Abstract

Background: Alcoholic neuropathy is a common complication among patients with alcohol abuse disorder. It is often asymptomatic and the frequency of occurrence varies. We propose that the deficit of protease inhibitors could be a causal factor of alcoholic neuropathy. If this is true, it would contribute to understanding of the pathophysiology, explain variability in individual response, and explain variability in individual response, and facilitate the search for prevention therapy.Development: Alcoholic neuropathy is characterized by a pattern of symmetrical polyneuropathy with great involvement of the lower extremities. The mechanisms of axonal degeneration due to alcohol consumption are still unclear. It is known that alcohol inhibits protection mechanisms of the nervous system. Here, we discuss that the deficit of protease inhibitors could be a causal factor in the pathogenesis of alcoholic neuropathy. If this is true, it would contribute to an understanding of the pathophysiology, explain variability in individual response, and facilitate the search for prevention therapy.Conclusions: The protease inhibitors play a significant role in the origin of peripheral neuropathies. There is strong evidence to suggest that proteases and their inhibitors are related to processes that allow the development and maintenance of peripheral nerves, and alterations in their proportions favor the development of anomalies in such structures. The mechanisms through which these molecules trigger the disease are unclear in most cases. An increase in the number of investigations in this area would undoubtedly contribute to preventing and combating a disease which strikes a significant number of people.