Interference with the normal function of peripheral nerve underlies a variety of neurologic diseases and provides a window for elucidation of basic mechanisms of axonal function. Our research involves the determination of the mechanisms underlying the response of the PNS to various forms of toxic, infectious, immunologic, age-related and metabolic injury. We have developed and characterized several animal models of diabetic autonomic neuropathy involving rats and mice with streptozotocin-induced diabetes and genetically diabetic NOD mice using biochemical, immunohistochemical, physiologic and ultrastructural techniques. We examine the potential of insulin therapy and treatment with newer therapeutic agents and neurotrophic substances (IGF-I, NGF, NT-3) to prevent neuropathy and reverse established neuropathic lesions. Our working hypothesis is that oxidative stress causes nerve terminal injury and is the initiating stimulus in the development of neuroaxonal dystrophy and that there is an age- and diabetes-related defect in synaptic plasticity which is secondary to an abnormal neurotrophic milieu.

Peripheral neuropathy, white matter diseases including multiple sclerosis, brain tumors, general neuropathology

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