The association between neuronal XXXX synthase and neuronal sensitivity in the brain after brain injury.

@entity1 @entity2227 @entity66 @entity39 @entity130 @entity75 @entity26 @entity149 @entity842 @entity460 @entity528 @entity855 @entity2383
@entity149 is the leading cause of disability in the United States. @entity528 is one of the causes of disability. Among @entity1 who survive this @entity130 , various degrees of recovery in brain function are observed. The molecular basis of functional recovery is poorly understood. Clinical observations and research using experimental injury models have implicated several metabolites in the cascade of events that lead to @entity528 . The levels of intracellular @entity855 (energy source) and pH are decreased, whereas levels of extracellular @entity2227 , intracellular @entity460 ions, and oxidative damage to RNA/DNA, protein, and lipid are increased. These initiating events can be associated with energy failure and @entity2383 , resulting in functional or structural @entity75 . The injured brain is known to express immediate early genes. Recent studies show that reactive @entity26 species (ROS) cause lesions in genes from which mRNA is transcribed as part of the endogenous neuroprotective response. Although degenerating proteins and lipids may contribute to @entity39 significantly after severe @entity66 in genetic material, if not repaired, disturb cellular function at every level by affecting replication, transcription, and translation. These lesions include abnormal nucleic acids, known as oxidative lesions of DNA (ODLs) or of RNA (ORLs). In this review, we focus on our current understanding of the various effects of neuronal @entity842 synthase on the formation of modified bases in DNA and RNA that are induced in the brain after injury, and how ODLs and ORLs affect cell function.
