N-acetyl aspartate (NAA) enjoys its position as the most prominent cerebral metabolite visualized during clinical brain examinations with magnetic resonance spectroscopy because it is a 'neuronal-marker' and because its steady-state concentration in the brain is extraordinary constant. Thus normative data for [NAA] (or NAA/Cr) vary by less than 5% in the normal adult population1. In one rare disease, Canavan's disease, [NAA] is dramatically increased, while in a single case to date, [NAA] is essentially zero (see Burlina article, this volume). In between, there are literally dozens of brain disorders in which steady state [NAA] is significantly reduced (Table 1)2.

The explanations for these alterations are generally to hand - absence of NAA-deacylase, destruction of neurons by hypoxia, ischemia, toxins or degenerative processes, or displacement by masses of NAA-depleted cells, as in primary glioma. However, this interpretation may be incomplete. In this paper we address another question, whether the rate of NAA-synthesis is regulated, and if so, whether in any of these well recognized disease states, altered [NAA] can be attributed to altered rates of NAA-synthesis (Figure 1). We could hypothesize for example that reduced [NAA] might be a result of reduced NAA synthesis.

Magnetic Resonance Unit, Huntington Medical Research Institutes, Pasadena, CA; Rudi Schulte Research

Institute, Santa Barbara CA and NARSAD.

Table 1. Some diseases that decrease NAA levels.


Unknown or Questionable




Chronic Fatique Syndrome

Multiple sclerosis (WM)

Attention Deficit Disorder


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