The cellular target site in distal axonopathies.
Spencer PS; Politis MJ; Pellegrino RG; Schaumburg HH
Disorders of the motor unit. Schotland DL, ed., New York: John Wiley and Sons, 1982 Jan; :87-101
Direct evidence was presented to support the idea that the causation of axonal degeneration in central/peripheral distal axonopathies should be sought in the nerve fiber rather than in the neuronal perikaryon. Evidence suggested that abnormalities of slow and fast axonal transport are responsible for the fine structural changes that precede nerve fiber breakdown. The usefulness of experimental toxicants for exploring the etiology and pathogenesis of human axonal neuropathies was discussed. Several factors must be included in choosing an appropriate toxicant to test hypotheses of direct toxic damage to the nerve fiber. The compound must be a primary neurotoxic agent, not one that requires metabolic activation to exert its effect. It must cause a pathologic change of a characteristic and readily recognizable type, and a chemically related nonneurotoxic compound must be available for negative control. According to the authors, axonal neurotoxins such as 2,5- hexanedione (110134) (2,5-HD) may continue to be important in the elucidation of these diseases, as well as in the expansion of the understanding of the biochemical mechanisms underlying axonal transport.
NIOSH-Grant; Neurotoxic-effects; Nervous-system-disorders; Cell-damage; Cell-function; Neuropathology; Toxic-effects
Pathology Albert Einstein Coll of Med 1300 Morris Park Avenue Bronx, N Y 10461
Disorders of the motor unit
Yeshiva University, New York, New York