The majority of research into the causes of autism has concentrated on the brain. David Ginty, a Professor of Neurobiology at Harvard Medical School and a Howard Hughes Medical Institute researcher, is the first to show that the typical symptoms of autism can be created in mice by the alteration of two genes in the peripheral nerve system.
The Mecp2 and the Gabrb3 genes are known to be associated with autism and are necessary for the proper transmission of nerve impulses from the skin to the brain through the peripheral nervous system. The mutated genes were synthetically introduced into a population of mice. The mice exhibited the typical symptoms of autism including heightened sensitivity to touch stimuli, an inability to distinguish between textures, heightened anxiety, and lowered interest in interacting with others. The discovery is not the entire answer to autism but it is the first to show that the disease is not necessarily centered in the brain.
The researchers liken the effect of the genetic mutations that produce autistic behavior to a volume control on the nerve impulses being left fully open all of the time. The discovery of a cause of autistic behavior external to the brain gives researchers a new target for drug therapy. Genetic modifications of one gene are possible with present technology. Individual gene reconstruction that alters each of the mutated genes that produce sensory overload in autism may mean the end of the symptoms but could not be considered a cure.
