Separating primary from secondary changes in the autistic brain has long been a research goal. With knowledge of wide-ranging molecular deficits, identification of the best therapeutic targets becomes a priority. See Letter p.380
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References
Geschwind, D. H. & Levitt, P. Curr. Opin. Neurobiol. 17, 103–111 (2007).
Voineagu, I. et al. Nature 474, 380–384 (2011).
Dennis, G. et al. Genome Biol. 4, P3 (2003).
Langfelder, P. & Horvath, S. BMC Bioinformatics 9, 559 (2008).
Judson, M. C., Eagleson, K. L. & Levitt, P. J. Neurodev. Disord. doi:10.1007/s11689-011-9081-8 (2011).
Garbett, K. et al. Neurobiol. Dis. 30, 303–311 (2008).
Martin, C. L. et al. Am. J. Med. Genet. B 144B, 869–876 (2007).
Wang, K. et al. Nature 459, 528–533 (2009).
Williams, N. M. et al. Lancet 376, 1401–1408 (2010).
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Korade, Ž., Mirnics, K. The autism disconnect. Nature 474, 294–295 (2011). https://doi.org/10.1038/474294a
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DOI: https://doi.org/10.1038/474294a