More neurexin would in turn not only enhance the presence of nicotinic acetylcholine receptors, but also a host of other proteins that are important for the proper formation and maturation of synapses. Proper synapse function is critical to the nervous system's ability to connect to and control other systems of the body.
"Now that these associations have been made, we believe that nicotine in smokers' brains possibly increases the level of neurexin-1 and, as a consequence, helps bring more receptors to the synapses and makes those circuits highly efficient, reinforcing the addiction. In autism, we have the opposite problem. We have a lack of these receptors, and we speculate that neurexin levels are lower," he said.
Anand presented the research Monday (11/17) at the Society for Neuroscience meeting in Washington, D.C.
Autism symptoms include impaired social interaction, problems with verbal and nonverbal communication, and repetitive or severely limited activities and interests. An estimated three to six of every 1,000 children are diagnosed with autism, and boys are four times more likely than girls to have the disorder, according to the National Institute of Neurological Disorders and Stroke.
Anand and colleagues were studying drug abuse and addiction when they discovered the neurexin-1 beta protein's relationship to a certain type of nicotinic receptor. The timing of the discovery was key, as it built upon two other research groups' previous observations: The brains of people with autism and other neurological disorders that were examined after their death showed a 60-percent to 70-percent decrease in specific nicotinic receptors, and some patients with autism have mutations in the neurexin-1 gene that suggest the gene's improper functions could play a role in the disorder.
"These have all been 'association studies.' None has been able to prove what causes autism," Anand said. "And then we accidentally discovered t
|Contact: Rene Anand|
Ohio State University