A ketogenic diet increases succinic dehydrogenase (SDH) activity and recovers age-related decrease in numeric density of SDH-positive mitochondria in cerebellar Purkinje cells of late-adult rats

Balietti, Marta; Giorgetti, Belinda; Stefano, Giuseppina Di; Casoli, Tiziana; Platano, Daniela; Solazzi, Moreno; Bertoni–Freddari, Carlo; Aicardi, Giorgio; Lattanzio, Fabrizia; Fattoretti, Patrizia

doi:10.1016/j.micron.2009.08.010

Cited by 47 publications

(32 citation statements)

References 43 publications

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“…Certainly, the metabolic state established by a KD might be disrupted during tissue preparation for in vitro work. As introduced briefly above, one of the biochemical effects associated with a KD is an abundance of high-energy molecules (DeVivo et al, 1978; Nakazawa et al, 1983; Pan et al, 1999; Masino et al, 2007), as well as increased mitochondrial biogenesis, respiration, and expression of ATP synthesis-related proteins (Noh et al, 2004; Sullivan et al, 2004; Bough et al, 2006; Nylen et al, 2009; Balietti et al, 2010). Several lines of evidence suggest that reduced glucose is critical for antiseizure effects.…”

Section: Ketogenic Diet For a Brain Slice: Relaxing In Reduced Glucose?mentioning

confidence: 99%

“…Positive effects of KD feeding have been found in models of amyotrophic lateral sclerosis (Zhao et al, 2006), Parkinson’s disease (Cheng et al, 2009; Yang and Cheng, 2010), and Alzheimer’s disease (Van der Auwera et al, 2005; Mohamed et al, 2010). In addition, KD feeding reverses aging-related impairments in brain biochemistry in animals (Studzinski et al, 2008; Balietti et al, 2010). Direct application of ketones is also beneficial in models of Parkinson’s disease (Kashiwaya et al, 2000; Tieu et al, 2003) and Alzheimer’s disease (Kashiwaya et al, 2000).…”

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: Ketogenic Diet For a Brain Slice: Relaxing In Reduced Glucose?mentioning

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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“…After exposure to the 20% MCT diet, these rats showed an increase in numerical density of succinate dehydrogenase-positive mitochondria in Purkinje cells from the cerebellar vermis (an area that shows age-related degeneration) (Balietti et al, 2010). Conflicting findings between neurons in various regions suggest that metabolism-based therapy has different effects that may be specific for a given cell type.…”

Section: Neurological Illnesses Modeled In Rodentsmentioning

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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“…However, we found that KDs may exert even opposite effects on the synaptic structure in different brain regions, presumably depending on the different neuronal vulnerability to age among different brain areas. Only the cells that maintain a good functional profile during aging may be able to reactivate ketone bodies uptake and catabolism, allowing exploitation of the beneficial properties of KDs [27][28][29] (for review, see Balietti et al 26 ).…”

Section: Age-and Ad-related Synaptic Structural Changesmentioning

confidence: 99%

Impairments of Synaptic Plasticity in Aged Animals and in Animal Models of Alzheimer's Disease

Balietti

Tamagnini

Fattoretti

et al. 2012

Rejuvenation Research

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Aging is associated with a gradual decline in cognitive functions, and more dramatic cognitive impairments occur in patients affected by Alzheimer's disease (AD). Electrophysiological and molecular studies performed in aged animals and in animal models of AD have shown that cognitive decline is associated with significant modifications in synaptic plasticity (i.e., activity-dependent changes in synaptic strength) and have elucidated some of the cellular mechanisms underlying this process. Morphological studies have revealed a correlation between the quality of memory performance and the extent of structural changes of synaptic contacts occurring during memory consolidation. We briefly review recent experimental evidence here.

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A ketogenic diet increases succinic dehydrogenase (SDH) activity and recovers age-related decrease in numeric density of SDH-positive mitochondria in cerebellar Purkinje cells of late-adult rats

Cited by 47 publications

References 43 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

Impairments of Synaptic Plasticity in Aged Animals and in Animal Models of Alzheimer's Disease

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