Evidence map›Paper›PMID 17415598›Full record

ArticleNeurogenetics2007

Evaluation of autism traits in Angelman syndrome: a resource to unfold autism genes.

Maria Teresa Bonati, Silvia Russo, Palma Finelli, Maria Rosa Valsecchi, Francesca Cogliati, Florinda Cavalleri, Wendy Roberts, Maurizio Elia, Lidia Larizza

Abstract read
PubMed Publisher
In one paragraph

Article in Neurogenetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 2 pooled it
3.1field-weighted citation impact, top 8% 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

40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 98 citations in OpenAlex.

  1. Meta-Analysis of BDNF Levels in Autism.Cellular and molecular neurobiology · 2017
    Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Remote EEG acquisition in Angelman syndrome using PANDABox-EEG.Journal of neurodevelopmental disorders · 2025
    Article
  7. Age-Related Trajectories of Autistic Traits in Children With Angelman Syndrome.Autism research : official journal of the International Society for Autism Research · 2025
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
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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

9 authors at 4 institutions in 2 countries.

Maria Teresa BonatiClinic of Medical Genetics, IRCCS Istituto Auxologico Italiano, Milan, Italy. mt.bonati@auxologico.it
Silvia Russo
Palma Finelli
Maria Rosa Valsecchi
Francesca Cogliati
Florinda Cavalleri
Wendy Roberts
Maurizio Elia
Lidia Larizza
IRCCS Istituto Auxologico Italiano · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITOasi Maria SS · ITSickKids Foundation · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Linkage and cytogenetics studies have found the Angelman syndrome (AS) chromosomal region to be of relevance to autism disorder (AD) or autism spectrum disorder (ASD). Autism is considered part of the behavioural phenotype in AS based on formal autism assessments (autism diagnostic interview-revised [ADI-R] and autism diagnostic observation schedule [ADOS]), which have mainly addressed the deleted AS group. We explored 23 AS patients including all genetic subtypes and made a co-morbid diagnosis of AD/ASD in 14/23 (61%), which does not include 4 cases classified within the broader autism spectrum disorder (bASD). Deletions accounted for the main fraction (35%), ubiquitin-protein ligase E3A (UBE3A) mutation represented 13%, imprinting defects and uniparental disomy 9 and 4%, respectively. UBE3A mutations due to lack of the homologous to the E6-associated protein carboxyl terminus domain (n = 3) were associated with the ASD, while more distal mutations (n = 3) seem to escape from a co-morbid diagnosis of autism/autism spectrum. Differences in severity of autistic features were seen across subtypes of AS, with some behavioural features being unique to AS and some representing all forms of developmental disability. Autism signs (poor/lack of eye contact, showing, spontaneous initiation of joint attention, social quality of overtures [ADOS algorithm items for Diagnostic and Statistical Manual of Mental Disorders-IV (DSM-IV)/International Statistical Classification of Diseases and Related Health Problems-10 (ICD-10) autism diagnosis belonging to the reciprocal social interaction domain]) discriminating all the co-morbid AS categories from non-autistic AS belonged to the social interaction domain. Impairments in the communication domain (gestures, pointing, use of another's body, frequency of vocalisation towards others [ADOS algorithm items for DSM-IV/ICD-10 autism diagnosis belonging to the communication domain]) justified classification of co-morbid AD/ASD vs the classification of less affected bASD. Evaluation of the behaviour domain suggested that repetitive sensory and motor behaviours correlate with a low developmental profile rather than being specific to autism.

Indexed as

Angelman SyndromeAutistic DisorderChildDevelopmental DisabilitiesFemaleHumansMaleMutationPhenotypeSequence DeletionUbiquitin-Protein LigasesUBE3A protein, humanUbiquitin-Protein Ligases

Identifiers

PMID17415598
OpenAlexW2013013633

What OpenQuestion holds

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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.