Jan. 26 (UPI) -- A new study from the University of Philadelphia used a tuberculosis drug in autism mouse models resulting in improved social deficits in the mice.
Researchers found that reducing the function of the gene Pcdh10 led to impairments in social behavior and disrupted the structure and function of circuitry in the amygdala, a region of the brain responsible for behavioral symptoms of the autism spectrum disorder, or ASD.
The study found that neurons in the amygdala of mice lacked one copy of Pcdh10 and had reduced levels of NMDA glutamate receptor subunits resulting in disrupted excitatory neural circuitry.
"Our study of Pcdh10+/- mice gives us greater insight into the biology of social behaviors and into the function of a gene associated with ASD," Professor Edward Brodkin of the University of Pennsylvania and senior author of the study, said in a press release.
Researchers gave the mice d-cycloserine, an older medication commonly used to treat tuberculosis, and saw improvements in impaired social behavior. D-cycloserine targets the NMDA receptor enhancing its function.
The function of Pcdh10 was more prominent in male mice than female mice and follows the male predominance of ASD in humans.
The study was published in Biological Psychiatry.
"This study is an example of a principle that we will hold for more psychiatric conditions," John Krystal, editor of Biological Psychiatry. "That hypothesis is that when psychiatric syndromes can be targeted to specific genes, then specific treatments may be implicated."
