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Altered Cell Membranes in Creutzfeldt-Jakob DiseaseMicrochemical Studies
Norman H. Bass, MD;
Helen H. Hess, MD;
Alfred Pope, MD
Arch Neurol. 1974;31(3):174-182.
Abstract
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Quantitative microchemical assays with histologic controls were used to study biochemical structural components in specimens of frontal cortex from patients with Creutzfeldt-Jakob disease (two cases) as compared with normal cortex (eight cases). Neuronal damage at an early stage of the disease was evidenced by depletion of ribosomal organelles (RNA per cell) and disintegration of axodendritic membranes and synapses (loss of ganglioside sialic acid). Distention of neuronal processes in association with cytoplasmic membrane-bound vacuoles resulted in status spongiosus (decreased total solids per unit volume). While astrocytes hypertrophy and proliferate, neurons are progressively destroyed leading to secondary myelin destruction (cerebroside depletion). Chloroform: methanol soluble proteins (proteolipid proteins) were increased, possibly representing membrane fragments that electron microscopists have shown to occupy intracellular vacuoles in neurons and postulated to harbor the infectious agent.
Author Affiliations
From the McLean Hospital Biological Research Laboratory, Belmont, Mass, and the Department of Neurology and Neuropathology, Harvard Medical School, Boston (Dr. Pope); Department of Neurology, University of Virginia School of Medicine, Charlottesville (Dr. Bass); and the Laboratory of Vision Research, National Eye Institute, National Institutes of Health, Bethesda, Md (Dr. Hess).
Footnotes
Accepted for publication Jan 23, 1974.
Reprint requests to Department of Neurology, University of Virginia School of Medicine, Charlottesville, VA 22901 (Dr. Bass).
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