Evidence map›Paper›PMID 40170060›Full record

ArticleBMC neurology2025

Growth associated protein 43 (GAP-43) predicts brain amyloidosis in Alzheimer's dementia continuum: an [

Rezvan Nemati, Ahmadreza Sohrabi-Ashlaghi, Parsa Saberian, Mohammad Sadeghi, Sajjad Mardani, Amir Sina Jafari Hossein Abadi, Ali Yaghoobpoor, Atefeh Heydari, Niloofar Khoshroo, Yassin Rahnama and 2 more

Abstract read
In one paragraph

Article in BMC neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Rezvan NematiDepartment of Psychology, Islamic Azad University Arak branch, Arak, Iran.
Ahmadreza Sohrabi-AshlaghiDepartment of Physiology, Faculty of Medicine, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Parsa SaberianStudent Research Committee, Faculty of Medicine, Hormozgan University of Medical Sciences, Bandar Abbas, Hormozgan Province, 7916969573, Iran. ar1sohrabi@gmail.com.
Mohammad SadeghiSchool of Medicine, Tehran University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0000-0003-0351-7876
Sajjad MardaniSchool of Medicine, Urmia University of Medical Sciences, Urmia, Iran.
Amir Sina Jafari Hossein AbadiIslamic Azad University, Shahr-e-Qods Branch, Tehran, Iran.
Ali YaghoobpoorStudent's Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Atefeh HeydariTehran University, Tehran, Iran.
Niloofar KhoshrooSchool of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Yassin RahnamaSchool of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Mahsa MayeliSchool of Medicine, Tehran University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0000-0003-4656-156X
Hamide NasiriStudent Research Committee, School of Medicine, Zanjan University of Medical Science, Zanjan, Iran. hnasiri@sina.zums.ac.ir.

Funding

Project 1U19AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI MONICA G. RIVERA-MINDT · 2016 to 2026
$226.7M
NIA NIH HHS U19 AG024904
6 · The paper itself

Abstract

backgroundGrowth-associated protein 43 (GAP-43) is a key protein involved in neuronal growth and synaptic plasticity. Alterations in GAP-43 levels have been associated with Alzheimer's Disease (AD), potentially reflecting synaptic dysfunction. We evaluated the potential of GAP-43 as a biomarker for AD and explored its association with amyloid-beta (Aβ) levels, as well as its correlation with Aβ plaque burden in the brain.

methodsWe screened 1,639 participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort. A total of 226 individuals met the eligibility criteria and were enrolled. Participants were classified into three groups: 77 cognitively normal (CN) individuals, 111 with mild cognitive impairment (MCI), and 38 with a diagnosis of AD. The associations between cerebrospinal fluid (CSF) GAP-43 levels with other biomarkers as well as [¹⁸F] AV-45 (Florbetapir) PET Standardized Uptake Value Ratios (SUVR) were investigated.

resultsOur findings revealed significantly elevated CSF GAP-43 levels in individuals with AD compared to CN and MCI groups. Furthermore, GAP-43 levels showed a significant positive correlation with tau pathology. Notably, we observed a significant association between GAP-43 and [¹⁸F] Florbetapir PET SUVR in the MCI group, suggesting that GAP-43 may serve as a reliable biomarker in the early stages of AD.

conclusionThis study provides evidence supporting the role of GAP-43 as a potential biomarker for AD, particularly in relation to predicting the amyloid pathology pattern in the brain in the MCI stage.

Indexed as

Alzheimer DiseaseAmyloidosisBrainGAP-43 ProteinAgedAged, 80 and overAmyloid beta-PeptidesAniline CompoundsBiomarkersCognitive DysfunctionCohort StudiesEthylene GlycolsFemaleFluorine RadioisotopesHumansMaleAmyloid beta-PeptidesAniline CompoundsBiomarkersEthylene GlycolsflorbetapirFluorine RadioisotopesGAP-43 ProteinAlzheimer’s diseaseGrowth associated protein 43Mild cognitive impairmentPositron emission tomography

Identifiers

PMID40170060
PMCPMC11959801

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.