Background and Purpose: Peripheral neuropathies, disorders of peripheral ne
rves, result from genetic alterations or from metabolic, inflammatory, infe
ctious, or chemical insults. Experimental animal models, spontaneous or ind
uced, exist for many of the common human peripheral neuropathies. Recent ad
vances in human genetics have led to identification of several specific gen
e defects involved in heritable neuropathies and have allowed reproduction
of the molecular defects in experimental animals.
Methods: Genetic modifications in mice and rats, similar to those seen in h
umans, along with animal models of specific gene defects are presented and
discussed.
Results and Conclusion: Chemotherapeutic agents administered to affected an
imals mimic the dose-dependent neuropathies similar to those seen in humans
, Availability of the experimental animal models has been invaluable to an
understanding of the pathogenesis of disease and the development of new tre
atments.