Mice are certainly not our closest mammalian relatives, yet they have been key in helping enlighten us with respect to the minutiae of our own neurology. Autism is a prime example of one of the most mysterious afflictions that rodents have helped us to better understand. It would seem, at first glance, to be a very uniquely human disorder, but continuing research implies that biological and behavioral patterns observed in modified test mice very closely mirror those of autistic individuals and may ultimately serve to enhance our knowledge of and ability to treat this most perplexing condition.
Researchers have bred and genetically altered mice in order to create approximations of various mental illnesses with surpising success, and the symptomatic similarities between affected humans and their rodent counterparts, united by common genetic mutations, are far too great to ignore. In a recent study performed at Stanford University, researchers developed a new mouse model which will almost certainly provide a greater understanding of autism's biological roots and may, with time, lead to the development of more refined treatments. The study's rodent subjects had been bred to lack Gabrb3, a gene responsible for the design of certain proteins; mutations in the same gene have long been observed in autistic individuals, though the precise origin of these abnormalities remains unknown.
Autism has three defining behaviors: an inability to communicate effectively (most often presenting as a problem forming and interpreting language), difficulty or lack of interest in performing standard social activities, and a tendency toward repetitive physical and linguistic tics. Mice lack the gift of language by our definition, but the remaining symptoms were observed among these "autistic" rodents. The experiments involved placing the mice into a structure with several compartments that they could easily access and then placing other mice in cages located within these tiny "rooms". Researchers compared the behaviors of the modified mice with those of control rodents and found that the differences were nearly identical to those among similar groups of humans.
The control mice behaved exactly as expected, making concerted efforts to communicate with their caged peers, while the affected subjects simply did not seem to feel the same need to socialize. They displayed, more than anything, a muted disinterest in their new cellmates, spending just as much time exploring the far corners of the research space. Like mice in previous related studies, they were just as interested in exploring an empty cage as they were in a cage containing an unfamiliar peer. Among humans, this aloofness is often misinterpreted as avoidant or antisocial behavior. Affected mice in older, similar studies have also had a particularly hard time coupling, forming nests, and engaging in maternal behavior. Autistic humans similarly rarely form long-term relationships or have and raise children. Researchers found even deeper biological similarities, noting that test mice displayed the same abnormally large brains and heads common to ASD individuals.
This study's true significance arises from the possibility that the human brain will react to new treatments in a manner very similar to the rodent brain. Recent experiments in genetic modification allowed for a reversal of autistic symptoms in engineered mice suffering from (the approximation of) a rare developmental disorder called Rett syndrome, which is closely related to autism but often more severe. By using chemical supplements to create a biological on/off switch for this mutation, researchers brought about dramatic reversals in the conditions of these mice, nearly eliminating symptoms altogether. At the present time, these methods are too extreme to be applied to humans. But their potential warrants further experiments in the same mold, and in coming decades we may well witness the development of effective autism treatments that do not amount to genetic engineering. Our interest, to say the least, is piqued.
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