Evidence map›Paper›PMID 42625899›Full record

ArticleAlzheimer's & dementia (Amsterdam, Netherlands)

Cerebrospinal fluid biomarkers for cerebral amyloid angiopathy with non-hemorrhagic imaging marker.

Alexander Sekita, Maximilian I Sprügel, Stefanie Balk, David Haupenthal, Tobias Engelhorn, Manuel Alexander Schmidt, Arnd Doerfler, Timo Jan Oberstein, Juan Manuel Maler, Johannes Kornhuber and 5 more

Abstract read
In one paragraph

Article in Alzheimer's & dementia (Amsterdam, Netherlands). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. 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

15 authors.

Alexander SekitaDepartment of Neurology University Hospital Erlangen and Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen Germany.
Maximilian I SprügelDepartment of Neurology University Hospital Erlangen and Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen Germany.
Stefanie BalkDepartment of Neurology University Hospital Erlangen and Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen Germany.
David HaupenthalDepartment of Neurology University Hospital Erlangen and Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen Germany.
Tobias EngelhornDepartment of Neuroradiology University Hospital Erlangen and Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen Germany.
Manuel Alexander SchmidtDepartment of Neuroradiology University Hospital Erlangen and Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen Germany.
Arnd DoerflerDepartment of Neuroradiology University Hospital Erlangen and Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen Germany.
Timo Jan ObersteinDepartment of Psychiatry and Psychotherapy University Hospital Erlangen and Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen Germany.
Juan Manuel MalerDepartment of Psychiatry and Psychotherapy University Hospital Erlangen and Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen Germany.
Johannes KornhuberDepartment of Psychiatry and Psychotherapy University Hospital Erlangen and Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen Germany.
Piotr LewczukDepartment of Neurology University Hospital Erlangen and Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen Germany.
Veit RothhammerDepartment of Neurology University Hospital Erlangen and Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen Germany.
Stefan SchwabDepartment of Neurology University Hospital Erlangen and Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen Germany.
Joji B KuramatsuDepartment of Neurology University Hospital Erlangen and Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen Germany.
Jochen A SembillDepartment of Neurology University Hospital Erlangen and Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionReduced cerebrospinal fluid (CSF) amyloid beta (Aβ) 40 has been reported in cerebral amyloid angiopathy (CAA) diagnosed by hemorrhagic magnetic resonance imaging (MRI) markers. Whether similar alterations occur when fulfilling Boston Criteria 2.0 solely through non-hemorrhagic markers remains unclear.

methodsWe analyzed 358 memory clinic patients undergoing MRI and CSF assessment. CAA was categorized by hemorrhagic markers (CAA 1.5 H) or exclusively non-hemorrhagic markers (CAA 2.0 NH) per Boston Criteria 1.5 and 2.0, respectively. Primary comparison of CSF-Aβ40 between CAA groups was complemented by secondary (Aβ42, phosphorylated tau [p-tau181], total tau [t-tau]) and exploratory analyses including Alzheimer's disease (AD), mild cognitive impairment (MCI), and healthy controls, adjusted for age, sex, MRI characteristics, and assay type.

resultsSixty-five patients were reclassified as CAA 2.0 NH. Aβ40 was higher in CAA 2.0 NH than CAA 1.5 H (15,808 vs. 13,792 pg/ml, DISCUSSION: Non-hemorrhagic imaging markers alone were not associated with characteristic CAA-related CSF alterations, suggesting biological heterogeneity, limited specificity, or lesion type-dependent variability.

Indexed as

amyloidBoston Criteriacerebral amyloid angiopathycerebrospinal fluid biomarkersnon‐hemorrhagic markers

Identifiers

PMID42625899
PMCPMC13490837

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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 OpenQuestion graph.