Evidence map›Paper›PMID 8815899›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1996

Consequences of trisomy 16 for mouse brain development: corticogenesis in a model of Down syndrome.

T F Haydar, M E Blue, M E Molliver, B K Krueger, P J Yarowsky

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.6field-weighted citation impact, top 6% 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

16 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Absence of Prenatal Forebrain Defects in the Dp(16)1Yey/+ Mouse Model of Down Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  9. Review
  10. New Perspectives for the Rescue of Cognitive Disability in Down Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  11. Article
  12. Trisomy 21 and early brain development.Trends in neurosciences · 2012
    Review
  13. Article
  14. Defects in embryonic neurogenesis and initial synapse formation in the forebrain of the Ts65Dn mouse model of Down syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  15. Review
  16. Role of founder cell deficit and delayed neuronogenesis in microencephaly of the trisomy 16 mouse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000
    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

5 authors at 3 institutions in 1 country.

T F HaydarDepartment of Physiology, University of Maryland School of Medicine, Baltimore 21201, USA.
M E Blue
M E Molliver
B K Krueger
P J Yarowsky
Johns Hopkins Medicine · USNeurology, Inc · USUniversity of Maryland, Baltimore · US

Funding

TRAINING PROGRAM IN INTEGRATIVE MEMBRANE BIOLOGYT32GM008181 · NIGMS · UNIVERSITY OF MARYLAND BALTIMORE · PI RIZZO, MEGAN A, TRUDEAU, MATTHEW C · 1987 to 2022
$4.9M
GLIAL/NEURONAL INTERACTIONS IN NEURODENGENERATIONR01AG010686 · NIA · UNIVERSITY OF MARYLAND BALTIMORE · PI KRUEGER, BRUCE K · 1991 to 2000
$91k
ROLE OF EXCITATORY AMINO ACIDS IN CORTEX DEVELOPMENTR29NS029167 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI BLUE, MARY E · 1992 to 1996
–
NIA NIH HHS AG10686NICHD NIH HHS HD20461NIGMS NIH HHS T32 GM008181NINDS NIH HHS NS29167
6 · The paper itself

Abstract

We have studied abnormalities in the tangential and radial expansion of the cerebral cortex during fetal development in the trisomy 16 (Ts16) mouse, a model for human trisomy 21 (Down syndrome). Slowed tangential expansion of the neuroepithelium in Ts16 resulted in a reduction of final telencephalic size and is predicted to decrease the number of radial cortical units in the mature brain. In addition, radial growth of the Ts16 cortex was delayed at the time of peak cortical neurogenesis in normal mice, but by embryonic day 18 the cortex reached normal thickness. Because mouse chromosome 16 shares many genes with human chromosome 21, abnormalities in Ts16 brain development may parallel abnormalities in trisomy 21.

Indexed as

Embryonic and Fetal DevelopmentTrisomyAnimalsBrainCerebral CortexDown SyndromeMiceMice, Inbred C57BL

Identifiers

PMID8815899
PMCPMC6579184
OpenAlexW2097351341

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.