterioration, to help prioritise the work of the outreach team. This system takes data from the electronic medical record in real-time and creates a discrete tokenized trajectory, which is fed into a recurrent neural network model. These models achieve an AUROC of 0.928 for inpatient death and 0.778 for unplanned ICU admission (within 24 hours), which compares favourably with existing early warning scores and is comparable with proof of concept deep learning systems requiring significantly more input data. Based on these results, we can conclude that it is technically feasible to build a set of predictive models that meet the needs of the critical care outreach role, based on a limited set of real-time clinical data.
Publisher: Wiley
Date: 13-05-2017
DOI: 10.1002/MDS.27034
Publisher: Springer Science and Business Media LLC
Date: 11-04-2018
DOI: 10.1038/S41398-017-0049-7
Abstract: Neurodegenerative diseases likely share common underlying pathobiology. Although prior work has identified susceptibility loci associated with various dementias, few, if any, studies have systematically evaluated shared genetic risk across several neurodegenerative diseases. Using genome-wide association data from large studies (total n = 82,337 cases and controls), we utilized a previously validated approach to identify genetic overlap and reveal common pathways between progressive supranuclear palsy (PSP), frontotemporal dementia (FTD), Parkinson’s disease (PD) and Alzheimer’s disease (AD). In addition to the MAPT H1 haplotype, we identified a variant near the chemokine receptor CXCR4 that was jointly associated with increased risk for PSP and PD. Using bioinformatics tools, we found strong physical interactions between CXCR4 and four microglia related genes, namely CXCL12 , TLR2, RALB, and CCR5 . Evaluating gene expression from post-mortem brain tissue, we found that expression of CXCR4 and microglial genes functionally related to CXCR4 was dysregulated across a number of neurodegenerative diseases. Furthermore, in a mouse model of tauopathy, expression of CXCR4 and functionally associated genes was significantly altered in regions of the mouse brain that accumulate neurofibrillary tangles most robustly. Beyond MAPT , we show dysregulation of CXCR4 expression in PSP, PD, and FTD brains, and mouse models of tau pathology. Our multi-modal findings suggest that abnormal signaling across a ‘network’ of microglial genes may contribute to neurodegeneration and may have potential implications for clinical trials targeting immune dysfunction in patients with neurodegenerative diseases.
Publisher: Hindawi Limited
Date: 2018
DOI: 10.1111/JONM.12533
Publisher: Informa UK Limited
Date: 04-05-2019
Publisher: Informa UK Limited
Date: 02-01-2016
Location: Germany
No related grants have been discovered for John Rihari-Thomas.