Abstract
Four ataxic mice (axJ/axJ) and 4 littermate controls were studied with regard to major brain lipid classes, fatty acids, nucleic acids, and "neurokeratin" amino acid content. No significant differences were found between affected and control animals. An arrest or retardation of myelination was implied rather than amyelination, dysmyelination, or demyelination. This conclusion is in accord with histological evidence. Retarded myelin growth is merely part of a retardation in total brain growth. A similar process was reported in a case of Pelizaeus-Merzbacher disease suggesting that the ataxic mouse will provide a valuable laboratory biochemical model for future investigation.

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