Evidence map›Paper›PMID 33514010›Full record

ArticleInternational journal of molecular sciences2021

Nuclear Reorganization in Hippocampal Granule Cell Neurons from a Mouse Model of Down Syndrome: Changes in Chromatin Configuration, Nucleoli and Cajal Bodies.

Alba Puente-Bedia, María T Berciano, Olga Tapia, Carmen Martínez-Cué, Miguel Lafarga, Noemí Rueda

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. 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
2.4field-weighted citation impact, top 12% 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. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Epigenetic Regulation in Neurodegeneration Disease.International journal of molecular sciences · 2022
    Article
  12. Nuclear Architecture in the Nervous System.Results and problems in cell differentiation · 2022
    Review
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

6 authors at 2 institutions in 1 country.

Alba Puente-BediaDepartment of Physiology and Pharmacology, Faculty of Medicine, University of Cantabria, 39011 Santander, Spain.
María T BercianoDepartment of Molecular Biology, University of Cantabria-IDIVAL, and "Red sobre Enfermedades Neurodegenerativas (CIBERNED)", 39011 Santander, Spain.
Olga TapiaInstituto de Investigación Sanitaria Valdecilla (IDIVAL), "Red sobre Enfermedades Neurodegenerativas (CIBERNED)" and Universidad Europea del Atlántico, 39011 Santander, Spain.ORCID 0000-0002-0802-7975
Carmen Martínez-CuéDepartment of Physiology and Pharmacology, Faculty of Medicine, University of Cantabria, 39011 Santander, Spain.ORCID 0000-0002-2137-1156
Miguel LafargaDepartment of Anatomy and Cell Biology, University of Cantabria-IDIVAL, and "Red sobre Enfermedades Neurodegenerativas (CIBERNED)", 39011 Santander, Spain.
Noemí RuedaDepartment of Physiology and Pharmacology, Faculty of Medicine, University of Cantabria, 39011 Santander, Spain.
Universidad de Cantabria · ESBiomedical Research Networking Center on Neurodegenerative Diseases · ES

Funding

Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas" Spain (CIBERNED; CB06/05/0037)Instituto de Investigación Valdecilla, Santander, Spain IDIVAL; NVAL 19/23
6 · The paper itself

Abstract

Down syndrome (DS) or trisomy of chromosome 21 (Hsa21) is characterized by impaired hippocampal-dependent learning and memory. These alterations are due to defective neurogenesis and to neuromorphological and functional anomalies of numerous neuronal populations, including hippocampal granular cells (GCs). It has been proposed that the additional gene dose in trisomic cells induces modifications in nuclear compartments and on the chromatin landscape, which could contribute to some DS phenotypes. The Ts65Dn (TS) mouse model of DS carries a triplication of 92 genes orthologous to those found in Hsa21, and shares many phenotypes with DS individuals, including cognitive and neuromorphological alterations. Considering its essential role in hippocampal memory formation, we investigated whether the triplication of this set of Hsa21 orthologous genes in TS mice modifies the nuclear architecture of their GCs. Our results show that the TS mouse presents alterations in the nuclear architecture of its GCs, affecting nuclear compartments involved in transcription and pre-rRNA and pre-mRNA processing. In particular, the GCs of the TS mouse show alterations in the nucleolar fusion pattern and the molecular assembly of Cajal bodies (CBs). Furthermore, hippocampal GCs of TS mice present an epigenetic dysregulation of chromatin that results in an increased heterochromatinization and reduced global transcriptional activity. These nuclear alterations could play an important role in the neuromorphological and/or functional alterations of the hippocampal GCs implicated in the cognitive dysfunction characteristic of TS mice.

Indexed as

AnimalsBrainCell NucleolusChromatinCognitionCoiled BodiesDisease Models, AnimalDown SyndromeHippocampusHumansMemoryMiceMice, TransgenicNeurogenesisNeuronsChromatinCajal bodychromatinDown syndromehippocampusNORsnucleolusTs65Dn

Identifiers

PMID33514010
PMCPMC7865916
OpenAlexW3125109270

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.