Evidence map›Paper›PMID 40314736›Full record

ArticleEuropean archives of psychiatry and clinical neuroscience2025

Plasma biomarkers of amyloid, tau & neuroinflammation in Alzheimer's disease and corticobasal syndrome.

Carolin Kurz, Laura Carli, Selim Üstün Gürsel, Isabelle Schrurs, Alexander Jethwa, Margherita Carboni, Tobias Bittner, Sayuri Hortsch, Daniel Keeser, Matthias Brendel and 15 more

Abstract read
In one paragraph

Article in European archives of psychiatry and clinical neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

25 authors.

Carolin KurzDepartment of Psychiatry and Psychotherapy, LMU University Hospital, LMU Munich, Nußbaumstr. 7, 80336, Munich, Germany. carolin.kurz@med.uni-muenchen.de.ORCID http://orcid.org/0000-0003-4299-6240
Laura CarliDepartment of Psychiatry and Psychotherapy, LMU University Hospital, LMU Munich, Nußbaumstr. 7, 80336, Munich, Germany.
Selim Üstün GürselDepartment of Psychiatry and Psychotherapy, LMU University Hospital, LMU Munich, Nußbaumstr. 7, 80336, Munich, Germany.
Isabelle SchrursRoche Diagnostics International Ltd, 6343, Rotkreuz, Switzerland.
Alexander JethwaRoche Diagnostics GmbH, 82377, Penzberg, Germany.
Margherita CarboniRoche Diagnostics International Ltd, 6343, Rotkreuz, Switzerland.
Tobias BittnerF. Hoffmann-La Roche Ltd, 4070, Basel, Switzerland.
Sayuri HortschRoche Diagnostics GmbH, 82377, Penzberg, Germany.
Daniel KeeserDepartment of Psychiatry and Psychotherapy, LMU University Hospital, LMU Munich, Nußbaumstr. 7, 80336, Munich, Germany.
Matthias BrendelMunich Cluster for Systems Neurology (SyNergy), 80336, Munich, Germany.
Lena BurowDepartment of Psychiatry and Psychotherapy, LMU University Hospital, LMU Munich, Nußbaumstr. 7, 80336, Munich, Germany.
Jan HaeckertDepartment of Psychiatry and Psychotherapy, LMU University Hospital, LMU Munich, Nußbaumstr. 7, 80336, Munich, Germany.
Carolin A M KoriathDepartment of Psychiatry and Psychotherapy, LMU University Hospital, LMU Munich, Nußbaumstr. 7, 80336, Munich, Germany.
Maia TatòDepartment of Psychiatry and Psychotherapy, LMU University Hospital, LMU Munich, Nußbaumstr. 7, 80336, Munich, Germany.
Julia UtechtDepartment of Psychiatry and Psychotherapy, LMU University Hospital, LMU Munich, Nußbaumstr. 7, 80336, Munich, Germany.
Boris PapazovClinic for Psychiatry, Psychotherapy and Psychosomatics at the University of Augsburg, Augsburg, Germany.
Estrella Morenas-RodriguezGerman Center for Neurodegenerative Diseases (DZNE), 81377, Munich, Germany.
Oliver PogarellDepartment of Psychiatry and Psychotherapy, LMU University Hospital, LMU Munich, Nußbaumstr. 7, 80336, Munich, Germany.
Carla PalleisGerman Center for Neurodegenerative Diseases (DZNE), 81377, Munich, Germany.
Endy WeidingerDepartment of Neurology, LMU Hospital Munich, LMU Munich, 81377, Munich, Germany.
Sophia StoeckleinDepartment of Radiology, LMU Hospital Munich, LMU Munich, 81377, Munich, Germany.
Johannes LevinGerman Center for Neurodegenerative Diseases (DZNE), 81377, Munich, Germany.
Günter HöglingerGerman Center for Neurodegenerative Diseases (DZNE), 81377, Munich, Germany.
Boris-Stephan RauchmannDepartment of Psychiatry and Psychotherapy, LMU University Hospital, LMU Munich, Nußbaumstr. 7, 80336, Munich, Germany.
Robert PerneczkyDepartment of Psychiatry and Psychotherapy, LMU University Hospital, LMU Munich, Nußbaumstr. 7, 80336, Munich, Germany.

Funding

Deutsche Forschungsgemeinschaft 390857198
6 · The paper itself

Abstract

backgroundBlood-based biomarkers (BBBMs) could significantly facilitate the diagnosis of Alzheimer's disease (AD) and non-AD dementia by providing less invasive alternatives to cerebrospinal fluid (CSF) and positron emission tomography (PET) imaging.

objectiveThis study investigated how well the BBBMs-amyloid-β (Aβ) 1-42/1-40 ratio, phosphorylated tau181 (pTau181), apolipoprotein E4 (ApoE4), glial fibrillary acidic protein (GFAP), and neurofilament light chain (NfL)-reflect thorough clinical work-up validated by PET and CSF biomarkers in participants with AD (n = 27), Aβ-negative CBS (n = 26), and agematched healthy controls (HC) (n = 17).

methodsFactor and correlation explored biomarker associations. Bayesian regression, backward selection regression, and ROC curve analysis were applied to identify optimal biomarker combinations and diagnostic cut-offs.

resultsIn AD cases, pTau181 and ApoE4 levels were elevated, and the Aβ1-42/1-40 ratio was reduced. ROC analysis showed high accuracy for pTau181, ApoE4 and Aβ1-42/1-40 in discriminating AD from HC, with a combination significantly improving performance. However, limited fold change, and high variability reduced the diagnostic applicability of Aβ1-42/1-40 ratio. Elevated NfL levels were the most reliable biomarker for CBS-Aβ(-) cases. GFAP showed limited discriminatory power due to overlapping levels, suggesting that it may not serve as a disease-specific biomarker but may be indicative of general neurodegeneration.

conclusionsThis study highlights the diagnostic utility of pTau181, ApoE4 and the Aβ1-42/1-40 ratio for AD and NfL in the CBS-Aβ(-) cases and emphasizes the added value of combined biomarker models for group differentiation. Prospective studies will help validate these findings and refine clinical thresholds.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesCorticobasal DegenerationNeuroinflammatory DiseasesPeptide Fragmentstau ProteinsAgedAged, 80 and overApolipoprotein E4BiomarkersFemaleGlial Fibrillary Acidic ProteinHumansMaleMiddle AgedNeurofilament ProteinsAmyloid beta-Peptidesamyloid beta-protein (1-40)amyloid beta-protein (1-42)Apolipoprotein E4BiomarkersGFAP protein, humanGlial Fibrillary Acidic ProteinMAPT protein, humanneurofilament protein LNeurofilament ProteinsPeptide Fragmentstau ProteinsApolipoprotein E (ApoE4)Beta-amyloid 1-40 (Aβ1-40)Beta-amyloid 1-42 (Aβ1-42)Glial fibrillary acidic protein (GFAP)Neurofilament light chain (NfL)Non-Alzheimer's disease dementia; betaPhosphorylated tau (pTau)

Identifiers

PMID40314736
PMCPMC12638345

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.