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Christopher A. Walsh

Researcher at Howard Hughes Medical Institute

Publications -  470
Citations -  62520

Christopher A. Walsh is an academic researcher from Howard Hughes Medical Institute. The author has contributed to research in topics: Cerebral cortex & Microcephaly. The author has an hindex of 123, co-authored 455 publications receiving 55874 citations. Previous affiliations of Christopher A. Walsh include University of Liverpool & Newcastle University.

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Multiple Recurrent De Novo CNVs, Including Duplications of the 7q11.23 Williams Syndrome Region, Are Strongly Associated with Autism

Stephen Sanders, +66 more
- 09 Jun 2011 - 
TL;DR: A genome-wide analysis of rare copy-number variation in 1124 autism spectrum disorder families, each comprised of a single proband, unaffected parents, and, in most kindreds, an unaffected sibling, finds significant association of ASD with de novo duplications of 7q11.23, where the reciprocal deletion causes Williams-Beuren syndrome.
Journal ArticleDOI

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.
Journal ArticleDOI

Directed migration of neural stem cells to sites of CNS injury by the stromal cell-derived factor 1α/CXC chemokine receptor 4 pathway

TL;DR: The data implicate SDF-1α/CXCR4, representative of the inflammatory milieu characterizing many pathologies, as a pathway that activates NSC molecular programs during injury and suggest that inflammation may be viewed not simply as playing an adverse role but also as providing stimuli that recruit cells with a regenerative homeostasis-promoting capacity.