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Intracellular Distribution and Chromatographic Fractionation

HUNTINGTON PORTER, MD

Arch Neurol. 1964;11(4):341-349.

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

Abnormalities in copper metabolism are a consistent feature of Wilson's disease,¹ and it has been demonstrated that these abnormalities antedate both pathological lesions and the onset of clinical illness² and can be detected in infancy.³ The occurrence of elevated tissue copper early in life relative to the onset of symptoms^2,4 and the improvement which may follow treatment with copper mobilizing agents^5,6 suggest that accumulation of copper in the tissues is the primary factor in the production of the characteristic deficits in neurological, hepatic, and renal function. Among the manifestations of this abnormal copper metabolism in Wilson's disease are two which are similar to the condition of the normal newborn infant; first, a reduced amount of normal plasma ceruloplasmin,⁷ and, second, a greatly elevated concentration of copper in the liver.^8,9 One phase of the present investigation deals with the possible relationship between the type . . . [Full Text PDF of this Article]

Author Affiliations
BOSTON

From the Department of Neurology, New England Center Hospital, and Department of Medicine (Neurology), Tufts University School of Medicine.

Footnotes
Presented at the 88th Annual Meeting of the American Neurological Association, Atlantic City, NJ, June 10-12, 1963.

This investigation was supported by research grant NB 01733-05,06 from the National Institute of Neurological Diseases and Blindness, United States Public Health Service.

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