Evidence map›Paper›PMID 24252600›Full record

ArticleActa neuropathologica communications2013

NG2 cells, a new trail for Alzheimer's disease mechanisms?

Henrietta M Nielsen, Danyal Ek, Una Avdic, Camilla Orbjörn, Oskar Hansson, Netherlands Brain Bank, Robert Veerhuis, Annemieke Jm Rozemuller, Arne Brun, Lennart Minthon and 1 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Acta neuropathologica communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 2 pooled it
1.5field-weighted citation impact, top 19% 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

45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 69 citations in OpenAlex.

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  7. Emerging Role of Oligodendrocytes Malfunction in the Progression of Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
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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

11 authors at 3 institutions in 2 countries.

Henrietta M NielsenDepartment of Clinical Sciences Malmö, Molecular Memory Research Unit, Lund University, The Wallenberg Laboratory 2nd floor, Inga Marie Nilssons gata, entrance 53, Skåne University Hospital, Malmö, 205 02, Sweden. malin.wennstrom@med.lu.se.
Danyal Ek
Una Avdic
Camilla Orbjörn
Oskar Hansson
Netherlands Brain Bank
Robert Veerhuis
Annemieke Jm Rozemuller
Arne Brun
Lennart Minthon
Malin Wennström
Lund University · SEAmsterdam Neuroscience · NLMalmö University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuron Glial 2 (NG2) cells are glial cells known to serve as oligodendrocyte progenitors as well as modulators of the neuronal network. Altered NG2 cell morphology and up-regulation as well as increased shedding of the proteoglycan NG2 expressed on the cell surface have been described in rodent models of brain injury. Here we describe alterations in the human NG2 cell population in response to pathological changes characteristic of Alzheimer's disease (AD).

resultsImmunohistological stainings of postmortem brain specimens from clinically diagnosed and postmortem verified AD patients and non-demented controls revealed reduced NG2 immunoreactivity as well as large numbers of NG2 positive astrocytes in individuals with high amyloid beta plaque load. Since fibrillar amyloid beta (Aβ)1-42 is the major component of AD-related senile plaques, we exposed human NG2 cells to oligomer- and fibril enriched preparations of Aβ1-42. We found that both oligomeric and fibrillar Aβ1-42 induced changes in NG2 cell morphology. Further, in vitro exposure to fibrillar Aβ1-42 decreased the NG2 concentrations in both cell lysates and supernatants. Interestingly, we also found significantly decreased levels of soluble NG2 in the cerebrospinal fluid (CSF) from clinically diagnosed AD patients compared to non-demented individuals. Additionally, the CSF NG2 levels were found to significantly correlate with the core AD biomarkers Aß1-42, T-tau and P-tau.

conclusionOur results demonstrate major alterations in the NG2 cell population in relation to AD pathology which highlights the NG2 cell population as a new attractive research target in the search for cellular mechanisms associated with AD pathogenesis.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesAntigensAstrocytesBiomarkersBrainCells, CulturedCell SurvivalChondroitin Sulfate Proteoglycan 4FemaleHumansMaleMiddle AgedNeurogliaAmyloid beta-Peptidesamyloid beta-protein (1-42)AntigensBiomarkersChondroitin Sulfate Proteoglycan 4MAPT protein, humanPeptide FragmentsProteoglycanstau Proteins

Identifiers

PMID24252600
PMCPMC4046664
OpenAlexW2165533183

What OpenQuestion holds

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LicenceCC BY
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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.