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Neurotoxic chemicals as probes of cellular mechanisms of neuromuscular disease.
Neurotoxicology Unit, Rose F. Kennedy Center for Research in Mental Retardation and Human Development, Albert Einstein College of Medicine, Bronx, New York 1979 Jan; :1-7
Possible cell mechanisms of toxic diseases of neurons and myelinating cells are discussed based on principles of cell biology. The authors mention that neuronopathies and schwannopathies are considered to be diseases of the perikaryon process of the cell, resulting in protein synthesis shutdown and axonal death from cessation of material transport. Distal axonopathies are the most common type of neurocellular intoxication response, in which toxins gaining access to the entire neuron and axon bind to and inactivate protein in the cytoplasm and cause a critical protein shortage in the distal parts of long and large axons. The toxins spare the neuronal perikaryon and affect large axons before they affect smaller, shorter ones. The affected axons undergo distal and retrograde degeneration, but neurons survive and can support axonal regeneration. Some toxins may cause accumulation of neurofilaments and block material transport. Proximal axonopathy has occurred only in response to one specific toxin, and may result from neurofilament blockades. No proximal myelinopathies are known to exist, but one possible reaction may involve Schwann cell demyelination.
NIOSH-Grant; Neurotoxic-effects; Cellular-reactions; Biochemical-reactions; Neurotoxic-agents; Neuropathology; Neuromuscular-system-disorders; Cell-metabolism; Chemical-binding; Membrane-dysfunction; Nuclear-membrane
Pathology Albert Einstein Coll of Med 1300 Morris Park Avenue Bronx, N Y 10461
Final Grant Report
Neurotoxic Disorders; Neurotoxic-effects
Neurotoxicology Unit, Rose F. Kennedy Center for Research in Mental Retardation and Human Development, Albert Einstein College of Medicine, Bronx, New York
Yeshiva University, New York, New York
Page last reviewed: September 2, 2020
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