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Articles by Jong M. Rho
Symptom impact and safety of ketogenic therapy in adults with anorexia nervosa: a feasibility trial
Abstract Anorexia nervosa (AN) is a severe psychiatric disorder characterized by food restriction and significantly low body weight. Even after weight restoration, core symptoms such as body dissatisfaction, intense fear of eating, and preoccupation with body shape and weight often persist, contributing to a high risk of relapse.
Role of cholesterol in modulating brain hyperexcitability
Brain cholesterol is metabolized by CH24H into 24HC; this pathway has important impacts on disorders of neuronal hyperexcitability. 24HC is a positive allosteric modulator of NMDA receptors; activation can trigger cholesterol metabolism in a vicious cycle of neuronal hyperexcitability. 24HC can upregulate TNF-α-mediated inflammation to increase extracellular glutamate. Blocking CH24H reduced seizures and improved survival in multiple animal models of epilepsy.
Improving vocal communication with a ketogenic diet in a mouse model of autism
Abstract Background: Deficits in social communication and language development is a hallmark of autism spectrum disorder currently with no cure. Interventional studies using animal models have been very limited in demonstrating improved vocal communication. Autism has been proposed to involve metabolic dysregulation. Ketogenic diet (KD) is a metabolism-based therapy for medically intractable epilepsy, and its applications in other neurological conditions have been increasingly tested.
Intermittent vs continuous ketogenic diet: Impact on seizures, gut microbiota, and mitochondrial metabolism
Abstract We have shown previously that the ketogenic diet (KD) is effective in reducing seizures associated with infantile spasms syndrome (ISS) and that this benefit is related to alterations in the gut microbiota. However, it remains unclear whether the efficacy of the KD persists after switching to a normal diet. Employing a neonatal rat model of ISS, we tested the hypothesis that the impact of the KD would diminish when switched to a normal diet.
The metabolic basis of epilepsy - Nature Reviews Neurology
References Devinsky, O. et al. Epilepsy. Nat. Rev. Dis. Prim. 4, 18024 (2018). PubMed Google Scholar Hall, C. N., Klein-Flugge, M. C., Howarth, C. & Attwell, D. Oxidative phosphorylation, not glycolysis, powers presynaptic and postsynaptic mechanisms underlying brain information processing. J. Neurosci. 32, 8940–8951 (2012). CAS PubMed PubMed Central Google Scholar Rangaraju, V., Calloway, N. & Ryan, T. A. Activity-driven local ATP synthesis is required for synaptic function. Cell 156, 825–835 (2014).
Probiotics counteract hepatic steatosis caused by ketogenic diet and upregulate AMPK signaling in a model of infantile epilepsy
Summary Background Infantile spasms syndrome (IS) is a type of epilepsy affecting 1.6 to 4.5 per 10,000 children in the first year of life, often with severe lifelong neurodevelopmental consequences. Only two first-line pharmacological treatments currently exist for IS and many children are refractory to these therapies. In such cases, children are treated with the ketogenic diet (KD). While effective in reducing seizures, the diet can result in dyslipidemia over time.
Ketone Bodies in the Brain Beyond Fuel Metabolism: From Excitability to Gene Expression and Cell Signaling
Introduction Ketone bodies (KBs) were long considered mere by-products of fatty acid breakdown that increase during fasting and other situations of glucose shortage, which can be physiological, including extenuating exercise, or pathological, such as diabetes. In fact, their relationship with starvation and fat mobilization has been studied for several decades (Edson and Leloir, 1936), but their physiological function was not fully understood at the time.
The Ketogenic Diet as a Treatment Paradigm for Diverse Neurological Disorders
The ketogenic diet (KD) is now a proven therapy for drug-resistant epilepsy (Vining et al., 1998; Neal et al., 2008), and while the mechanisms underlying its anticonvulsant effects remain incompletely understood (Hartman et al., 2007; Bough and Stafstrom, 2010; Rho and Stafstrom, 2011), there is mounting experimental evidence for its broad neuroprotective properties and in turn, emerging data supporting its use in multiple neurological disease states (Baranano and Hartman, 2008).
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