Animal model of autism

One of the more common rodent models is the Norway rat (Rattus norvegicus).[3] More recent research has used the house mouse (Mus musculus) to model autism because it is a social species. Other strains of mice used include mu opioid receptor knockout mice, as well as Fmr1 knockout mice; the latter are also used as animal models of Fragile X syndrome.[4]

The Norway rat has been used, for example, by Mady Hornig to implicate thiomersal in autism.[5][6] The current scientific consensus is that no convincing scientific evidence supports these claims,[7][8] and major scientific and medical bodies such as the Institute of Medicine[7] and World Health Organization[9] (WHO) as well as governmental agencies such as the U.S. Food and Drug Administration[10] (FDA) and Centers for Disease Control and Prevention[11] (CDC) reject any role for thiomersal in autism or other neurodevelopmental disorders.

Behaviors measured in these models include "approach to olfactory pheromones emitted by other mice, approach to familiar and new conspecifics, reciprocal social interactions, ultrasonic vocalizations, communal nesting, sexual and parenting behaviors, territorial scent marking, and aggressive behaviors."[12] Social interaction is measured by how the mouse interacts with a stranger mouse introduced in the opposite side of a test box.[13]

Researchers from the University of Florida have used deer mice to study restricted and repetitive behavior such as compulsive grooming, and how these behaviors may be caused by specific gene mutations.[14] In addition, Craig Powell of the University of Texas Southwestern Medical Center, with a grant from Autism Speaks,[15] is currently using mice to examine the potential role of neuroligin gene mutations in causing autism. Much research has been done into the use of a rat model to show how Borna virus infection,[16][17] exposure to valproic acid in utero,[18] and maternal immune activation[19] may cause autism.

Another goal of the use of rodent models to study autism is to identify the mechanism by which autism develops in humans.[1] Other researchers have developed an autism severity score to measure the degree of severity of the mice's autism, as well as the use of scent marking behavior[20] and vocalization distress[13] as models for communication.

It has been observed that mice lacking the gene for oxytocin exhibit deficits in social interaction, and that it may be possible to develop treatments for autism based on abnormalities in this and other neuropeptides.[21][22]

In 2012, a researcher from the University of Nebraska at Kearney published a study reviewing research that had been done using the songbird as a model for autism spectrum disorders, noting that the neurobiology of vocalization is similar between humans and songbirds, and that, in both species, social learning plays a central role in the development of the ability to vocalize.[23] Other research using this model has been done by Stephanie White at the University of California Los Angeles, who studied mutations in the FOXP2 gene and its potential role in learned vocalization in both songbirds (specifically the zebra finch) and humans.[24][25]

In 2013, a study was published by Swiss researchers which concluded that 91% (31 out of the 34 studies reviewed) of valproic acid-autism studies using animal models suffered from statistical flaws—specifically, they had failed to correctly use the litter as a level of statistical analysis rather than just the individual (i.e., an individual mouse or rat).[26][27]