Converging evidence for brain stem injury in autism.
The hypothesis that brain stem injury plays a role in the autism spectrum disorders was suggested by evidence that exposure to thalidomide during the earliest stages of brain development increases the risk of autism spectrum disorders. The implications for the embryological origin of autism first led to studies of neuroanatomy in a human case and an animal model and then to examinations of minor craniofacial features in autism. But the general hypothesis had much broader implications. It has now generated studies of the behavioral and neurological symptoms of human patients, of human molecular genetics and population genetics, and of animal behavioral teratology and molecular pharmacology. The collection of this range of data was made possible by adding experts from many fields to the research team. They worked both independently and collaboratively to try to unravel the etiology of autism.
D001321:Autistic Disorder / Q000235:genetics / Q000503:physiopathology*; D001933:Brain Stem / Q000187:drug effects* / Q000503:physiopathology*; D002648:Child; D020022:Genetic Predisposition to Disease; D018398:Homeodomain Proteins / Q000235:genetics; D006801:Humans; D006993:Hypnotics and Sedatives / Q000009:adverse effects*; D008967:Molecular Biology / Q000379:methods; D016133:Polymerase Chain Reaction; D013792:Thalidomide / Q000009:adverse effects*; D014157:Transcription Factors / Q000235:genetics; D000099261:Homeobox A1 Protein
D018398:Homeodomain Proteins; D006993:Hypnotics and Sedatives; D013792:Thalidomide; D014157:Transcription Factors; D000099261:Homeobox A1 Protein