Evidence map›Paper›PMID 40690136›Full record

ReviewMolecular neurobiology2025

The Role of Glial Fibrillary Acidic Protein in the Neuropathology of Alzheimer's Disease and Its Potential as a Blood Biomarker for Early Diagnosis and Progression.

Ekanayaka M S Bandara, Prita R Asih, Steve Pedrini, Eugene Hone, Warnakulasuriya Mary Ann Dipika Binosha Fernando, Ralph N Martins

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Trial
  2. Review
  3. Article
  4. Observational
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Special Issue: "New Insights of Biomarkers in Neurodegenerative Diseases".International journal of molecular sciences · 2025
    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.

Ekanayaka M S BandaraCentre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Joondalup, WA, Australia.ORCID http://orcid.org/0000-0002-2263-4720
Prita R AsihAlzheimer's Research Australia, Ralph and Patricia Sarich Neuroscience Research Institute, Nedlands, WA, 6009, Australia.ORCID http://orcid.org/0000-0002-1973-9628
Steve PedriniCentre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Joondalup, WA, Australia.ORCID http://orcid.org/0000-0002-6409-8022
Eugene HoneCentre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Joondalup, WA, Australia.ORCID http://orcid.org/0000-0001-6708-3718
Warnakulasuriya Mary Ann Dipika Binosha FernandoCentre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Joondalup, WA, Australia. w.fernando@ecu.edu.au.ORCID http://orcid.org/0000-0002-8364-7808
Ralph N MartinsCentre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Joondalup, WA, Australia.ORCID http://orcid.org/0000-0002-4828-9363

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disease characterised by neuropathological hallmarks, including extracellular amyloid plaques and neurofibrillary tangles. The disease is clinically defined by cognitive dysfunction, including learning, memory deficits, and behavioural changes. With the rising global prevalence of AD, early diagnosis is critical for implementing effective interventions before irreversible neuronal damage occurs. Biomarkers correlating amyloid deposition, tau pathology, neuroinflammation, and neurodegeneration are currently being investigated using cerebrospinal fluid analysis and positron emission tomography imaging. These methods are invasive or costly, limiting their widespread clinical utility. Blood-based biomarkers offer a promising alternative due to accessibility, cost-effectiveness, and feasibility for large-scale screening. Among blood-based biomarkers, plasma glial fibrillary acidic protein (GFAP) levels have gained interest in identifying individuals at risk of AD at preclinical stages. However, significant challenges remain, including methodological inconsistencies, analytical variability, and the need for standardisation across immunoassay platforms to ensure the clinical applicability of plasma GFAP measurement in AD diagnosis. Additionally, the specificity of GFAP for AD needs further evaluation, as increased plasma levels are also observed in other diseases. Similar issues are found with p-tau 217, the blood biomarker candidate for AD that has received the most attention. This review summarises the role of GFAP in the neuropathology of AD, provides evidence on plasma GFAP as an early blood biomarker for AD and identifies key knowledge gaps that need to be addressed. Future advancements in assay development and large-scale longitudinal studies are essential to validate its diagnostic and prognostic potential for community-based AD screening.

Indexed as

Alzheimer DiseaseDisease ProgressionGlial Fibrillary Acidic ProteinAnimalsBiomarkersEarly DiagnosisHumansBiomarkersGFAP protein, humanGlial Fibrillary Acidic ProteinADAlzheimer’s diseaseBlood biomarkersGFAPGFAP isoformsGlial fibrillary acidic protein

Identifiers

PMID40690136
PMCPMC12559115

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.