3.5.1.15	additional information	the enzyme functions in concert with the plasma membrane transporter NaDC3, that specifically transports N-acetylaspartic acid into the cell	
3.5.1.15	N-acetyl-L-aspartate + H2O	-	
3.5.1.15	N-acetyl-L-aspartate + H2O	aspartoacylase is a key enzyme in the human central nervous system. N-Acetyl-L-aspartate is a precursor for the synthesis of the dipeptide N-acetylaspartyl-glutamate, which participates in the neuromodulation of metabotropic and NMDA receptors (NMDA is N-methyl-D-aspartate), regulates the intracellular pressure in neurons and is involved in the energy generation from glutamate anions in neuronal mitochondria. N-Acetyl-L-aspartate is a source of acetyl groups for the construction of myelin sheath in the brain. Therefore, maintenance of the N-acetyl-L-aspartate level ensures proper development and functions of white matter	
3.5.1.15	N-acetyl-L-aspartate + H2O	the enzyme hydrolyzes one of the most abundant amino acid derivatives in the brain, N-acetyl-aspartate	
3.5.1.15	N-acetyl-L-aspartate + H2O	enzyme mutations cause the Canavan disease	
3.5.1.15	N-acetyl-L-aspartate + H2O	deficiency in enzyme activity leads to spongiform degeneration of the white matter of the brain and is the established cause of Canavan disease	
3.5.1.15	N-acetyl-L-aspartate + H2O	malfunction of the enzyme causes Canavan disease	
3.5.1.15	N-acetyl-L-aspartic acid + H2O	-	
3.5.1.15	N-acetylaspartate + H2O	-	
3.5.1.15	N-acetylaspartate + H2O	aspartocylase deficiency results in elevated levels of substrate, brain edema and dysmyelination	
3.5.1.15	N-acetylaspartic acid + H2O	-	
3.5.1.15	N-acetylaspartic acid + H2O	enzyme deficiency causes the Canavan disease, an autosomal-recessive neurodegenerative disorder	
3.5.1.15	N-acetylaspartic acid + H2O	enzyme deficiency, due to mutations of aspartoacylase II, causes the Canavan disease, which is associated with optical neuropathy	
3.5.1.15	N-acetylaspartic acid + H2O	enzyme mutations cause the Canavan disease	
3.5.1.15	N-acetylaspartic acid + H2O	hydrolysis of N-acetylaspartic acid is important to maintain healthy neurons, the enzyme is upregulated in duodenum of obesity-induced diabetic mice, which might be responsible for diabetic neuropathy, overview	
3.5.1.15	N-acetylaspartic acid + H2O	restoration of deficient enzyme activity by enzyme expression in CNS neurons does not ameliorate motor deficits and demyelination in a model of Canavan disease, which is caused by elevated levels of N-acetylaspartic acid, NAA, neuronal expression of ASPA can compensate for NAA-mediated neuronal hyperexcitation, but not for oligodebdrocyte dysfunciton, overview	
3.5.1.15	N-acetylaspartic acid + H2O	the enzyme is involved in negative regulation of brain-derived neurotrophic factor, BDNF, and timing of postnatal oligodendrogenesis, overview	
3.5.1.15	N-acetylaspartic acid + H2O	enzyme mutations cause the Canavan disease and type 2 diabetes