Evidence map›Paper›PMID 38558318›Full record

ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2024

Plasma concentrations of glial fibrillary acidic protein, neurofilament light, and tau in Alexander disease.

Nicholas J Ashton, Guglielmo Di Molfetta, Kübra Tan, Kaj Blennow, Henrik Zetterberg, Albee Messing

Open access · hybridAbstract read
In one paragraph

Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Rigorous genetic diagnosis review in natural history studies.Orphanet journal of rare diseases · 2026
    Article
  5. 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

6 authors at 4 institutions in 6 countries.

Nicholas J AshtonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.ORCID http://orcid.org/0000-0002-3579-8804
Guglielmo Di MolfettaDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.ORCID http://orcid.org/0009-0001-5339-933X
Kübra TanDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.ORCID http://orcid.org/0000-0002-1890-4193
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.ORCID http://orcid.org/0000-0003-3930-4354
Albee MessingWaisman Center, University of Wisconsin-Madison, Madison, WI, 53705, USA. amessing@wisc.edu.ORCID http://orcid.org/0000-0001-6049-0521
University of Gothenburg · SEUniversity of Wisconsin–Madison · USKing's College London · GBUniversity of Science and Technology of China · CN

Funding

Validation of the GMFC-MLDU54NS115052 · NINDS · CHILDREN'S HOSP OF PHILADELPHIA · PI Laura Ann Adang · 2019 to 2026
$14.3M
Astrocyte-synapse interactions in a rat model of Alexander diseaseR01NS110719 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI HAGEMANN, TRACY · 2019 to 2023
$2.1M
AD Strategic Fund and Alzheimer's Association ADSF-21-831376-CAD Strategic Fund and Alzheimer's Association ADSF-21-831377-CAD Strategic Fund and Alzheimer's Association ADSF-21-831381-CALF Agreement ALFGBG-715986ALF Agreement ALFGBG-965240Alzheimer's Association 2021 Zenith Award ZEN-21-848495Alzheimer's Association 2022-2025 Grant SG-23-1038904 QCAlzheimer's Drug Discovery Foundation 201809-2016862EU Joint Programme - Neurodegenerative Disease Research JPND2019-466-236European Union Joint Programme - Neurodegenerative Disease Research JPND2021-00694Hjärnfonden ALZ2022-0006)Hjärnfonden FO2017-0243Hjärnfonden FO2022-0270HORIZON EUROPE Marie Sklodowska-Curie Actions 860197 (MIRIADE)Horizon Europe Research and Innovation Programme 101053962National Institute for Health Research Collaboration for Leadership in Applied Health Research and Care Yorkshire and Humber UKDRI-1003NIH HHS R01 NS110719NIH HHS U54 NS115052NINDS NIH HHS R01 NS110719NINDS NIH HHS U54 NS115052Swedish Alzheimer Foundation AF-930351Swedish Alzheimer Foundation AF-939721Swedish Alzheimer Foundation AF-968270Swedish Research Council 2017-11915Swedish Research Council 2019-02397Swedish Research Council 2022-00732)Swedish Research Council 2022-01018Swedish State Support for Clinical Research ALFGBG-71320UK Dementia Research Institute UKDIR-1003)
6 · The paper itself

Abstract

introductionAlexander disease (AxD) is a rare leukodystrophy caused by dominant gain-of-function mutations in the gene encoding the astrocyte intermediate filament, glial fibrillary acidic protein (GFAP). However, there is an urgent need for biomarkers to assist in monitoring not only the progression of disease but also the response to treatment. GFAP is the obvious candidate for such a biomarker, as it is measurable in body fluids that are readily accessible for biopsy, namely cerebrospinal fluid and blood. However, in the case of ASOs, the treatment that is furthest in development, GFAP is the target of therapy and presumably would go down independent of disease status. Hence, there is a critical need for biomarkers that are not directly affected by the treatment strategy.

methodsWe explored the potential utility of biomarkers currently being studied in other neurodegenerative diseases and injuries, specifically neurofilament light protein (NfL), phosphorylated forms of tau, and amyloid-β peptides (Aβ42/40). RESULTS AND

conclusionsHere, we report that GFAP is elevated in plasma of all age groups afflicted by AxD, including those with adult onset. NfL and p-tau are also elevated, but to a much lesser extent than GFAP. In contrast, the levels of Aß40 and Aß42 are not altered in AxD.

Indexed as

Alexander DiseaseAmyloid beta-PeptidesBiomarkersGlial Fibrillary Acidic ProteinNeurofilament Proteinstau ProteinsAdolescentAdultAgedChildChild, PreschoolFemaleHumansInfantMaleMiddle AgedAmyloid beta-Peptidesamyloid beta-protein (1-42)BiomarkersGFAP protein, humanGlial Fibrillary Acidic ProteinMAPT protein, humanneurofilament protein LNeurofilament ProteinsPeptide Fragmentstau ProteinsAlexander diseaseGFAPLeukodystrophyNeurofilamentsPlasmaTau

Identifiers

PMID38558318
PMCPMC11305938
OpenAlexW4393391801

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.