Like detectives trying to solve a murder case, researchers searching for the biological cause of autism have come up with some surprising suspects.
They've found that different genes may be responsible for causing autism in boys than in girls.
In addition, the researchers also have discovered that other genes may play a role in the early onset form of the developmental disorder and in the recently verified regression, or late onset, type of autism, according to a new study published today in the online edition of the journal Molecular Genetics.
The study also provides new evidence for the idea that multiple genes contribute to autism, said lead author Gerard Schellenberg, a researcher at the Puget Sound Veterans Affairs Medical Center and a research professor of medicine at the University of Washington. The research team was headed by Schellenberg, Ellen Wijsman, a UW research professor of medical genetics and Geraldine Dawson, director of the UW's Autism Center.
"It is highly unlikely that there is only one gene responsible for autism," said Schellenberg. "There may be four to six major genes and 20 to 30 others that might contribute to autism to a lesser degree.
"If an individual only gets three high-risk variants of these genes, it could mean a less-severe form of autism. And because autism is rarer in females, it may take more risk genes for a female to have autism. There also is the possibility that there might be a biological difference in autism for females versus males," he said.
"What is meaningful is that we have found evidence for two genetic subtypes of autism, male versus female and early versus late onset," added Geraldine Dawson, a professor of psychology. "This is a critical piece of information. With Alzheimer's disease research, one big breakthrough was segregating the late and early onset forms of the disease, and this led to important genetic discoveries."
Schellenberg said the study came up with "strong support" for an autism gene on chromosome 7 and "less, but still compelling evidence" for genes on chromosomes 3, 4 and 11. These results confirm some data from previous studies, particularly involving chromosome 7.