Caring for an individual with autism involves many unique considerations, such as managing a special diet and accommodating a range of behavioral difficulties. In order to determine the best way to treat people diagnosed with this condition, scientists are constantly working to determine the root causes of these specific symptoms.
On August 10, the peer-reviewed open-access scientific journal PLoS One published findings from a UC Davis study regarding this element of autism. ScienceDaily reports that researchers at the university's MIND institute have zeroed in on how the function of one specific gene may cause an individual to show anti-social characteristics on par with an autistic person's behavior.
The study was led by Professor Cecilia Giulivi, who specializes in molecular biosciences in the School of Veterinary Medicine and also works with the MIND institute. The source reports that Giulivi and her team focused on a gene that has already been found to function incorrectly in autistic children. While Giulivi acknowledges that many factors influence the onset of autism, she believed that a targeted investigation could help determine how to address its behavioral effects in the future.
"This study points to a mechanism – how one gene defect may trigger this type of neurological behavior," she explains. "Once you understand the mechanism, that opens the way for developing drugs to treat the condition."
The study involved manipulating a gene in the brains of lab mice so that it did not release the correct amount of protein. That deficiency ultimately prevented the neurons from using energy correctly. After between 20 and 30 weeks, this reportedly led the affected mice to withdraw from other subjects and also engage in repetitive actions. This led researchers to conclude that this genetic disruption could be responsible for similar behavior in autism patients.
Targeted medication based on these findings, paired with a consideration for autism nutrition, may lead to great strides in the treatment of this condition.