Research conducted on mice has shown that Autism Spectrum Disorders may be partially caused by faulty receptors in the nerves in the skin responsible for touch, a study suggests.
Autism Spectrum Disorders (ASD) are generally thought to be disorders of the brain, often presenting with issues in social communication, along with repetitive behaviour and, in some, problems with the sensory perception. However, new research on mice has shown that the high levels of anxiety and social impairment seen in people with Autism may be – in part – due to disruption of nerves in the skin responsible for sensing touch.
The sensation of touch starts in receptors at the surface of the skin in the peripheral nervous system. Once an item is touched, these receptors send a signal along nerves that connect to the central nervous system – completing the journey at the brain. Autism researchers have focused on the brain, but others have wondered about the first part of the trip and what role – if any – this may play in the formation of autism.
The study, published in Cell, describes how mutations were introduced in the genes associated with autism in mice. The mutations were added in a way that restricted the effects to the cells in the peripheral nervous system, causing the mice to be more sensitive to touch. These changes made a small blow of air on the neck startle the mice in a similar way seen in those with ASD.
“Our behavioural findings are reminiscent of human, non-human primate, and rodent tactile deprivation studies, which showed that early life experiences and developmental tactile stimulation are essential for proper brain development, cognition, and adult social behaviors,” the study says.
One gene, Mecp2, was singled out. This gene’s role is to regulate the connection between nerve cells, and when faulty, the study suggests that an increased perception to touch is the result. Additionally, the mice with the mutation were unable to distinguish between soft and rough textures when compared with a control group. A ‘standard’ mouse would not be keen to play with the rough surface of wood, yet the mutated mice showed no preference for any object or type of surface.
It was also reported that the mutated mice showed “autism-like behaviours” that went beyond sensory issues. The mice without the Mecp2 gene showed increased levels of anxiety, were less sociable, and preferred to be alone – shunning other mice. Tests were performed to examine how anxious the mice appeared to be. Normal mice will explore a new environment, whereas the mutant mice hugged the edges of the area they were introduced, showing heightened levels of anxiety.
In recent years, more focus has been put into the sensory part of the disorder, with the sensory part officially being added to the 2013 American Diagnostic and Statistical Manual of Mental Disorders, fifth version (DSM-V).