Evidence map›Paper›PMID 21179413›Full record

ArticlePloS one2010

Β-amyloid 1-42 oligomers impair function of human embryonic stem cell-derived forebrain cholinergic neurons.

Linn Wicklund, Richardson N Leão, Anne-Marie Strömberg, Malahat Mousavi, Outi Hovatta, Agneta Nordberg, Amelia Marutle

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 49 citations in OpenAlex.

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  17. Treatment Efficacy of NGF Nanoparticles Combining Neural Stem Cell Transplantation on Alzheimer's Disease Model Rats.Medical science monitor : international medical journal of experimental and clinical research · 2015
    Article
  18. Article
  19. Amyloid-β immunization enhances neurogenesis and cognitive ability in neonatal mice.International journal of clinical and experimental medicine · 2015
    Article
  20. Probing the secrets of Alzheimer's disease using human-induced pluripotent stem cell technology.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015
    Review
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

7 authors at 2 institutions in 1 country.

Linn WicklundDepartment of Neurobiology, Care Sciences and Society, Division of Alzheimer Neurobiology, Karolinska Institutet, Stockholm, Sweden.
Richardson N Leão
Anne-Marie Strömberg
Malahat Mousavi
Outi Hovatta
Agneta Nordberg
Amelia Marutle
Karolinska Institutet · SEKarolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cognitive impairment in Alzheimer's disease (AD) patients is associated with a decline in the levels of growth factors, impairment of axonal transport and marked degeneration of basal forebrain cholinergic neurons (BFCNs). Neurogenesis persists in the adult human brain, and the stimulation of regenerative processes in the CNS is an attractive prospect for neuroreplacement therapy in neurodegenerative diseases such as AD. Currently, it is still not clear how the pathophysiological environment in the AD brain affects stem cell biology. Previous studies investigating the effects of the β-amyloid (Aβ) peptide on neurogenesis have been inconclusive, since both neurogenic and neurotoxic effects on progenitor cell populations have been reported. In this study, we treated pluripotent human embryonic stem (hES) cells with nerve growth factor (NGF) as well as with fibrillar and oligomeric Aβ1-40 and Aβ1-42 (nM-µM concentrations) and thereafter studied the differentiation in vitro during 28-35 days. The process applied real time quantitative PCR, immunocytochemistry as well as functional studies of intracellular calcium signaling. Treatment with NGF promoted the differentiation into functionally mature BFCNs. In comparison to untreated cells, oligomeric Aβ1-40 increased the number of functional neurons, whereas oligomeric Aβ1-42 suppressed the number of functional neurons. Interestingly, oligomeric Aβ exposure did not influence the number of hES cell-derived neurons compared with untreated cells, while in contrast fibrillar Aβ1-40 and Aβ1-42 induced gliogenesis. These findings indicate that Aβ1-42 oligomers may impair the function of stem cell-derived neurons. We propose that it may be possible for future AD therapies to promote the maturation of functional stem cell-derived neurons by altering the brain microenvironment with trophic support and by targeting different aggregation forms of Aβ.

Indexed as

Amyloid beta-PeptidesBenzothiazolesCell DifferentiationCell SurvivalCholinergic AgentsElectrophysiologyEmbryonic Stem CellsHumansImmunohistochemistryNerve Growth FactorNeuronsPeptide FragmentsProsencephalonProto-Oncogene Proteins c-aktThiazolesAmyloid beta-Peptidesamyloid beta-protein (1-42)BenzothiazolesCholinergic AgentsNerve Growth FactorPeptide FragmentsProto-Oncogene Proteins c-aktThiazolesthioflavin T

Identifiers

PMID21179413
PMCPMC3003688
OpenAlexW2125991715

What OpenQuestion holds

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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.