Ketogenic diet protects the hippocampus from kainic acid toxicity by inhibiting the dissociation of bad from 14‐3‐3

Noh, Hae Sook; Kim, Yoon Sook; Kim, Young Hee; Han, Jae Yoon; Park, Chang Hwan; Kang, Ahn Ki; Shin, Hee Suk; Kang, Sang Soo; Cho, Gyeong Jae; Choi, Wan Sung

doi:10.1002/jnr.21057

Cited by 36 publications

(22 citation statements)

References 46 publications

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“…Animal studies have found find that the KD protects against seizure-induced neurodegeneration and related sequelae (such as aberrant neurite sprouting; Muller-Schwarze et al, 1999; Noh et al, 2003, 2005, 2006b; Linard et al, 2010). The KD is also neuroprotective against ischemic damage (Tai et al, 2008, 2009), hypoglycemic damage (Yamada et al, 2005), and traumatic brain and spinal injury (Prins et al, 2005; Appelberg et al, 2009; Hu et al, 2009a,b; Prins and Hovda, 2009; Schwartzkroin et al, 2010; Streijger et al, 2011), and improves injury-related deficits in cognition and movement after traumatic brain and spinal injury, respectively (Appelberg et al, 2009; Streijger et al, 2011).…”

Section: Attenuating Brain Injury and Neurodegenerationmentioning

confidence: 99%

“…The KD is also neuroprotective against ischemic damage (Tai et al, 2008, 2009), hypoglycemic damage (Yamada et al, 2005), and traumatic brain and spinal injury (Prins et al, 2005; Appelberg et al, 2009; Hu et al, 2009a,b; Prins and Hovda, 2009; Schwartzkroin et al, 2010; Streijger et al, 2011), and improves injury-related deficits in cognition and movement after traumatic brain and spinal injury, respectively (Appelberg et al, 2009; Streijger et al, 2011). Ketosis is apparently crucial to these effects as direct application of ketones to in vitro tissue is also protective against hypoglycemia and ischemia (Samoilova et al, 2010), oxidative stress (Kim et al, 2007), and excitotoxicity (Massieu et al, 2003; Noh et al, 2006b; Maalouf et al, 2007; Samoilova et al, 2010). The mechanisms are likely to involve reduced reactive oxygen species, reduced tissue excitability, and enhanced production of high-energy molecules.…”

Section: Attenuating Brain Injury and Neurodegenerationmentioning

confidence: 99%

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The Nervous System and Metabolic Dysregulation: Emerging Evidence Converges on Ketogenic Diet Therapy

Ruskin¹,

Masino²

2012

Front. Neurosci.

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A link between metabolism and brain function is clear. Since ancient times, epileptic seizures were noted as treatable with fasting, and historical observations of the therapeutic benefits of fasting on epilepsy were confirmed nearly 100 years ago. Shortly thereafter a high fat, low-carbohydrate ketogenic diet (KD) debuted as a therapy to reduce seizures. This strict regimen could mimic the metabolic effects of fasting while allowing adequate caloric intake for ongoing energy demands. Today, KD therapy, which forces predominantly ketone-based rather than glucose-based metabolism, is now well-established as highly successful in reducing seizures. Cellular metabolic dysfunction in the nervous system has been recognized as existing side-by-side with nervous system disorders – although often with much less obvious cause-and-effect as the relationship between fasting and seizures. Rekindled interest in metabolic and dietary therapies for brain disorders complements new insight into their mechanisms and broader implications. Here we describe the emerging relationship between a KD and adenosine as a way to reset brain metabolism and neuronal activity and disrupt a cycle of dysfunction. We also provide an overview of the effects of a KD on cognition and recent data on the effects of a KD on pain, and explore the relative time course quantified among hallmark metabolic changes, altered neuron function and altered animal behavior assessed after diet administration. We predict continued applications of metabolic therapies in treating dysfunction including and beyond the nervous system.

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Section: Attenuating Brain Injury and Neurodegenerationmentioning

confidence: 99%

Section: Attenuating Brain Injury and Neurodegenerationmentioning

confidence: 99%

The Nervous System and Metabolic Dysregulation: Emerging Evidence Converges on Ketogenic Diet Therapy

Ruskin¹,

Masino²

2012

Front. Neurosci.

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“…One potential neuroprotective effect of a ketogenic diet may be to prevent dissociation of the pro-apoptosis protein Bad from its binding partner 14-3-3 (Noh et al, 2006). Dissociation of Bad from 14-3-3 is one way to activate the apoptosis cascade.…”

Section: Potential Mechanisms Of Neuroprotectionmentioning

confidence: 99%

Neuroprotection in metabolism-based therapy

Hartman

2012

Epilepsy Research

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Metabolism-based therapy has been used successfully in the treatment of seizures but study of its use in other neurodegenerative disorders is growing. Data demonstrating the use of different forms of metabolism-based therapy in human trials of Alzheimer disease and Parkinson disease are discussed. Animal and in vitro studies have shed light on metabolism-based therapy’s mechanisms in these diseases, as well as ALS, aging, ischemia, trauma and mitochondrial cytopathies. Additional insights may be obtained by considering the role of metabolism-based therapy in cell disability and death (specifically apoptosis, excitotoxicity, and autophagy).

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“…In mice treated with ketone diet blood DbHB increases and halts kainic acid-induced hippocampal cell death [29][30][31][32][33]. DbHB prevents glutamate-mediated striatal neuronal damage in vivo [25].…”

Section: Discussionmentioning

confidence: 99%

D-β-Hydroxybutyrate Prevents MPP+-Induced Neurotoxicity in PC12 Cells

et al. 2009

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Numerous studies show that D-beta-Hydroxybutyrate (DbetaHB) is neuroprotective. The present study was to explore the neuroprotective effects of DbetaHB against the cell death and apoptosis induced by 1-methyl-4-phenylpyridinium ion (MPP+) in PC12 cells. PC12 cells were pretreated with DbetaHB and followed by MPP+ exposure. The cell viability was determined by MTT assay. The morphological characteristics of apoptosis was observed by Acridine Orange (AO) staining and apoptotic rates were measured by flow cytometer. The product of lipid peroxidation, malondialdehyde (MDA), was measured using thiobarbituric acid method. The mitochondrial membrane potential (MMP), intracellular ROS and total glutathione were detected by microplate reader. In PC12 cells, pretreatment with DbetaHB significantly reduced MPP+-induced the decrease of cell viability. AO staining and flow cytometric analysis found DbetaHB inhibited MPP+-induced apoptosis. The measurement of MDA formation showed that DbetaHB alleviated lipid peroxidation induced by MPP+. The loss of MMP induced by MPP+ was preventive by DbetaHB. The changes of intracellular ROS and total glutathione induced by MPP+ were reversed by DbetaHB. DbetaHB protected PC12 cells against MPP+-induced death and apoptosis.

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Ketogenic diet protects the hippocampus from kainic acid toxicity by inhibiting the dissociation of bad from 14‐3‐3

Cited by 36 publications

References 46 publications

The Nervous System and Metabolic Dysregulation: Emerging Evidence Converges on Ketogenic Diet Therapy

The Nervous System and Metabolic Dysregulation: Emerging Evidence Converges on Ketogenic Diet Therapy

Neuroprotection in metabolism-based therapy

D-β-Hydroxybutyrate Prevents MPP+-Induced Neurotoxicity in PC12 Cells

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