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Mitochondrial DNA Damage in Autism

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Part of the book series: Advances in Biochemistry in Health and Disease ((ABHD,volume 16))

Abstract

Mitochondria are organelles involved in essential roles in intermediary metabolism, perinatal neurodevelopment, immunity, bioenergetics, neurotransmitter metabolism, among other critical pathways. As such, mitochondrial dysfunction (MD) has deleterious effects with the potential of contributing to neurological diseases or enhancing their morbidity (e.g., autism and schizophrenia). Therefore, accumulation of mitochondrial damage is interpreted as a key element of the development of aging as well as neurodegenerative diseases. With the rise in the prevalence of autism spectrum disorders (ASD), there has been an increased interest in the etiology and contributors of this disorder. MD caused by genetics alone or by gene and environment interactions, may play a role in the etiology of ASD and holds promise for developing future therapies and/or interventions to help manage its symptoms or delaying its onset. Here we explore findings from our research and others analyzing the role of mitochondrial DNA damage as a contributor to ASD morbidity.

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Acknowledgements

We thank the families that participated in this study as well as the technical and intellectual contributions over the years of Catherine Ross-Inta, Alicja Omanska-Klusek, Gyu Song, Yi-Fan Zhang, Daniel Sakaguchi, Casey Bronec, Erica Santos, Nadia Dueñas, Joel Ramirez, Prithvi Bomdica, Allegra De Sandri, and Drs. Eleonora Napoli, Siming Liu, Kazu Kato and Yasuko Fujisawa. We are grateful for the scientific collaborations with Drs. Irva Hertz-Picciotto, Sally Ozonoff, Randi Hagerman, and Flora Tassone that made these studies possible. The research in this article was supported by grants from the Simons Foundation (SFARI 271406) and National Institute of Environmental Health Sciences R01-ES011269, R01-ES015359, R01-ES020392, and P30-ES023513. The National Institute of Child and Human Development: U45-HD079125; EPA Science to Achieve Results (STAR): R-829388 and R833292; and the University of California Davis MIND Institute. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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Correspondence to Cecilia Giulivi .

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Rose, S., Wong, S., Giulivi, C. (2016). Mitochondrial DNA Damage in Autism. In: Gelpi, R., Boveris, A., Poderoso, J. (eds) Biochemistry of Oxidative Stress. Advances in Biochemistry in Health and Disease, vol 16. Springer, Cham. https://doi.org/10.1007/978-3-319-45865-6_21

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