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Int. J. Mol. Sci. 2015, 16(12), 28194-28217;

Old Things New View: Ascorbic Acid Protects the Brain in Neurodegenerative Disorders

Instituto de Bioquímica y Microbiología, Facultad de Ciencias, Universidad Austral de Chile, Valdivia 5090000, Chile
Center for Interdisciplinary Studies on the Nervous system (CISNe), Universidad Austral de Chile, Casilla 547, Valdivia 5090000, Chile
Author to whom correspondence should be addressed.
Academic Editor: Guido Haenen
Received: 22 July 2015 / Revised: 23 September 2015 / Accepted: 14 October 2015 / Published: 27 November 2015
(This article belongs to the Special Issue Antioxidant 2.0——Redox Modulation by Food and Drugs)
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Ascorbic acid is a key antioxidant of the Central Nervous System (CNS). Under brain activity, ascorbic acid is released from glial reservoirs to the synaptic cleft, where it is taken up by neurons. In neurons, ascorbic acid scavenges reactive oxygen species (ROS) generated during synaptic activity and neuronal metabolism where it is then oxidized to dehydroascorbic acid and released into the extracellular space, where it can be recycled by astrocytes. Other intrinsic properties of ascorbic acid, beyond acting as an antioxidant, are important in its role as a key molecule of the CNS. Ascorbic acid can switch neuronal metabolism from glucose consumption to uptake and use of lactate as a metabolic substrate to sustain synaptic activity. Multiple evidence links oxidative stress with neurodegeneration, positioning redox imbalance and ROS as a cause of neurodegeneration. In this review, we focus on ascorbic acid homeostasis, its functions, how it is used by neurons and recycled to ensure antioxidant supply during synaptic activity and how this antioxidant is dysregulated in neurodegenerative disorders. View Full-Text
Keywords: oxidative stress; brain energy metabolism oxidative stress; brain energy metabolism

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Covarrubias-Pinto, A.; Acuña, A.I.; Beltrán, F.A.; Torres-Díaz, L.; Castro, M.A. Old Things New View: Ascorbic Acid Protects the Brain in Neurodegenerative Disorders. Int. J. Mol. Sci. 2015, 16, 28194-28217.

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