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Elise B. Robinson

Researcher at Broad Institute

Publications -  98
Citations -  14888

Elise B. Robinson is an academic researcher from Broad Institute. The author has contributed to research in topics: Autism & Population. The author has an hindex of 40, co-authored 80 publications receiving 10786 citations. Previous affiliations of Elise B. Robinson include Boston Children's Hospital & Harvard University.

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Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder

Ditte Demontis, +126 more
- 01 Jan 2019 - 
TL;DR: A genome-wide association meta-analysis of 20,183 individuals diagnosed with ADHD and 35,191 controls identifies variants surpassing genome- wide significance in 12 independent loci and implicates neurodevelopmental pathways and conserved regions of the genome as being involved in underlying ADHD biology.
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Analysis of shared heritability in common disorders of the brain

Verneri Anttila, +720 more
- 22 Jun 2018 - 
TL;DR: It is demonstrated that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine, and it is shown that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures.
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Insights into Autism Spectrum Disorder Genomic Architecture and Biology from 71 Risk Loci.

TL;DR: Analysis of de novo CNVs from the full Simons Simplex Collection replicates prior findings of strong association with autism spectrum disorders (ASDs) and confirms six risk loci, including 6 CNV regions.
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Large-Scale Exome Sequencing Study Implicates Both Developmental and Functional Changes in the Neurobiology of Autism

F. Kyle Satterstrom, +201 more
- 06 Feb 2020 - 
TL;DR: The largest exome sequencing study of autism spectrum disorder (ASD) to date, using an enhanced analytical framework to integrate de novo and case-control rare variation, identifies 102 risk genes at a false discovery rate of 0.1 or less, consistent with multiple paths to an excitatory-inhibitory imbalance underlying ASD.