Heritability of autism

The heritability of autism is how much of people getting autism is because of their genes. It is also the way that the genes create autism. Autism is mostly genetic, and it has a heritability of 80% to 90%.^[1] Heritability is how much genes can explain who gets autism and who doesn't. The environment can still be very important even with a large heritability. Heritability is estimated by studying twins. Since both twins have autism most of the time, it is more genetic. It is caused by many different genes working together, not just one.^[2]^[3]

References[change | change source]

↑ Sandin, Sven; Lichtenstein, Paul; Kuja-Halkola, Ralf; Hultman, Christina; Larsson, Henrik; Reichenberg, Abraham (2017-09-26). "The Heritability of Autism Spectrum Disorder". JAMA. 318 (12): 1182–1184. doi:10.1001/jama.2017.12141. ISSN 0098-7484. PMC 5818813. PMID 28973605.
↑ Abrahams BS, Geschwind DH (May 2008). "Advances in autism genetics: on the threshold of a new neurobiology". Nature Reviews. Genetics. 9 (5): 341–55. doi:10.1038/nrg2346. PMC 2756414. PMID 18414403.
↑ Weiner, Daniel J.; Wigdor, Emilie M.; Ripke, Stephan; Walters, Raymond K.; Kosmicki, Jack A.; Grove, Jakob; Samocha, Kaitlin E.; Goldstein, Jacqueline I.; Okbay, Aysu; Bybjerg-Grauholm, Jonas; Werge, Thomas; Hougaard, David M.; Taylor, Jacob; Skuse, David; Devlin, Bernie (2017-05-15). "Polygenic transmission disequilibrium confirms that common and rare variation act additively to create risk for autism spectrum disorders". Nature Genetics. 49 (7): 978–985. doi:10.1038/ng.3863. ISSN 1546-1718. PMC 5552240. PMID 28504703. Common polygenic variation, distributed across the genome, accounts for at least 20% of ASD liability. De novo single-nucleotide and copy number variants can have a strong effect on the individuals who carry them but account for less liability at a population level (<10%).

[1] Sandin, Sven; Lichtenstein, Paul; Kuja-Halkola, Ralf; Hultman, Christina; Larsson, Henrik; Reichenberg, Abraham (2017-09-26). "The Heritability of Autism Spectrum Disorder". JAMA. 318 (12): 1182–1184. doi:10.1001/jama.2017.12141. ISSN 0098-7484. PMC 5818813. PMID 28973605.

[2] Abrahams BS, Geschwind DH (May 2008). "Advances in autism genetics: on the threshold of a new neurobiology". Nature Reviews. Genetics. 9 (5): 341–55. doi:10.1038/nrg2346. PMC 2756414. PMID 18414403.

[3] Weiner, Daniel J.; Wigdor, Emilie M.; Ripke, Stephan; Walters, Raymond K.; Kosmicki, Jack A.; Grove, Jakob; Samocha, Kaitlin E.; Goldstein, Jacqueline I.; Okbay, Aysu; Bybjerg-Grauholm, Jonas; Werge, Thomas; Hougaard, David M.; Taylor, Jacob; Skuse, David; Devlin, Bernie (2017-05-15). "Polygenic transmission disequilibrium confirms that common and rare variation act additively to create risk for autism spectrum disorders". Nature Genetics. 49 (7): 978–985. doi:10.1038/ng.3863. ISSN 1546-1718. PMC 5552240. PMID 28504703. Common polygenic variation, distributed across the genome, accounts for at least 20% of ASD liability. De novo single-nucleotide and copy number variants can have a strong effect on the individuals who carry them but account for less liability at a population level (<10%).

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