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Neural Plasticity
Volume 2015, Article ID 972791, 15 pages
Review Article

Zinc in Gut-Brain Interaction in Autism and Neurological Disorders

1Zinpro Corporation, Eden Prairie, MN 55344, USA
2Autismo ABP, 64639 Monterrey, NL, Mexico
3WG Molecular Analysis of Synaptopathies, Neurology Department, Neurocenter of Ulm University, 89081 Ulm, Germany
4Institute for Anatomy and Cell Biology, Ulm University, 89081 Ulm, Germany

Received 2 February 2015; Accepted 5 March 2015

Academic Editor: Richard Dyck

Copyright © 2015 Guillermo Vela et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


A growing amount of research indicates that abnormalities in the gastrointestinal (GI) system during development might be a common factor in multiple neurological disorders and might be responsible for some of the shared comorbidities seen among these diseases. For example, many patients with Autism Spectrum Disorder (ASD) have symptoms associated with GI disorders. Maternal zinc status may be an important factor given the multifaceted effect of zinc on gut development and morphology in the offspring. Zinc status influences and is influenced by multiple factors and an interdependence of prenatal and early life stress, immune system abnormalities, impaired GI functions, and zinc deficiency can be hypothesized. In line with this, systemic inflammatory events and prenatal stress have been reported to increase the risk for ASD. Thus, here, we will review the current literature on the role of zinc in gut formation, a possible link between gut and brain development in ASD and other neurological disorders with shared comorbidities, and tie in possible effects on the immune system. Based on these data, we present a novel model outlining how alterations in the maternal zinc status might pathologically impact the offspring leading to impairments in brain functions later in life.