Autism. It seems as if everyone knows someone diagnosed with autism in today's society. Living with autism is no walk in the park and is sometimes harder for those surrounding the person, than the actual person diagnosed with autism, because of their behavior. Since mice models for autism began, about ten years ago, researchers have discovered a slew of new information, including genes liked to the disorder. While the ultimate purpose of mouse models is to provide testing grounds for drugs and to understand the molecular underpinnings of autism in the brain, sometimes research needs some regulations in order to reach that goal.
Nature Neuroscience is in the middle of presenting a special on autism titled, "The Autism Enigma." The special includes a variety of topics, blogs, papers, and news on autism to choose from, all of it great information. After reading several articles, one titled "New mouse models of autism highlight need for standardized tests." Williams argues that as more and more models are being made, it is necessary for standardized tests to be created in order to study and compare the effects of the various genetic mutations more clearly "that are collectively providing the field with a window into the brain structure, neuron function and cellular pathways associated with autism, as well as a platform for testing new drugs." Also, similar in most research, people have different ideas of what something is; for example, the paper uses repetitive behavior, for what one person may call repetitive behavior, like the repetitive licking of it's paw, another may not. Therefore standardized testing is required in order to further improve research in mouse models of autism.
Williams' paper also details information on current research being conducted. She reports results from Daniel Geschwind of UCLA, Matthew Anderson of Beth Israel Deaconess Medical Center, Guoping Feng of the Massachusetts Institute of Technology's McGovern Institute for Brain Research, Paul Worley of Johns Hopkins University, Jacqueline Crawley of NIMH, and Alea Mills of the Cold Spring Harbor Laboratory. Geschwind's mouse model had a mutation in CNTNAP2, which has been linked to both a familial epilepsy disorder and autism. This relation between epilepsy and severe autism, I have seen in a family friend so the fact that they are discovering genetic links is very promising. Anderson created a model with duplications in Ube3a, a gene involved in protein degradation which is linked to autism in humans. His mice ignored other mice, avoided new toys, and were abnormally quiet. Feng presented the newest model, showing that deleting Shank3, "which encodes a protein that helps stabilize synapses between neurons, in mice produced the same three core symptoms of autism as seen in people: abnormal social interactions, communication deficits and repetitive behavior." Worley also worked with Shank3, except they deleted only one exon of the Shank3 gene and found similar social problems within the mice's behavior. Crawley and Mills seem to have taken a different approach in which they observe communication and movements in the mice through highly sensitive microphones and video tracking technology. They hope to look at it from a behavioral aspect instead of neurogenetical in order to "take the blinders off" and view every aspect of the mouse.