Mutations in four identified genes (peripheral myelin protein 22, P-0, conn
exin 32, and the early growth response 2 zinc finger protein) are the cause
for several forms of inherited peripheral neuropathies that are still incu
rable disorders. Some forms of these disorders are well mimicked by enginee
red or spontaneous rodent mutants that might be instrumental for developing
treatment strategies. This review focusses on common pathways of pathogene
sis of the disorders and emphasizes strategies that might be suitable to am
eliorate disease expression. (C) 2000 Wiley-Liss, Inc.