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Frontiers in molecular neuroscience, 2017-02, Vol.10, p.34-34
2017

Details

Autor(en) / Beteiligte
Titel
Metabolic Dysfunction Underlying Autism Spectrum Disorder and Potential Treatment Approaches
Ist Teil von
  • Frontiers in molecular neuroscience, 2017-02, Vol.10, p.34-34
Ort / Verlag
Switzerland: Frontiers Research Foundation
Erscheinungsjahr
2017
Link zum Volltext
Quelle
EZB-FREE-00999 freely available EZB journals
Beschreibungen/Notizen
  • Autism spectrum disorder (ASD) is characterized by deficits in sociability and communication, and increased repetitive and/or restrictive behaviors. While the etio-pathogenesis of ASD is unknown, clinical manifestations are diverse and many possible genetic and environmental factors have been implicated. As such, it has been a great challenge to identify key neurobiological mechanisms and to develop effective treatments. Current therapies focus on co-morbid conditions (such as epileptic seizures and sleep disturbances) and there is no cure for the core symptoms. Recent studies have increasingly implicated mitochondrial dysfunction in ASD. The fact that mitochondria are an integral part of diverse cellular functions and are susceptible to many insults could explain how a wide range of factors can contribute to a consistent behavioral phenotype in ASD. Meanwhile, the high-fat, low-carbohydrate ketogenic diet (KD), used for nearly a century to treat medically intractable epilepsy, has been shown to enhance mitochondrial function through a multiplicity of mechanisms and affect additional molecular targets that may address symptoms and comorbidities of ASD. Here, we review the evidence for the use of metabolism-based therapies such as the KD in the treatment of ASD as well as emerging co-morbid models of epilepsy and autism. Future research directions aimed at validating such therapeutic approaches and identifying additional and novel mechanistic targets are also discussed.
Sprache
Englisch
Identifikatoren
ISSN: 1662-5099
eISSN: 1662-5099
DOI: 10.3389/fnmol.2017.00034
Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5318388

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