Introduction

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.

Regional

Unknown or Questionable

Epilepsy

Schizophrenia

Demyelination

Chronic Fatique Syndrome

Multiple sclerosis (WM)

Attention Deficit Disorder

Adrenoleukodystrophy

0 0

Post a comment