COMMENTARY Translating Preclinical Environmental Enrichment Studies for the Treatment of Autism and Other Brain Disorders: Comment on Woo and Leon (2013) Elisa L. Hill-Yardin and Anthony J. Hannan The University of Melbourne Environmental enrichment (EE) has been shown to induce beneficial effects in mouse models of autism spectrum disorder (ASD), as well as animal models of a variety of other neurological and psychiatric disorders. Investigation of the mechanisms responsible for these changes in animal models will facilitate translation of EE and associated therapies to patient cohorts. In the accompanying article, Woo and Leon demonstrate clinical benefits of sensorimotor enrichment in patients with ASD. We discuss the impli- cations of these findings for future development of therapeutic approaches for ASD and other brain disorders. Keywords: environmental enrichment, Autism Spectrum Disorder, sensory, animal models, treatment Woo and Leon’s (2013, pp. 487– 497) study applies environ- mental enrichment (EE) in the form of increased sensorimotor stimulation to patients and identifies significant improvements in subjects exposed to EE compared with controls. This work is important, as it attempts to directly translate work from animal models to benefit patients with autism spectrum disorder (ASD). The fact that this study shows improvements in cogni- tive performance and autism severity following sensory enrich- ment in this relatively small cohort is promising. Following appropriate follow-up on a larger scale, this EE approach for ASD could be developed for widespread applications. The effective treatment of behavioral aspects of ASD with sensori- motor enrichment holds several lifestyle advantages for indi- vidual patients, in addition to socioeconomic benefits to general communities. Sensory abnormalities are present in the overwhelming majority of ASD patients (Leekam, Nieto, Libby, Wing, & Gould, 2007) and pose significant challenges for these patients and their families (Schaaf, Toth-Cohen, Johnson, Outten, & Benevides, 2011). Such abnormal- ities may present as apparent indifference to pain/heat/cold, adverse response to specific sounds or textures, excessive smelling or touch- ing of objects, and/or fascination with lights or spinning objects. The fact that sensory processing abnormalities are a prominent feature of ASD further reinforces the need for treatment of these symptoms in patients and the potential for impacting other symptoms of ASD by manipulating neural pathways involved in sensory processing. Sen- sory alterations are emerging as an integral component of ASD, and modulation of sensory processing may assist in improving other core behavioral features of ASD, for example, stereotypy (Sidener, Carr, & Firth, 2005). In light of the high prevalence and impact of inappropriate sensory processing in ASD, the implementation of EE paradigms to benefit ASD patients is a logical and positive step. However, there are a number of issues to consider in order for such an approach to be optimized for wider clinical implementation. Pa- tient heterogeneity predicts that individuals with ASD will respond to EE in differing ways. These responses may be due to complex genetics and environmental influences resulting in differing levels of sensory abnormalities or responsiveness of people with ASD at baseline. The study by Woo and Leon (2013) identifies a potential therapy that has several practical advantages for patients and their families. The implementation of an EE protocol that can be conducted by parents (following minimal training) in the home using inexpensive materials has broad applications. For the community, it is clear that there are substantial socioeconomic advantages to undertaking this kind of approach. For families and individuals, timely access to services (including diagnostic evaluation) is a major issue, and per- haps if these treatments are targeted to patients for whom this will be effective, accessibility to other services in general can be improved. The benefits to patients (who, together with sensory issues, often exhibit anxiety disorders) and families in having the ability to carry Elisa L. Hill-Yardin, Enteric Neuroscience Laboratory, Department of Physiology, The University of Melbourne, Parkville, Victoria, Australia; Anthony J. Hannan, Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Victoria, Australia. Elisa L. Hill-Yardin and Anthony J. Hannan are supported by the following awards regarding neural plasticity and Autism Spectrum Disor- der: NHMRC 1047674 (Anthony J. Hannan and Elisa L. Hill-Yardin), NHMRC 1034785, ARC Future Fellowship FT3 (Anthony J. Hannan), and US DoD AR110134 (Elisa L. Hill-Yardin). Correspondence concerning this article should be addressed to Anthony J. Hannan, Florey Institute of Neuroscience and Mental Health, Melbourne Brain Centre, University of Melbourne, at Genetics Lane, Royal Parade, Parkville, Victoria 3010, Australia. E-mail: anthony.hannan@florey.edu.au This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. Behavioral Neuroscience © 2013 American Psychological Association 2013, Vol. 127, No. 4, 606 – 609 0735-7044/13/$12.00 DOI: 10.1037/a0033319 606