Primal Health Databank: Study
| Entry No: | 0774 |
| Title: | beta2-adrenergic receptor activation and genetic polymorphisms in autism: data from dizygotic twins |
| Author(s): | Connors SL, Crowell DE, Eberhart CG, et al. |
| Reference: | J Child Neurol. 2005 Nov;20(11):876-84 |
| Place of Study: | USA |
| Abstract: | The authors investigated the effects of prenatal overstimulation of the beta2-adrenergic receptor in dizygotic twins who were exposed to terbutaline, a selective beta2-adrenergic receptor agonist used to treat premature labor, as a gestational factor. As a possible genetic mechanism, we studied two beta2-adrenergic receptor polymorphisms in twins from whom DNA was available: glycine substitution at codon 16 (16G) and glutamic acid substitution at codon 27 (27E), which show diminished desensitization in vivo compared with the wild-type receptor. Continuous terbutaline exposure for 2 weeks or longer was associated with increased concordance for autism spectrum disorders in dizygotic twins (relative risk = 2.0), with a further increase in the risk for male twins with no other affected siblings (relative risk = 4.4). A significant association was found between the presence of 16G and 27E polymorphisms in autistic patients compared with population controls (P = .006). Prenatal overstimulation of the beta2-adrenergic receptor by terbutaline or by increased signaling of genetic polymorphisms of the beta2-adrenergic receptor that have diminished desensitization can affect cellular responses and developmental programs in the fetal brain, leading to autism. |
| Keyword(s): | autism, autistic spectrum disorder, betamimetic drug, forceps delivery, jaundice, psychopathologic problem |
| Discussion: | No discussion mentioned for this entry |
| See Also: | No related entries mentioned for this entry |
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