Evidence map›Paper›PMID 30321501›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2019

Elevated CSF GAP-43 is Alzheimer's disease specific and associated with tau and amyloid pathology.

Åsa Sandelius, Erik Portelius, Åsa Källén, Henrik Zetterberg, Uros Rot, Bob Olsson, Jon B Toledo, Leslie M Shaw, Virginia M Y Lee, David J Irwin and 11 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 3 pooled it
9.8field-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

101 citing papers in PubMed, 3 syntheses or guidelines pooled it, 207 citations in OpenAlex.

  1. Pooled it
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  4. Review
  5. Sex-specific brain reserve and progression from mild cognitive impairment to Alzheimer's disease dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  12. Hippocampal volume moderates the association between cerebrospinal fluid growth-associated protein 43 and episodic memory performance in older adults.Neuropsychology, development, and cognition. Section B, Aging, neuropsychology and cognition · 2025
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  19. Development and validation of a novel Simoa assay for NPTX2 in Alzheimer's disease and Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  20. Article

41 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

21 authors at 7 institutions in 5 countries.

Åsa SandeliusInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. Electronic address: asa.sandelius@neuro.gu.se.
Erik PorteliusInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Åsa KällénClinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Henrik ZetterbergInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden; UK Dementia Research Institute, London, UK; Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK.
Uros RotDepartment of Neurology, University Medical Centre, Ljubljana, Slovenia.
Bob OlssonInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Jon B ToledoDepartment of Pathology and Laboratory Medicine, Institute on Aging, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, PA, USA; Department of Neurology, Houston Methodist Hospital, Houston, TX, USA.
Leslie M ShawDepartment of Pathology and Laboratory Medicine, Institute on Aging, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
Virginia M Y LeeDepartment of Pathology and Laboratory Medicine, Institute on Aging, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
David J IrwinDepartment of Pathology and Laboratory Medicine, Institute on Aging, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
Murray GrossmanDepartment of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
Daniel WeintraubDepartment of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA; Department of Psychiatry, University of Pennsylvania School of Medicine, Philadelphia, PA, USA; Parkinson's Disease and Mental Illness Research, Education and Clinical Centers (PADRECC and MIRECC), Philadelphia Veterans Affairs Medical Center, Philadelphia, PA, USA.
Alice Chen-PlotkinDepartment of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
David A WolkDepartment of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
Leo McCluskeyDepartment of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
Lauren ElmanDepartment of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
Vesna KostanjeveckiFujirebio Europe nv, Ghent, Belgium.
Manu VandijckFujirebio Europe nv, Ghent, Belgium.
Jennifer McBrideDepartment of Pathology and Laboratory Medicine, Institute on Aging, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
John Q TrojanowskiDepartment of Pathology and Laboratory Medicine, Institute on Aging, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
Kaj BlennowInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
University of Pennsylvania · USSahlgrenska University Hospital · SEUniversity of Gothenburg · SEFujirebio (Belgium) · BEInstitute on Aging · USLjubljana University Medical Centre · SIMental Illness Research, Education and Clinical Centers · US

Funding

Transgenic Mouse Models of Tau PathologiesP01AG017586 · NIA · UNIVERSITY OF PENNSYLVANIA · PI LEE, VIRGINIA M · 2000 to 2021
$37.3M
UPenn ADCC Biomarker CoreP30AG010124 · NIA · UNIVERSITY OF PENNSYLVANIA · PI XIE, SHARON XIANGWEN · 1991 to 2020
$35.1M
Project IV: "Alpha-Synuclein Strains & Diverse Synucleinopathies"P50NS053488 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI TROJANOWSKI, JOHN Q. · 2007 to 2017
$20.9M
Towards a blood-based diagnostic panel for confirmation of Parkinson's diseaseU01NS097056 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI CHEN-PLOTKIN, ALICE S · 2017 to 2019
$785k
NIA NIH HHS P01 AG017586NIA NIH HHS P30 AG010124NINDS NIH HHS P50 NS053488NINDS NIH HHS U01 NS097056
6 · The paper itself

Abstract

introductionThe level of the presynaptic protein growth-associated protein 43 (GAP-43) in cerebrospinal fluid (CSF) has previously been shown to be increased in Alzheimer's disease (AD) and thus may serve as an outcome measure in clinical trials and facilitate earlier disease detection.

methodsWe developed an enzyme-linked immunosorbent assay for CSF GAP-43 and measured healthy controls (n = 43), patients with AD (n = 275), or patients with other neurodegenerative diseases (n = 344). In a subpopulation (n = 93), CSF GAP-43 concentrations from neuropathologically confirmed cases were related to Aβ plaques, tau, α-synuclein, and TDP-43 pathologies.

resultsGAP-43 was significantly increased in AD compared to controls and most neurodegenerative diseases and correlated with the magnitude of neurofibrillary tangles and Aβ plaques in the hippocampus, amygdala, and cortex. GAP-43 was not associated to α-synuclein or TDP-43 pathology. DISCUSSION: The presynaptic marker GAP-43 is associated with both diagnosis and neuropathology of AD and thus may be useful as a sensitive and specific biomarker for clinical research.

Indexed as

Agedalpha-SynucleinAlzheimer DiseaseAmyloid beta-PeptidesBiomarkersEnzyme-Linked Immunosorbent AssayFemaleGAP-43 ProteinHumansMiddle AgedPlaque, Amyloidtau Proteinsalpha-SynucleinAmyloid beta-PeptidesBiomarkersGAP-43 Proteintau ProteinsAlzheimer's diseaseCSF biomarkerDifferential diagnosisEnzyme-linked immunosorbent assayGAP-43

Identifiers

PMID30321501
PMCPMC6333489
OpenAlexW2897287578

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.