{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T15:06:25Z","timestamp":1787497585122,"version":"build-2736575974"},"reference-count":55,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2012,2,22]],"date-time":"2012-02-22T00:00:00Z","timestamp":1329868800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Autism Research"],"published-print":{"date-parts":[[2012,4]]},"abstract":"<jats:p>\n                    Homeobox A1 (\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">HOXA<\/jats:styled-content>\n                      1\n                    <\/jats:italic>\n                    ) has been proposed as a candidate gene for autism spectrum disorder (\n                    <jats:styled-content style=\"fixed-case\">ASD<\/jats:styled-content>\n                    ) as it regulates embryological patterning of hind\u2010brain structures implicated in autism neurobiology. In line with this notion, a nonsynonymous single nucleotide polymorphism within a highly conserved domain of\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">HOXA<\/jats:styled-content>\n                      1\n                    <\/jats:italic>\n                    \u2014\n                    <jats:styled-content style=\"fixed-case\">A218G<\/jats:styled-content>\n                    (rs10951154)\u2014has been linked to both\n                    <jats:styled-content style=\"fixed-case\">ASD<\/jats:styled-content>\n                    risk, and cross\u2010sectional differences in superior posterior lobar cerebellar anatomy in late adulthood. Despite evidence for early onset and developmentally dynamic cerebellar involvement in\n                    <jats:styled-content style=\"fixed-case\">ASD<\/jats:styled-content>\n                    , little is known of the relationship between\n                    <jats:styled-content style=\"fixed-case\">A218G<\/jats:styled-content>\n                    genotype and maturation of the cerebellum over early development. We addressed this issue using 296 longitudinally acquired structural magnetic resonance imaging brain scans from 116 healthy individuals between 5 and 23 years of age. Mixed models were used to compare the relationship between age and semi\u2010automated measures of cerebellar volume in\n                    <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>\n                    \u2010homozygotes (\n                    <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>\n                    ) and carriers of the\n                    <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>\n                    allele (\n                    <jats:styled-content style=\"fixed-case\">Gcar<\/jats:styled-content>\n                    ). Total cerebellar volume increased between ages of 5 and 23 years in both groups. However, this was accelerated in the\n                    <jats:styled-content style=\"fixed-case\">Gcar<\/jats:styled-content>\n                    relative to the\n                    <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>\n                    group (\n                    <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>\n                    enotype\u2010by\u2010age interaction term,\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>\n                    <\/jats:italic>\n                    \u2009=\u20090.03), and driven by genotype\u2010dependent differences in the rate of bilateral superior posterior lobar volume change with age (\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>\n                    <\/jats:italic>\n                    \u2009=\u20090.002). Resultantly, although superior posterior lobar volume did not differ significantly between genotype groups at age 5 (\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>\n                    <\/jats:italic>\n                    \u2009=\u20090.9), by age 23 it was 12% greater in\n                    <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>\n                    car than\n                    <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>\n                    (\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>\n                    <\/jats:italic>\n                    \u2009=\u20090.002). Our results suggest that common genetic variation within this putative\n                    <jats:styled-content style=\"fixed-case\">ASD<\/jats:styled-content>\n                    risk gene has the capacity to modify the development of cerebellar systems implicated in\n                    <jats:styled-content style=\"fixed-case\">ASD<\/jats:styled-content>\n                    neurobiology.\n                  <\/jats:p>","DOI":"10.1002\/aur.238","type":"journal-article","created":{"date-parts":[[2012,2,22]],"date-time":"2012-02-22T21:14:49Z","timestamp":1329945289000},"page":"93-100","source":"Crossref","is-referenced-by-count":10,"title":["Allelic Variation Within the Putative Autism Spectrum Disorder Risk Gene\n                    <scp>H<\/scp>\n                    omeobox\n                    <scp>A<\/scp>\n                    1 and Cerebellar Maturation in Typically Developing Children and Adolescents"],"prefix":"10.1002","volume":"5","author":[{"given":"Armin","family":"Raznahan","sequence":"first","affiliation":[{"name":"Child Psychiatry Branch National Institute of Mental Health, National Institutes of Health  Bethesda MD USA"},{"name":"Child Psychiatry Department King's College London, Institute of Psychiatry  London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yohan","family":"Lee","sequence":"additional","affiliation":[{"name":"Child Psychiatry Branch National Institute of Mental Health, National Institutes of Health  Bethesda MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catherine","family":"Vaituzis","sequence":"additional","affiliation":[{"name":"Child Psychiatry Branch National Institute of Mental Health, National Institutes of Health  Bethesda MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lan","family":"Tran","sequence":"additional","affiliation":[{"name":"Child Psychiatry Branch National Institute of Mental Health, National Institutes of Health  Bethesda MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susan","family":"Mackie","sequence":"additional","affiliation":[{"name":"Child Psychiatry Branch National Institute of Mental Health, National Institutes of Health  Bethesda MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henning","family":"Tiemeier","sequence":"additional","affiliation":[{"name":"Child Psychiatry Branch National Institute of Mental Health, National Institutes of Health  Bethesda MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liv","family":"Clasen","sequence":"additional","affiliation":[{"name":"Child Psychiatry Branch National Institute of Mental Health, National Institutes of Health  Bethesda MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francois","family":"Lalonde","sequence":"additional","affiliation":[{"name":"Child Psychiatry Branch National 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