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Elise Ng-Cordell

Researcher at Cognition and Brain Sciences Unit

Publications -  17
Citations -  137

Elise Ng-Cordell is an academic researcher from Cognition and Brain Sciences Unit. The author has contributed to research in topics: Autism & Intellectual disability. The author has an hindex of 4, co-authored 11 publications receiving 51 citations. Previous affiliations of Elise Ng-Cordell include Durham University & University of British Columbia.

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The neurodevelopmental spectrum of synaptic vesicle cycling disorders.

TL;DR: Understanding the common cellular and systems mechanisms underlying neurodevelopmental phenotypes in SVC disorders, and the factors responsible for variation in clinical presentations and outcomes, may translate to personalized clinical management and improved quality of life for patients and families.
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Childhood intellectual disability and parents' mental health: integrating social, psychological and genetic influences.

TL;DR: The mental health of parents caring for a child with intellectual disability is influenced by child and family factors, converging on parental appraisal of impact, found that genetic aetiologies, broadly categorised, also influence impact and thereby family risks.
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STXBP1 -associated neurodevelopmental disorder: a comparative study of behavioural characteristics

TL;DR: De novo mutations in STXBP1 are associated with complex and variable neurodevelopmental impairments, which are severe language impairment and difficulties managing social interactions, despite strong social motivation.
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Anxiety in Williams Syndrome: The Role of Social Behaviour, Executive Functions and Change over Time.

TL;DR: Investigation of parent-reports of anxiety in Williams syndrome indicated that high anxiety persisted over time, and anxiety was related to impairments in both social and executive functioning.
Posted ContentDOI

Saturation genome editing of DDX3X clarifies pathogenicity of germline and somatic variation

TL;DR: A machine learning classifier is trained to identify functionally abnormal variants of NDD-relevance, which could account for almost all of the excess nonsynonymous DDX3X somatic mutations seen in DDx3X-driven cancers.