Evidence map›Paper›PMID 28624415›Full record

ArticleNeurobiology of disease2017

Aging rather than aneuploidy affects monoamine neurotransmitters in brain regions of Down syndrome mouse models.

Alain D Dekker, Yannick Vermeiren, Christelle Albac, Eva Lana-Elola, Sheona Watson-Scales, Dorota Gibbins, Tony Aerts, Debby Van Dam, Elizabeth M C Fisher, Victor L J Tybulewicz and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Neurobiology of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Outer Brain Oscillations in Down Syndrome.Frontiers in systems neuroscience · 2019
    Review
  10. Article
  11. Article
  12. 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

12 authors at 5 institutions in 4 countries.

Alain D DekkerDepartment of Neurology and Alzheimer Research Center, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands; Laboratory of Neurochemistry and Behaviour, Institute Born-Bunge, University of Antwerp, Universiteitsplein 1, 2610 Wilrijk, Antwerp, Belgium; Sorbonne Universités, UPMC Université Paris 06, INSERM, CNRS (U75, U1127, U7225) and Institut du Cerveau et de la Moelle Epinière (ICM), Boulevard de l'Hôpital, 75013 Paris, France.
Yannick VermeirenDepartment of Neurology and Alzheimer Research Center, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands; Laboratory of Neurochemistry and Behaviour, Institute Born-Bunge, University of Antwerp, Universiteitsplein 1, 2610 Wilrijk, Antwerp, Belgium.
Christelle AlbacSorbonne Universités, UPMC Université Paris 06, INSERM, CNRS (U75, U1127, U7225) and Institut du Cerveau et de la Moelle Epinière (ICM), Boulevard de l'Hôpital, 75013 Paris, France.
Eva Lana-ElolaThe Francis Crick Institute, Midland Road, London NW1 1AT, United Kingdom.
Sheona Watson-ScalesThe Francis Crick Institute, Midland Road, London NW1 1AT, United Kingdom.
Dorota GibbinsThe Francis Crick Institute, Midland Road, London NW1 1AT, United Kingdom.
Tony AertsLaboratory of Neurochemistry and Behaviour, Institute Born-Bunge, University of Antwerp, Universiteitsplein 1, 2610 Wilrijk, Antwerp, Belgium.
Debby Van DamDepartment of Neurology and Alzheimer Research Center, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands; Laboratory of Neurochemistry and Behaviour, Institute Born-Bunge, University of Antwerp, Universiteitsplein 1, 2610 Wilrijk, Antwerp, Belgium.
Elizabeth M C FisherDepartment of Neurodegenerative Disease, Institute of Neurology, University College London, Queen Square, London WC1N 3BG, United Kingdom.
Victor L J TybulewiczThe Francis Crick Institute, Midland Road, London NW1 1AT, United Kingdom; Department of Medicine, Imperial College London, Du Cane Road, London W12 0NN, United Kingdom.
Marie-Claude PotierSorbonne Universités, UPMC Université Paris 06, INSERM, CNRS (U75, U1127, U7225) and Institut du Cerveau et de la Moelle Epinière (ICM), Boulevard de l'Hôpital, 75013 Paris, France.
Peter P De DeynDepartment of Neurology and Alzheimer Research Center, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands; Laboratory of Neurochemistry and Behaviour, Institute Born-Bunge, University of Antwerp, Universiteitsplein 1, 2610 Wilrijk, Antwerp, Belgium. Electronic address: p.p.de.deyn@umcg.nl.
The Francis Crick Institute · GBCentre National de la Recherche Scientifique · FRUniversity Medical Center Groningen · NLNational Hospital for Neurology and Neurosurgery · GBUniversity of Antwerp · BE

Funding

Alzheimer's Society 192Medical Research Council G0601056Wellcome Trust 098327Wellcome Trust 098328
6 · The paper itself

Abstract

Altered concentrations of monoamine neurotransmitters and metabolites have been repeatedly found in people with Down syndrome (DS, trisomy 21). Because of the limited availability of human post-mortem tissue, DS mouse models are of great interest to study these changes and the underlying neurobiological mechanisms. Although previous studies have shown the potential of Ts65Dn mice - the most widely used mouse model of DS - to model noradrenergic changes, a comprehensive monoaminergic characterization in multiple brain regions has not been performed so far. Here, we used RP-HPLC with electrochemical detection to quantify (nor)adrenergic (NA, adrenaline and MHPG), dopaminergic (DA, HVA and DOPAC), and serotonergic compounds (tryptophan, 5-HT and 5-HIAA) in ten regionally dissected brain regions of Ts65Dn mice, as well as in Dp1Tyb mice - a novel DS mouse model. Comparing young adult aneuploid mice (2.5-5.5months) with their euploid WT littermates did not reveal generalized monoaminergic dysregulation, indicating that the genetic overload in these mice barely affected the absolute concentrations at this age. Moreover, we studied the effect of aging in Ts65Dn mice: comparing aged animals (12-13months) with their younger counterparts revealed a large number of significant changes. In general, the (nor)adrenergic system appeared to be reduced, while serotonergic compounds were increased with aging. Dopaminergic alterations were less consistent. These overall patterns appeared to be relatively similar for Ts65Dn and WT mice, though more observed changes were regarded significant for WT mice. Similar human post-mortem studies are necessary to validate the monoaminergic construct validity of the Ts65Dn and Dp1Typ mouse models.

Indexed as

AgingAneuploidyAnimalsBiogenic MonoaminesBrainChromatography, High Pressure LiquidDisease Models, AnimalDown SyndromeElectrochemical TechniquesMaleMiceMice, Inbred C57BLNeurotransmitter AgentsStatistics, NonparametricBiogenic MonoaminesNeurotransmitter AgentsAgingDopamineDown syndromeDp1TybMonoaminesMouse modelsNoradrenalineRP-HPLCSerotoninTs65Dn

Identifiers

PMID28624415
PMCPMC5536154
OpenAlexW2625246179

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.