Evidence map›Paper›PMID 28694877›Full record

ReviewJournal of neurodevelopmental disorders2017

Attention deficit hyperactivity disorder (ADHD) in phenotypically similar neurogenetic conditions: Turner syndrome and the RASopathies.

Tamar Green, Paige E Naylor, William Davies

Open access · goldAbstract readReview
In one paragraph

Review in Journal of neurodevelopmental disorders, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 2 pooled it
3.1field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 38 citations in OpenAlex.

  1. Pooled it
  2. Guideline
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Syndrome-Specific Neuroanatomical Phenotypes in Girls With Turner and Noonan Syndromes.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2024
    Article
  13. Article
  14. Neuropsychiatric phenotypes in children with Noonan syndrome.Developmental medicine and child neurology · 2023
    Article
  15. Article
  16. Article
  17. Social behavior in RASopathies and idiopathic autism.Journal of neurodevelopmental disorders · 2022
    Article
  18. Article
  19. Review
  20. 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 at 3 institutions in 2 countries.

Tamar GreenCenter for Interdisciplinary Brain Sciences Research, Stanford University School of Medicine, Stanford, USA.
Paige E NaylorDepartment of Clinical Psychology, Palo Alto University, Palo Alto, CA USA.
William DaviesMedical Research Council Centre for Neuropsychiatric Genetics and Genomics and Division of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK.ORCID 0000-0002-7714-2440
Cardiff University · GBPalo Alto University · USStanford University · US

Funding

Medical Research Council MR/L010305/1
6 · The paper itself

Abstract

backgroundADHD (attention deficit hyperactivity disorder) is a common neurodevelopmental disorder. There has been extensive clinical and basic research in the field of ADHD over the past 20 years, but the mechanisms underlying ADHD risk are multifactorial, complex and heterogeneous and, as yet, are poorly defined. In this review, we argue that one approach to address this challenge is to study well-defined disorders to provide insights into potential biological pathways that may be involved in idiopathic ADHD. MAIN BODY: To address this premise, we selected two neurogenetic conditions that are associated with significantly increased ADHD risk: Turner syndrome and the RASopathies (of which Noonan syndrome and neurofibromatosis type 1 are the best-defined with regard to ADHD-related phenotypes). These syndromes were chosen for two main reasons: first, because intellectual functioning is relatively preserved, and second, because they are strikingly phenotypically similar but are etiologically distinct. We review the cognitive, behavioural, neural and cellular phenotypes associated with these conditions and examine their relevance as a model for idiopathic ADHD.

conclusionWe conclude by discussing current and future opportunities in the clinical and basic research of these conditions, which, in turn, may shed light upon the biological pathways underlying idiopathic ADHD.

Indexed as

Attention deficit hyperactivity disorderNeurofibromatosis type 1Noonan syndromeRASopathiesTurner syndromeX chromosome

Identifiers

PMID28694877
PMCPMC5502326
OpenAlexW2619202372

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.