Evidence map›Paper›PMID 29606902›Full record

ReviewCurrent genomics2018

Behavioral Variability and Somatic Mosaicism: A Cytogenomic Hypothesis.

Svetlana G Vorsanova, Maria A Zelenova, Yuri B Yurov, Ivan Y Iourov

Abstract readReview
In one paragraph

Review in Current genomics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Cytogenomic epileptology.Molecular cytogenetics · 2023
    Review
  2. Somatic mosaicism in the diseased brain.Molecular cytogenetics · 2022
    Review
  3. Svetlana G. Vorsanova (1945-2021).Molecular cytogenetics · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. 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

4 authors.

Svetlana G VorsanovaSeparated Structural Unit "Clinical Research Institute of Pediatrics at Pirogov Russian National Research Medical University named after Y.E Veltishev", Ministry of Health of Russian Federation, Moscow125412, Russian Federation.
Maria A ZelenovaSeparated Structural Unit "Clinical Research Institute of Pediatrics at Pirogov Russian National Research Medical University named after Y.E Veltishev", Ministry of Health of Russian Federation, Moscow125412, Russian Federation.
Yuri B YurovSeparated Structural Unit "Clinical Research Institute of Pediatrics at Pirogov Russian National Research Medical University named after Y.E Veltishev", Ministry of Health of Russian Federation, Moscow125412, Russian Federation.
Ivan Y IourovSeparated Structural Unit "Clinical Research Institute of Pediatrics at Pirogov Russian National Research Medical University named after Y.E Veltishev", Ministry of Health of Russian Federation, Moscow125412, Russian Federation.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Behavioral sciences are inseparably related to genetics. A variety of neurobehavioral phenotypes are suggested to result from genomic variations. However, the contribution of genetic factors to common behavioral disorders (i.e. autism, schizophrenia, intellectual disability) remains to be understood when an attempt to link behavioral variability to a specific genomic change is made. Probably, the least appreciated genetic mechanism of debilitating neurobehavioral disorders is somatic mosaicism or the occurrence of genetically diverse (neuronal) cells in an individual's brain. Somatic mosaicism is assumed to affect directly the brain being associated with specific behavioral patterns. As shown in studies of chromosome abnormalities (syndromes), genetic mosaicism is able to change dynamically the phenotype due to inconsistency of abnormal cell proportions. Here, we hypothesize that brain-specific postzygotic changes of mosaicism levels are able to modulate variability of behavioral phenotypes. More precisely, behavioral phenotype variability in individuals exhibiting somatic mosaicism might correlate with changes in the amount of genetically abnormal cells throughout the lifespan. If proven, the hypothesis can be used as a basis for therapeutic interventions through regulating levels of somatic mosaicism to increase functioning and to improve overall condition of individuals with behavioral problems.

Indexed as

BehaviorBrainChromosomeNeurobehavioral disordersPostzygotic changesSomatic mosaicism

Identifiers

PMID29606902
PMCPMC5850503

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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.