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Sven G. Eliasson, MD, PhD; JoAnne D. Scarpellini, BS; Richard R. Fox, PhD

Arch Neurol. 1967;17(6):661-665.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

HEREDITARY ataxia in rabbits is due to a recessive mutant gene (ax). The pathology begins in adolescence and progressively involves lateral brainstem nuclei and deep cerebellar nuclei. The clinical and morphological features have been described by Sawin et al¹ and by O'Leary and his associates.² Glycogen deposits in the neuropil of the involved areas have been demonstrated³ and a study of brain glycogen metabolism has been published by Tourtellotte and his co-workers.⁴ Glucose-6-phosphate was found to be significantly elevated with other intermediates at normal levels. Normal also were the amino acid spectra of brain and urine from ataxic rabbits as determined by Weinstein et al.⁵

Further biochemical studies were directed toward the lipid composition of the brainstem areas with histological evidence of lesions. A decrease in the concentration of inositolphosphatides was found⁶ and the present communication is an extension of these observations with . . . [Full Text PDF of this Article]

Author Affiliations
St. Louis; Bar Harbor, Me

From the Department of Neurology, Washington University School of Medicine, St. Louis (Dr. Eliasson and Mrs. Scarpellini) and The Jackson Laboratory, Bar Harbor, Me (Dr. Fox).

Footnotes
Received for publication July 6, 1967; accepted July 24.

Read in part before the American Oil Chemists' Society, Houston, April 26, 1965.

Reprint requests to 660 S Euclid, St. Louis 63110 (Dr. Eliasson).

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