Evidence map›Paper›PMID 31683073›Full record

ReviewPlacenta2020

Placental development and function in trisomy 21 and mouse models of Down syndrome: Clues for studying mechanisms underlying atypical development.

April D Adams, Faycal Guedj, Diana W Bianchi

Open access · greenAbstract readReview
In one paragraph

Review in Placenta, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Investigating the Origins of Biochemical Dysregulation in Trisomy 21 Pregnancy.The Journal of clinical endocrinology and metabolism · 2025
    Article
  4. Article
  5. A head start: The relationship of placental factors to craniofacial and brain development.Developmental dynamics : an official publication of the American Association of Anatomists · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Impact of fetal trisomy 21 on umbilical artery Doppler indices.The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2022
    Article
  10. Article
  11. Down syndrome and type I interferon: not so simple.Current opinion in immunology · 2021
    Review
  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

3 authors at 2 institutions in 1 country.

April D AdamsMedical Genetics Branch (Prenatal Genomics and Therapy Section), National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA. Electronic address: adams.aprild@gmail.com.
Faycal GuedjMedical Genetics Branch (Prenatal Genomics and Therapy Section), National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.
Diana W BianchiMedical Genetics Branch (Prenatal Genomics and Therapy Section), National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA; Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
National Human Genome Research Institute · USNational Institutes of Health · US

Funding

Prenatal Treatment of Down Syndrome to Improve Brain Development and NeurocognitionZIAHG200399 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI BIANCHI, DIANA · 2017 to 2025
$11.1M
Intramural NIH HHS ZIA HG200399
6 · The paper itself

Abstract

Down syndrome (DS) is the most common genetic disorder leading to developmental disability. The phenotypes associated with DS are complex and vary between affected individuals. Placental abnormalities in DS include differences in cytotrophoblast fusion that affect subsequent conversion to syncytiotrophoblast, atypical oxidative stress/antioxidant balance, and increased expression of genes that are also upregulated in the brains of individuals with Alzheimer's disease. Placentas in DS are prematurely senescent, showing atypical evidence of mineralization. Fetuses with DS are especially susceptible to adverse obstetric outcomes, including early in utero demise, stillbirth and growth restriction, all of which are related to placental function. The placenta, therefore, may provide key insights towards understanding the phenotypic variability observed in individuals with DS and aid in identifying biomarkers that can be used to evaluate phenotypic severity and prenatal treatments in real time. To address these issues, many different mouse models of DS have been generated to identify the mechanisms underlying developmental changes in many organ systems. Little is known, however, regarding placental development in the currently available mouse models of DS. Based upon the relative paucity of data on placental development in preclinical mouse models of DS, we recommend that future evaluation of new and existing models routinely include histologic and functional assessments of the placenta. In this paper we summarize studies performed in the placentas of both humans and mouse models with DS, highlighting gaps in knowledge and suggesting directions for future research.

Indexed as

AnimalsDisease Models, AnimalDown SyndromeFemaleMiceOxidative StressPlacentaPlacentationPregnancyBiomarkersDown syndromeMouse modelsPlacentaTrisomy 21

Identifiers

PMID31683073
PMCPMC10040210
OpenAlexW2977985081

What OpenQuestion holds

Textmetadata
LicenceTDM
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.