N-acetylaspartate (NAA) peak
Updates to Article Attributes
N-acetylaspartate (NAA) is one of the more important compounds assessed on MR spectroscopy, and resonates at 2.0 ppm chemical shift (its concentration in healthy adults is 8-10 mM) 1. The synthesis of NAA, adenosine diphosphate-dependent, occurs in the neuronal mitochondria 2.
NAA is the acetylated form of the amino acid, aspartate, which is found in high concentrations in neurons and is a marker of neuronal viability. It is therefore reduced in any process that destroys neurons, such as high grade tumours, radionecrosis, non-neuronal tumours (e.g. cerebral metastases and primary CNS lymphoma).
Markedly elevated NAA peak and NAA: creatinine ratio are pathognomonic for Canavan disease 7. The NAA peak level may decrease after gene therapy.
Many studies have shown the reduction of NAA, in specific brain areas, in schizophrenic patients: hippocampus, mesial regions of the temporal lobes and frontal lobes 3-6.
-<p><strong>N-acetylaspartate (NAA)</strong> is one of the more important compounds assessed on <a href="/articles/mr-spectroscopy-1">MR spectroscopy</a>, and resonates at 2.0 <a href="/articles/parts-per-million">ppm</a> chemical shift (its concentration in healthy adults is 8-10 mM) <sup>1</sup>. The synthesis of NAA, adenosine diphosphate-dependent, occurs in the mitochondria<sup> 2</sup>.</p><p>NAA is the acetylated form of the <a href="/articles/amino-acids-1">amino acid</a>, aspartate, which is found in high concentrations in neurons and is a marker of neuronal viability. It is therefore reduced in any process that destroys neurons, such as <a href="/articles/glioblastoma">high grade tumours</a>, <a href="/articles/cerebral-radiation-necrosis-1">radionecrosis</a>, non-neuronal tumours (e.g. <a href="/articles/brain-metastases">cerebral metastases</a> and <a href="/articles/primary-cns-lymphoma">primary CNS lymphoma</a>). </p><p>Markedly elevated NAA peak and NAA: creatinine ratio are pathognomonic for <a title="Canavan disease" href="/articles/canavan-disease">Canavan disease</a> <sup>7</sup>. The NAA peak level may decrease after gene therapy.</p><p>Many studies have shown the reduction of NAA, in specific brain areas, in <a href="/articles/schizophrenia">schizophrenic patients</a>: hippocampus, mesial regions of the temporal lobes and frontal lobes <sup>3-6</sup>.</p>- +<p><strong>N-acetylaspartate (NAA)</strong> is one of the more important compounds assessed on <a href="/articles/mr-spectroscopy-1">MR spectroscopy</a>, and resonates at 2.0 <a href="/articles/parts-per-million">ppm</a> chemical shift (its concentration in healthy adults is 8-10 mM) <sup>1</sup>. The synthesis of NAA, adenosine diphosphate-dependent, occurs in the neuronal mitochondria<sup> 2</sup>.</p><p>NAA is the acetylated form of the <a href="/articles/amino-acids-1">amino acid</a>, aspartate, which is found in high concentrations in neurons and is a marker of neuronal viability. It is therefore reduced in any process that destroys neurons, such as <a href="/articles/glioblastoma">high grade tumours</a>, <a href="/articles/cerebral-radiation-necrosis-1">radionecrosis</a>, non-neuronal tumours (e.g. <a href="/articles/brain-metastases">cerebral metastases</a> and <a href="/articles/primary-cns-lymphoma">primary CNS lymphoma</a>). </p><p>Markedly elevated NAA peak and NAA: creatinine ratio are pathognomonic for <a href="/articles/canavan-disease">Canavan disease</a> <sup>7</sup>. The NAA peak level may decrease after gene therapy.</p><p>Many studies have shown the reduction of NAA, in specific brain areas, in <a href="/articles/schizophrenia">schizophrenic patients</a>: hippocampus, mesial regions of the temporal lobes and frontal lobes <sup>3-6</sup>.</p>
References changed:
- 8. Martinez MA, Florenzano NV, Macchia EA. [Metabolism of N-acetyl-L-aspartate: its diagnostic and prognostic value]. (2016) Revista de neurologia. 62 (8): 361-70. <a href="https://www.ncbi.nlm.nih.gov/pubmed/27064916">Pubmed</a> <span class="ref_v4"></span>
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