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| 024 | 7 | _ | |a 10.1002/mds.70070 |2 doi |
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| 024 | 7 | _ | |a 0885-3185 |2 ISSN |
| 024 | 7 | _ | |a 1531-8257 |2 ISSN |
| 037 | _ | _ | |a DZNE-2026-00167 |
| 041 | _ | _ | |a English |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Palleis, Carla |0 P:(DE-2719)9000852 |b 0 |e First author |
| 245 | _ | _ | |a A Biomarker-Based Classification of Corticobasal Syndrome. |
| 260 | _ | _ | |a New York, NY |c 2026 |b Wiley |
| 336 | 7 | _ | |a article |2 DRIVER |
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| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1770628901_24270 |2 PUB:(DE-HGF) |
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| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a Corticobasal syndrome (CBS) is a clinically defined syndrome with progressive movement and cortical dysfunction, caused by various underlying pathologies, most commonly tau-predominant pathologies such as progressive supranuclear palsy and corticobasal degeneration, or Alzheimer's disease (AD). Lewy-type α-synucleinopathies (LTS), TDP-43 proteinopathies, and mixed pathologies may also underlie CBS. The clinical impact of these pathologies remains poorly understood.To subclassify CBS patients in vivo using biomarkers for amyloid-β (Aβ), Tau, and α-synuclein (αSyn), and assess the clinical relevance of this stratification.We conducted a prospective cohort study of 50 CBS patients at LMU University Hospital Munich. Biomarker analysis included cerebrospinal fluid (CSF) Aβ42 and Aβ42/40, [18F]flutemetamol Aβ-PET, [18F]PI-2620 tau-PET, and αSyn seed amplification assays in CSF. CSF neurofilament light chain (NfL) served as a marker of neurodegeneration. Patients were stratified into six groups based on biomarker positivity.Tau positivity was found in 90% of CBS cases, Aβ in 28%, and αSyn in 24%. Stratification identified: 52% consistent with tau-predominant pathology, 18% with AD, 10% with AD+LTS, 10% with tau-predominant+LTS, 4% with isolated LTS, and 6% unclassified. αSyn positivity was more frequent in AD-CBS (36%) than in tau-predominant-CBS (16%). Aβ-positive cases showed greater cognitive impairment; Tau positivity correlated with worse motor symptoms; αSyn-positive patients had milder motor symptoms, slower progression, and lower NfL levels.CBS is molecularly heterogeneous. Biomarker-based classification may enhance diagnostic precision and support personalized therapeutic strategies. © 2025 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society. |
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| 588 | _ | _ | |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de |
| 650 | _ | 7 | |a proteinopathies |2 Other |
| 650 | _ | 7 | |a tau‐PET |2 Other |
| 650 | _ | 7 | |a α‐synuclein seed amplification assay |2 Other |
| 650 | _ | 7 | |a β‐amyloid |2 Other |
| 650 | _ | 7 | |a Biomarkers |2 NLM Chemicals |
| 650 | _ | 7 | |a Amyloid beta-Peptides |2 NLM Chemicals |
| 650 | _ | 7 | |a tau Proteins |2 NLM Chemicals |
| 650 | _ | 7 | |a alpha-Synuclein |2 NLM Chemicals |
| 650 | _ | 7 | |a Peptide Fragments |2 NLM Chemicals |
| 650 | _ | 7 | |a amyloid beta-protein (1-42) |2 NLM Chemicals |
| 650 | _ | 2 | |a Humans |2 MeSH |
| 650 | _ | 2 | |a Male |2 MeSH |
| 650 | _ | 2 | |a Female |2 MeSH |
| 650 | _ | 2 | |a Aged |2 MeSH |
| 650 | _ | 2 | |a Biomarkers: cerebrospinal fluid |2 MeSH |
| 650 | _ | 2 | |a Amyloid beta-Peptides: cerebrospinal fluid |2 MeSH |
| 650 | _ | 2 | |a Middle Aged |2 MeSH |
| 650 | _ | 2 | |a tau Proteins: cerebrospinal fluid |2 MeSH |
| 650 | _ | 2 | |a Positron-Emission Tomography |2 MeSH |
| 650 | _ | 2 | |a alpha-Synuclein: cerebrospinal fluid |2 MeSH |
| 650 | _ | 2 | |a alpha-Synuclein: metabolism |2 MeSH |
| 650 | _ | 2 | |a Prospective Studies |2 MeSH |
| 650 | _ | 2 | |a Corticobasal Degeneration: classification |2 MeSH |
| 650 | _ | 2 | |a Corticobasal Degeneration: cerebrospinal fluid |2 MeSH |
| 650 | _ | 2 | |a Corticobasal Degeneration: diagnostic imaging |2 MeSH |
| 650 | _ | 2 | |a Peptide Fragments: cerebrospinal fluid |2 MeSH |
| 650 | _ | 2 | |a Aged, 80 and over |2 MeSH |
| 700 | 1 | _ | |a Bernhardt, Alexander Maximilian |0 P:(DE-2719)9002620 |b 1 |e First author |
| 700 | 1 | _ | |a Weidinger, Endy |0 P:(DE-2719)9000882 |b 2 |u dzne |
| 700 | 1 | _ | |a Fietzek, Urban M |0 P:(DE-2719)9001214 |b 3 |u dzne |
| 700 | 1 | _ | |a Jäck, Alexander |0 P:(DE-2719)9002626 |b 4 |u dzne |
| 700 | 1 | _ | |a Katzdobler, Sabrina |0 P:(DE-2719)9001160 |b 5 |
| 700 | 1 | _ | |a Gnoerich, Johannes |0 P:(DE-2719)9001652 |b 6 |u dzne |
| 700 | 1 | _ | |a Bauer, Theresa |b 7 |
| 700 | 1 | _ | |a Franzmeier, Nicolai |b 8 |
| 700 | 1 | _ | |a Perneczky, Robert |0 P:(DE-2719)2812234 |b 9 |u dzne |
| 700 | 1 | _ | |a Tauopathies, German Imaging Initiative for |b 10 |e Collaboration Author |
| 700 | 1 | _ | |a Brendel, Matthias |0 P:(DE-2719)9001539 |b 11 |e Last author |
| 700 | 1 | _ | |a Levin, Johannes |0 P:(DE-2719)2811659 |b 12 |e Last author |u dzne |
| 700 | 1 | _ | |a Höglinger, Günter U |0 P:(DE-2719)2811373 |b 13 |e Last author |u dzne |
| 773 | _ | _ | |a 10.1002/mds.70070 |g Vol. 41, no. 1, p. 129 - 142 |0 PERI:(DE-600)2041249-6 |n 1 |p 129 - 142 |t Movement disorders |v 41 |y 2026 |x 0885-3185 |
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