Evidence map›Paper›PMID 27383650›Full record

ArticleScientific reports2016

Amyloid precursor protein expression and processing are differentially regulated during cortical neuron differentiation.

Petra Bergström, Lotta Agholme, Faisal Hayat Nazir, Tugce Munise Satir, Jamie Toombs, Henrietta Wellington, Joakim Strandberg, Thomas Olsson Bontell, Hlin Kvartsberg, Maria Holmström and 9 more

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

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
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  11. The Amyloid Precursor Protein Regulates Synaptic Transmission at Medial Perforant Path Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  12. Article
  13. Review
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  15. Article
  16. Review
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  18. Review
  19. Role of Aβ in Alzheimer's-related synaptic dysfunction.Frontiers in cell and developmental biology · 2022
    Review
  20. 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

19 authors at 4 institutions in 2 countries.

Petra BergströmInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, S-405 30, Gothenburg, Sweden.
Lotta AgholmeInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, S-405 30, Gothenburg, Sweden.
Faisal Hayat NazirInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, S-405 30, Gothenburg, Sweden.
Tugce Munise SatirInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, S-405 30, Gothenburg, Sweden.
Jamie ToombsUCL Institute of Neurology, Department of Molecular Neuroscience, University College London, Queen Square, London, WC1N 3BG, UK.
Henrietta WellingtonUCL Institute of Neurology, Department of Molecular Neuroscience, University College London, Queen Square, London, WC1N 3BG, UK.
Joakim StrandbergInstitute of Neuroscience and Physiology, Department of Physiology, The Sahlgrenska Academy at the University of Gothenburg, S-405 30, Gothenburg, Sweden.
Thomas Olsson BontellInstitute of Neuroscience and Physiology, Department of Physiology, The Sahlgrenska Academy at the University of Gothenburg, S-405 30, Gothenburg, Sweden.
Hlin KvartsbergInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, S-431 80, Mölndal, Sweden.
Maria HolmströmInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, S-405 30, Gothenburg, Sweden.
Cecilia BoreströmInstitute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine, The Sahlgrenska Academy at the University of Gothenburg, S-405 30, Gothenburg, Sweden.
Stina SimonssonInstitute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine, The Sahlgrenska Academy at the University of Gothenburg, S-405 30, Gothenburg, Sweden.
Tilo KunathMRC Centre for Regenerative Medicine, School of Biological Sciences, University of Edinburgh, Edinburgh, EH16 4UU, UK.
Anders LindahlInstitute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine, The Sahlgrenska Academy at the University of Gothenburg, S-405 30, Gothenburg, Sweden.
Kaj BlennowInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, S-431 80, Mölndal, Sweden.
Eric HanseInstitute of Neuroscience and Physiology, Department of Physiology, The Sahlgrenska Academy at the University of Gothenburg, S-405 30, Gothenburg, Sweden.
Erik PorteliusInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, S-431 80, Mölndal, Sweden.
Selina WrayUCL Institute of Neurology, Department of Molecular Neuroscience, University College London, Queen Square, London, WC1N 3BG, UK.
Henrik ZetterbergUCL Institute of Neurology, Department of Molecular Neuroscience, University College London, Queen Square, London, WC1N 3BG, UK.
University of Gothenburg · SEUniversity College London · GBNational Hospital for Neurology and Neurosurgery · GBUniversity of Edinburgh · GB

Funding

Medical Research Council MR/J012831/1Parkinson's UK F-0902Parkinson's UK K-1205
6 · The paper itself

Abstract

Amyloid precursor protein (APP) and its cleavage product amyloid β (Aβ) have been thoroughly studied in Alzheimer's disease. However, APP also appears to be important for neuronal development. Differentiation of induced pluripotent stem cells (iPSCs) towards cortical neurons enables in vitro mechanistic studies on human neuronal development. Here, we investigated expression and proteolytic processing of APP during differentiation of human iPSCs towards cortical neurons over a 100-day period. APP expression remained stable during neuronal differentiation, whereas APP processing changed. α-Cleaved soluble APP (sAPPα) was secreted early during differentiation, from neuronal progenitors, while β-cleaved soluble APP (sAPPβ) was first secreted after deep-layer neurons had formed. Short Aβ peptides, including Aβ1-15/16, peaked during the progenitor stage, while processing shifted towards longer peptides, such as Aβ1-40/42, when post-mitotic neurons appeared. This indicates that APP processing is regulated throughout differentiation of cortical neurons and that amyloidogenic APP processing, as reflected by Aβ1-40/42, is associated with mature neuronal phenotypes.

Indexed as

Cell DifferentiationProtein Processing, Post-TranslationalAction PotentialsAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesCerebral CortexGene Expression RegulationHumansInduced Pluripotent Stem CellsNeuronsPeptide FragmentsRNA, MessengerSolubilityAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesPeptide FragmentsRNA, Messenger

Identifiers

PMID27383650
PMCPMC4935877
OpenAlexW2472933772

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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.