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

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 delet...

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Detalles Bibliográficos
Autores principales: Mitchell, Emma J., Thomson, David M., Openshaw, Rebecca L., Bristow, Greg C., Dawson, Neil, Pratt, Judith A., Morris, Brian J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7378168/
https://www.ncbi.nlm.nih.gov/pubmed/32704009
http://dx.doi.org/10.1038/s41598-020-69130-8

Internet

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7378168/
https://www.ncbi.nlm.nih.gov/pubmed/32704009
http://dx.doi.org/10.1038/s41598-020-69130-8

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