Modification of Astrocyte Metabolism as an Approach to the Treatment of @entity302 : XXXX and @entity4162 .

@entity1 @entity410 @entity16740 @entity3264 @entity1246 @entity16 @entity5093 @entity16374 @entity4162 @entity2134 @entity1315 @entity412 @entity302 @entity6626 @entity19722 @entity26543 @entity159 @entity49065
UNASSIGNED: @entity302 is a severe @entity16 characterized by altered electrical activity in the brain. Important pathophysiological mechanisms include disturbed metabolism and homeostasis of major excitatory and inhibitory neurotransmitters, @entity3264 and @entity1246 . Current drug treatments are largely aimed at decreasing neuronal excitability and thereby preventing the occurrence of @entity410 . However, many @entity1 are refractory to treatment and side effects are frequent. @entity1315 ( @entity1315 ) is the most common type of drug-resistant @entity302 in adults. In rodents, the @entity2134 - @entity159 model reflects the pathology and @entity1315 and the @entity5093 kindling model exhibits chronic induced limbic @entity410 . Accumulating evidence from studies on @entity1315 points to alterations in astrocytes and neurons as key metabolic changes. The present review describes interventions which alleviate these disturbances in astrocyte-neuronal interactions by supporting mitochondrial metabolism. The compounds discussed are the endogenous transport molecule @entity4162 and the @entity412 of @entity49065 , @entity26543 . Both provide @entity16374 moieties for oxidation in the @entity6626 cycle whereas @entity49065 is also provides @entity19722 , which after carboxylation can produce @entity16740 , resulting in anaplerosis-the refilling of the @entity6626 cycle.
