Abstract
Metabolic-based therapies such as nutritional ketosis have been proven effective for seizure disorders and various acute and chronic neurological pathologies. In a healthy brain, glucose is the primary metabolic fuel for cells. However, neurodegenerative disorders, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), seizure disorders, and traumatic brain injury (TBI) are associated with impaired glucose transport and metabolism and with mitochondrial dysfunction leading to energy deficit. Therapeutic ketosis can be considered as a form of metabolic therapy by providing alternative energy substrates. In addition, ketosis leads to metabolic adaptations that improve brain metabolism, restore mitochondrial ATP production, decrease reactive oxygen species production, reduce inflammation, and increase the activity of neurotrophic factors. Moreover, the synaptic activity between neurons is also stabilized through the increase of Szent-Györgyi–Krebs cycle intermediates, antioxidant effects, increased GABA-to-glutamate ratio, and activation of ATP-sensitive potassium channels.
Highlights
The Ketogenic Diet (KD) represents a well-known therapeutic option for refractory epilepsy [1], mechanisms regulating its anticonvulsant effects are currently object of study [2]
The mechanisms underlying the anti-seizure effects of the high-fat ketogenic diet (KD) remain unclear, it has been long-questioned whether ketone bodies (i.e., β-hydroxybutyrate, acetoacetate and acetone) provide any contribution from a mechanistic perspective
It has been observed that ketone bodies are responsible for enhanced fatty acid oxidation and for a global shift toward intermediary metabolism
Summary
The Ketogenic Diet (KD) represents a well-known therapeutic option for refractory epilepsy [1], mechanisms regulating its anticonvulsant effects are currently object of study [2]. In a metabolic state of ketosis, ketone body production is augmented when circulating carbohydrates decrease or fatty acids blood levels are raised [3].
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