Evidence map›Paper›PMID 36221099›Full record

ArticleAlzheimer's research & therapy2022

Diagnostic value of plasma p-tau181, NfL, and GFAP in a clinical setting cohort of prevalent neurodegenerative dementias.

Simone Baiardi, Corinne Quadalti, Angela Mammana, Sofia Dellavalle, Corrado Zenesini, Luisa Sambati, Roberta Pantieri, Barbara Polischi, Luciano Romano, Matteo Suffritti and 5 more

Open access · goldAbstract read
In one paragraph

Article in Alzheimer's research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 6 pooled it
18.9field-weighted citation impact, top 1% of its field
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

123 citing papers in PubMed, 6 syntheses or guidelines pooled it, 171 citations in OpenAlex.

  1. Pooled it
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  6. Pooled it
  7. Trial
  8. Pharmacodynamic effects of semorinemab on plasma and CSF biomarkers of Alzheimer's disease pathophysiology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Trial
  9. Article
  10. Article
  11. Alterations of gut microbiota in Down syndrome and their association with Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  12. Observational
  13. Article
  14. Review
  15. Article
  16. Article
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  18. Review
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  20. Observational

63 more citing papers are in PubMed but not listed here.

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 at 4 institutions in 1 country.

Simone BaiardiDepartment of Experimental, Diagnostic and Specialty Medicine (DIMES) University of Bologna, Bologna, Italy.
Corinne QuadaltiIRCCS Istituto delle Scienze Neurologiche di Bologna, Via Altura 1/8, 40139, Bologna, Italy.
Angela MammanaDepartment of Experimental, Diagnostic and Specialty Medicine (DIMES) University of Bologna, Bologna, Italy.
Sofia DellavalleIRCCS Istituto delle Scienze Neurologiche di Bologna, Via Altura 1/8, 40139, Bologna, Italy.
Corrado ZenesiniIRCCS Istituto delle Scienze Neurologiche di Bologna, Via Altura 1/8, 40139, Bologna, Italy.
Luisa SambatiIRCCS Istituto delle Scienze Neurologiche di Bologna, Via Altura 1/8, 40139, Bologna, Italy.
Roberta PantieriIRCCS Istituto delle Scienze Neurologiche di Bologna, Via Altura 1/8, 40139, Bologna, Italy.
Barbara PolischiIRCCS Istituto delle Scienze Neurologiche di Bologna, Via Altura 1/8, 40139, Bologna, Italy.
Luciano RomanoDepartment of Biomedical and Neuromotor Sciences University of Bologna (DIBINEM), Bologna, Italy.
Matteo SuffrittiDepartment of Biomedical and Neuromotor Sciences University of Bologna (DIBINEM), Bologna, Italy.
Giuseppe Mario BentivengaDepartment of Biomedical and Neuromotor Sciences University of Bologna (DIBINEM), Bologna, Italy.
Vanda RandiEmilia-Romagna Regional Blood Bank, Immunohematology and Transfusion Medicine Service, Bologna Metropolitan Area, Bologna, Italy.
Michelangelo Stanzani-MaseratiIRCCS Istituto delle Scienze Neurologiche di Bologna, Via Altura 1/8, 40139, Bologna, Italy.
Sabina CapellariIRCCS Istituto delle Scienze Neurologiche di Bologna, Via Altura 1/8, 40139, Bologna, Italy.
Piero ParchiIRCCS Istituto delle Scienze Neurologiche di Bologna, Via Altura 1/8, 40139, Bologna, Italy. piero.parchi@unibo.it.
Istituto delle Scienze Neurologiche di Bologna · ITUniversity of Bologna · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITRegione Emilia-Romagna

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreasing evidence supports the use of plasma biomarkers of neurodegeneration and neuroinflammation to screen and diagnose patients with dementia. However, confirmatory studies are required to demonstrate their usefulness in the clinical setting.

methodsWe evaluated plasma and cerebrospinal fluid (CSF) samples from consecutive patients with frontotemporal dementia (FTD) (n = 59), progressive supranuclear palsy (PSP) (n = 31), corticobasal syndrome (CBS) (n = 29), dementia with Lewy bodies (DLB) (n = 49), Alzheimer disease (AD) (n = 97), and suspected non-AD physiopathology (n = 51), as well as plasma samples from 60 healthy controls (HC). We measured neurofilament light chain (NfL), phospho-tau181 (p-tau181), and glial fibrillary acid protein (GFAP) using Simoa (all plasma biomarkers and CSF GFAP), CLEIA (CSF p-tau181), and ELISA (CSF NfL) assays. Additionally, we stratified patients according to the A/T/N classification scheme and the CSF α-synuclein real-time quaking-induced conversion assay (RT-QuIC) results.

resultsWe found good correlations between CSF and plasma biomarkers for NfL (rho = 0.668, p < 0.001) and p-tau181 (rho = 0.619, p < 0.001). Plasma NfL was significantly higher in disease groups than in HC and showed a greater increase in FTD than in AD [44.9 (28.1-68.6) vs. 21.9 (17.0-27.9) pg/ml, p < 0.001]. Conversely, plasma p-tau181 and GFAP levels were significantly higher in AD than in FTD [3.2 (2.4-4.3) vs. 1.1 (0.7-1.6) pg/ml, p < 0.001; 404.7 (279.7-503.0) vs. 198.2 (143.9-316.8) pg/ml, p < 0.001]. GFAP also allowed discriminating disease groups from HC. In the distinction between FTD and AD, plasma p-tau181 showed better accuracy (AUC 0.964) than NfL (AUC 0.791) and GFAP (AUC 0.818). In DLB and CBS, CSF amyloid positive (A+) subjects had higher plasma p-tau181 and GFAP levels than A- individuals. CSF RT-QuIC showed positive α-synuclein seeding activity in 96% DLB and 15% AD patients with no differences in plasma biomarker levels in those stratified by RT-QuIC result.

conclusionsIn a single-center clinical cohort, we confirm the high diagnostic value of plasma p-tau181 for distinguishing FTD from AD and plasma NfL for discriminating degenerative dementias from HC. Plasma GFAP alone differentiates AD from FTD and neurodegenerative dementias from HC but with lower accuracy than p-tau181 and NfL. In CBS and DLB, plasma p-tau181 and GFAP levels are significantly influenced by beta-amyloid pathology.

Indexed as

Alzheimer DiseaseFrontotemporal Dementiaalpha-SynucleinAmyloid beta-PeptidesBiomarkersGlial Fibrillary Acidic ProteinHumanstau Proteinsalpha-SynucleinAmyloid beta-PeptidesBiomarkersGFAP protein, humanGlial Fibrillary Acidic Proteintau ProteinsAlpha-synucleinAlzheimer diseaseCorticobasal syndromeFrontotemporal dementiaFTLDLewy bodiesProgressive supranuclear palsyRT-QuICTau

Identifiers

PMID36221099
PMCPMC9555092
OpenAlexW4304588918

What OpenQuestion holds

Textmetadata
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Registered trials

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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.