Evidence map›Paper›PMID 34571966›Full record

ReviewCells2021

Genomic Aberrations Associated with the Pathophysiological Mechanisms of Neurodevelopmental Disorders.

Toshiyuki Yamamoto

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. 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
1.6field-weighted citation impact, top 16% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Trial
  2. mRNA Isoforms and Variants in Health and Disease.International journal of molecular sciences · 2025
    Review
  3. Review
  4. Prenatal diagnosis of aFrontiers in genetics · 2025
    Article
  5. Article
  6. Article
  7. 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

1 author at 1 institution in 1 country.

Toshiyuki YamamotoInstitute of Medical Genetics, Tokyo Women's Medical University, Tokyo 162-8666, Japan.ORCID 0000-0002-9484-3505
Tokyo Women's Medical University · JP

Funding

Japan Society for the Promotion of Science JSPS KAKENHI JP18K07803
6 · The paper itself

Abstract

Genomic studies are increasingly revealing that neurodevelopmental disorders are caused by underlying genomic alterations. Chromosomal microarray testing has been used to reliably detect minute changes in genomic copy numbers. The genes located in the aberrated regions identified in patients with neurodevelopmental disorders may be associated with the phenotypic features. In such cases, haploinsufficiency is considered to be the mechanism, when the deletion of a gene is related to neurodevelopmental delay. The loss-of-function mutation in such genes may be evaluated using next-generation sequencing. On the other hand, the patients with increased copy numbers of the genes may exhibit different clinical symptoms compared to those with loss-of-function mutation in the genes. In such cases, the additional copies of the genes are considered to have a dominant negative effect, inducing cell stress. In other cases, not the copy number changes, but mutations of the genes are responsible for causing the clinical symptoms. This can be explained by the dominant negative effects of the gene mutations. Currently, the diagnostic yield of genomic alterations using comprehensive analysis is less than 50%, indicating the existence of more subtle alterations or genomic changes in the untranslated regions. Copy-neutral inversions and insertions may be related. Hence, better analytical algorithms specialized for the detection of such alterations are required for higher diagnostic yields.

Indexed as

Child DevelopmentChromosome AberrationsChromosomes, HumanGenetic VariationAge FactorsAnimalsChildChild, PreschoolDNA Copy Number VariationsGene DosageGenetic Predisposition to DiseaseGenetic TestingHaploinsufficiencyHumansInfantLoss of Function Mutationclassical microdeletion syndromecontiguous gene deletion syndromediagnostic yieldexome sequencinggenome diseasenonallelic homologous recombination (NAHR)

Identifiers

PMID34571966
PMCPMC8470284
OpenAlexW3197748668

What OpenQuestion holds

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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.