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Article

Drug-responsive autism phenotypes in the 16p11.2 deletion mouse model: a central role for gene-environment interactions.

Scientific reports - 23 Jul 2020

Mitchell Emma J, Thomson David M, Openshaw Rebecca L, Bristow Greg C, Dawson Neil, Pratt Judith A, Morris Brian J

Abstract excerpt

There are no current treatments for autism, despite its high prevalence. Deletions of chromosome 16p11.2 dramatically increase risk for autism, suggesting that mice with an equivalent genetic rearrangement may offer a valuable model for the testing of novel classes of therapeutic drug. 16p11.2 deletion (16p11.2 DEL) mice and wild-type controls were assessed using an ethological approach, with 24 h monitoring of...

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Identifiers

PMID: 32704009
DOI: 10.1038/s41598-020-69130-8
PMCID: PMC7378168

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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