ArticlePloS one2017
Ketogenic diet improves behaviors in a maternal immune activation model of autism spectrum disorder.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 101 citations in OpenAlex.
- β-hydroxybutyrate restores social deficits by suppressing HDAC9 in the ACC of Shank3B-deficient mice.EMBO molecular medicine · 2026Article
- Placental and juvenile immune responses to maternal immune activation are differentially regulated by sex chromosomes and gonads across gestation.Journal of neuroinflammation · 2026Article
- Autism-like phenotype across the lifespan of Shank3B-mutant mice of both sexes.Journal of neurodevelopmental disorders · 2025Article
- The role of nutrition and gut microbiome in childhood brain development and behavior.Frontiers in nutrition · 2025Review
- Ketogenic diet, adenosine, and dopamine in addiction and psychiatry.Frontiers in nutrition · 2025Review
- Brain-gut-brain axis, nutrition, and autism spectrum disorders: a review.Translational pediatrics · 2024Review
- Adult Inception of Ketogenic Diet Therapy Increases Sleep during the Dark Cycle in C57BL/6J Wild Type and Fragile X Mice.International journal of molecular sciences · 2024Article
- Review
- Exogenous ketone bodies and the ketogenic diet as a treatment option for neurodevelopmental disorders.Frontiers in nutrition · 2024Review
- Ketogenic diet and behavior: insights from experimental studies.Frontiers in nutrition · 2024Review
- Review
- Ketogenic Diet Affects Sleep Architecture in C57BL/6J Wild Type and Fragile X Mice.International journal of molecular sciences · 2023Article
- Ketogenic diet for mood disorders from animal models to clinical application.Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
- A Spectrum of Solutions: Unveiling Non-Pharmacological Approaches to Manage Autism Spectrum Disorder.Medicina (Kaunas, Lithuania) · 2023Review
- Interconnection between Microbiota-Gut-Brain Axis and Autism Spectrum Disorder Comparing Therapeutic Options: A Scoping Review.Microorganisms · 2023Article
- Neuroinflammation and Oxidative Stress in the Pathogenesis of Autism Spectrum Disorder.International journal of molecular sciences · 2023Review
- Influences of the Immune System and Microbiome on the Etiology of ASD and GI Symptomology of Autistic Individuals.Current topics in behavioral neurosciences · 2023Article
- Global metabolic profiles in a non-human primate model of maternal immune activation: implications for neurodevelopmental disorders.Molecular psychiatry · 2022Article
- 2-month ketogenic diet preferentially alters skeletal muscle and augments cognitive function in middle aged female mice.Aging cell · 2022Article
- Rescue of histone hypoacetylation and social deficits by ketogenic diet in a Shank3 mouse model of autism.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Prenatal factors influence autism spectrum disorder (ASD) incidence in children and can increase ASD symptoms in offspring of animal models. These may include maternal immune activation (MIA) due to viral or bacterial infection during the first trimesters. Unfortunately, regardless of ASD etiology, existing drugs are poorly effective against core symptoms. For nearly a century a ketogenic diet (KD) has been used to treat seizures, and recent insights into mechanisms of ASD and a growing recognition that immune/inflammatory conditions exacerbate ASD risk has increased interest in KD as a treatment for ASD. Here we studied the effects of KD on core ASD symptoms in offspring exposed to MIA. To produce MIA, pregnant C57Bl/6 mice were injected with the viral mimic polyinosinic-polycytidylic acid; after weaning offspring were fed KD or control diet for three weeks. Consistent with an ASD phenotype of a higher incidence in males, control diet-fed MIA male offspring were not social and exhibited high levels of repetitive self-directed behaviors; female offspring were unaffected. However, KD feeding partially or completely reversed all MIA-induced behavioral abnormalities in males; it had no effect on behavior in females. KD-induced metabolic changes of reduced blood glucose and elevated blood ketones were quantified in offspring of both sexes. Prior work from our laboratory and others demonstrate KDs improve relevant behaviors in several ASD models, and here we demonstrate clear benefits of KD in the MIA model of ASD. Together these studies suggest a broad utility for metabolic therapy in improving core ASD symptoms, and support further research to develop and apply ketogenic and/or metabolic strategies in patients with ASD.
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