Evidence map›Paper›PMID 30325080›Full record

ArticleBrain pathology (Zurich, Switzerland)2019

Subicular hypotrophy in fetuses with Down syndrome and in the Ts65Dn model of Down syndrome.

Fiorenza Stagni, Andrea Giacomini, Marco Emili, Beatrice Uguagliati, Maria Paola Bonasoni, Renata Bartesaghi, Sandra Guidi

Open access · bronzeAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Development of Molecular Neuropathology in Down Syndrome across the Lifespan.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Transcriptional consequences of trisomy 21 on neural induction.Frontiers in cellular neuroscience · 2024
    Article
  12. Review
  13. Article
  14. 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

7 authors at 2 institutions in 1 country.

Fiorenza StagniDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
Andrea GiacominiDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
Marco EmiliDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
Beatrice UguagliatiDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
Maria Paola BonasoniPathology Unit, Azienda Unità Sanitaria Locale, IRCCS, Reggio Emilia, Italy.
Renata BartesaghiDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.ORCID 0000-0002-1640-0995
Sandra GuidiDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
University of Bologna · ITAzienda Sanitaria Unità Locale di Reggio Emilia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intellectual disability in Down syndrome (DS) has been attributed to neurogenesis impairment during fetal brain development. Consistently with explicit memory alterations observed in children with DS, fetuses with DS exhibit neurogenesis impairment in the hippocampus, a key region involved in memory formation and consolidation. Recent evidence suggests that the subiculum plays a unique role in memory retrieval, a process that is also altered in DS. While much attention has been devoted to the hippocampus, there is a striking lack of information regarding the subiculum of individuals with DS and DS models. In order to fill this gap, in the current study, we examined the subiculum of fetuses with DS and of the Ts65Dn mouse model of DS. We found that in fetuses with DS (gestational week: 17-21), the subiculum had a reduced thickness, a reduced cell density, a reduced density of progenitor cells in the ventricular zone, a reduced percentage of neurons, and an increased percentage of astrocytes and of cells immunopositive for calretinin-a protein expressed by inhibitory interneurons. Similarly to fetuses with DS, the subiculum of neonate Ts65Dn mice was reduced in size, had a reduced number of neurons and a reduced number of proliferating cells. Results suggest that the developmental defects in the subiculum of fetuses with DS may underlie impairment in recall memory and possibly other functions played by the subiculum. The finding that the subiculum of the Ts65Dn mouse exhibits neuroanatomical defects resembling those seen in fetuses with DS further validates the use of this model for preclinical studies.

Indexed as

AnimalsAnimals, NewbornBrainCognitionDisease Models, AnimalDown SyndromeFemaleFetusHippocampusHumansMaleMemoryMiceMice, Inbred C57BLMice, TransgenicNeurogenesiscalretininDown syndromefetusesGFAPNeuNneurogenesissubiculumTs65Dn mouse

Identifiers

PMID30325080
PMCPMC8028278
OpenAlexW2897080667

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.