Title : The molecular mechanisms affecting N-acetylaspartate homeostasis following experimental graded traumatic brain injury.

Pub. Date : 2014 Mar 24

PMID : 24515258






2 Functional Relationships(s)
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1 The reversible changes in NAA induced by mild TBI were due to a combination of transient mitochondrial malfunctioning with energy crisis (decrease in ATP and in the ATP/ADP ratio) and modulation in the gene and protein levels of N-acetyltransferase 8-like and increase of aspartoacylase levels. N-acetylaspartate aspartoacylase Rattus norvegicus
2 The irreversible decrease in NAA following severe TBI, was instead characterized by profound mitochondrial malfunctioning (constant 65% decrease of the ATP/ADP indicating permanent impairment of the mitochondrial phosphorylating capacity), dramatic repression of the N-acetyltransferase 8-like gene and concomitant remarkable increase in the aspartoacylase gene and protein levels. N-acetylaspartate aspartoacylase Rattus norvegicus