NAA  immuno-histochemistry

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Canavan disease





3-Dimensional view of N-acetyl-L-aspartate

N-Acetylaspartate, or NAA, rivals glutamate as the most abundant metabolite in the human central nervous system (CNS). The functional significance of the high NAA concentration in the brain remains uncertain, but it confers on NAA a unique clinical significance due to the fact that NAA emits the strongest signal in magnetic resonance spectrograms of the human brain. NAA levels measured by magnetic resonance spectroscopy are changed in a wide array of CNS disorders, but it is unknown if the changes are etiological, or merely secondary. Magnetic resonance spectroscopy (MRS)studies of human brain disorders have invariably detected decreases in brain NAA concentrations when neuronal loss or dysfunction are involved, with one major exception. The autosomal genetic disease, Canavan disease, involves the accumulation of NAA in the brain due to the lack of degradative enzyme activity. Virtually all other neurological disorders involving neuronal loss or dysfunction result in reductions in brain NAA levels including Alzheimer disease, epilepsy, amyotrophic lateral sclerosis, schizophrenia, multiple sclerosis, AIDS, traumatic brain injury, stroke and non-neuronal brain tumors such as glioma.


3-Dimensional view of the binding site of the NAA biosynthetic enzyme "aspartate N-acetyltransferase". The two substrates, aspartate (ASP) and acetyl coenzyme A (COA) are shown in the binding pocket. A ribbon representation of the homology model  with residues  from L143 to L283 are shown. The α-helical segments are shown in red, β-strand segments are shown in magenta, and loop regions are shown in gray. Coenzyme A is given in stick representation and the docked aspartate is shown in ball-and-stick representation. The model indicates the restricted pocket size of the Asp-NAT binding site which excludes amino acids larger than aspartate.


NAA-immunoreactivity in the rat retrosplenial cortex. More here.

N-acetylaspartate.com 2015