Evidence map›Paper›PMID 26731442›Full record

ReviewTranslational psychiatry2016

A common molecular signature in ASD gene expression: following Root 66 to autism.

L Diaz-Beltran, F J Esteban, D P Wall

Abstract readReview
In one paragraph

Review in Translational psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 2 pooled it
–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

14 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. PTSD Blood Transcriptome Mega-Analysis: Shared Inflammatory Pathways across Biological Sex and Modes of Trauma.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
    Pooled it
  2. Blood transcriptomic comparison of individuals with and without autism spectrum disorder: A combined-samples mega-analysis.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2017
    Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Coalitional game theory as a promising approach to identify candidate autism genes.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2018
    Article
  12. Article
  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

3 authors.

L Diaz-BeltranDivision of Systems Medicine, Department of Pediatrics, School of Medicine, Stanford University, Stanford, CA, USA.
F J EstebanDepartment of Experimental Biology, Experimental Sciences Faculty, University of Jaen, Jaen, Spain.
D P WallDivision of Systems Medicine, Department of Pediatrics, School of Medicine, Stanford University, Stanford, CA, USA.

Funding

Characterizing the genetic systems of autism through multi-disease analysisR01MH090611 · NIMH · STANFORD UNIVERSITY · PI WALL, DENNIS PAUL · 2010 to 2014
$2.8M
NIMH NIH HHS 1R01MH090611NIMH NIH HHS R01 MH090611
6 · The paper itself

Abstract

Several gene expression experiments on autism spectrum disorders have been conducted using both blood and brain tissue. Individually, these studies have advanced our understanding of the molecular systems involved in the molecular pathology of autism and have formed the bases of ongoing work to build autism biomarkers. In this study, we conducted an integrated systems biology analysis of 9 independent gene expression experiments covering 657 autism, 9 mental retardation and developmental delay and 566 control samples to determine if a common signature exists and to test whether regulatory patterns in the brain relevant to autism can also be detected in blood. We constructed a matrix of differentially expressed genes from these experiments and used a Jaccard coefficient to create a gene-based phylogeny, validated by bootstrap. As expected, experiments and tissue types clustered together with high statistical confidence. However, we discovered a statistically significant subgrouping of 3 blood and 2 brain data sets from 3 different experiments rooted by a highly correlated regulatory pattern of 66 genes. This Root 66 appeared to be non-random and of potential etiologic relevance to autism, given their enriched roles in neurological processes key for normal brain growth and function, learning and memory, neurodegeneration, social behavior and cognition. Our results suggest that there is a detectable autism signature in the blood that may be a molecular echo of autism-related dysregulation in the brain.

Indexed as

Autism Spectrum DisorderBrainGene ExpressionHumans

Identifiers

PMID26731442
PMCPMC5068868

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.