
Frederik Barkhof
Articles
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Jan 5, 2025 |
jnnp.bmj.com | Mirthe Coenen |Xin Xu |Saima Hilal |Frederik Barkhof
X @MarcoDueringJMB and CHT contributed equally. Collaborators Alzheimer’s Disease Neuroimaging Initiative: data used in the preparation of this article were obtained from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database (https://adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in the analysis or writing of this report.
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Nov 26, 2024 |
alzres.biomedcentral.com | Antti Tolonen |Frederik Barkhof |Juha Koikkalainen |Sanna-Kaisa Herukka |Steen Gregers Hasselbalch |Patrizia Mecocci | +4 more
In an era where disease-modifying therapies are becoming available for the first time, timely and accurate diagnosis of dementia is more important than ever. A data-driven tool can be beneficial for assisting clinicians in determining which tests add value in different clinical contexts. In this study, we applied a data-driven stepwise testing approach using a CDSS in three clinical scenarios to assess its potential to guide diagnostic decision-making.
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Oct 12, 2024 |
alzres.biomedcentral.com | Anna Svenningsson |Diana I. Bocancea |Erik Stomrud |Frederik Barkhof |Niklas Mattsson-Carlgren |Sebastian Palmqvist | +3 more
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Sep 3, 2024 |
nature.com | Ruth Geraldes |Georgina Arrambide |Alex Rovira |Hans Lassmann |Patrick Waters |Declan T. Chard | +6 more
AbstractMyelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is an immune-mediated demyelinating disease that is challenging to differentiate from multiple sclerosis (MS), as the clinical phenotypes overlap, and people with MOGAD can fulfil the current MRI-based diagnostic criteria for MS. In addition, the MOG antibody assays that are an essential component of MOGAD diagnosis are not standardized.
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Jun 14, 2024 |
nature.com | Sophie E Mastenbroek |Jacob Vogel |Lyduine E. Collij |Alexandra Young |Frederik Barkhof |Rik Ossenkoppele
AbstractLewy body (LB) diseases, characterized by the aggregation of misfolded α-synuclein proteins, exhibit notable clinical heterogeneity. This may be due to variations in accumulation patterns of LB neuropathology. Here we apply a data-driven disease progression model to regional neuropathological LB density scores from 814 brain donors with Lewy pathology.
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