Alcoholic Neuropathy: Involvement of Multifaceted Signalling Mechanisms

Abstract

Background: Alcoholic neuropathy is a chronic disorder caused by excessive consumption of alcohol. Damage to the nerves results in unusual sensations in the limbs, decrease mobility and loss of some body functions. Objective: Alcohol is considered a major villain for exclusively creating the debilitating condition of the neuropathic state. This review critically examines the key mediators involved in the pathogenesis of alcoholic neuropathy and the targets which upon selective inhibition alleviates the progression of alcoholic neuropathy. Method: A thorough study of research and review articles available on the internet from PubMed, MEDLINE, and concerned sites was performed on alcoholic neuropathy. Result: A deal of impairment in axonal transportation is quiet common with the progression of alcoholic neuropathy. Nutritional deficiencies lead to axonal neuropathies that escalate a variety of complications that further worsens the state. PKC and PKA play a significant role in the pathogenesis of alcoholic neuropathy. PKC plays a well-marked role in modulating NMDA receptor currents manifesting to excitation in the neurons. MMPs are involved in the number of pathologies that destructs CNS and reduction in the level of endogenous antioxidants like -tocopherol, vitamin E with ethanol promotes oxidative stress by generating free radicals and lipid peroxidation. Conclusion: Oxidative stress is implicated in the activation of MMPs causing blood-brain barrier disruption, the latter involved in the trafficking and passages of molecules in and out of the cell. Chronic alcohol consumption leads to the downregulation of CNS receptors consequently precipitating the condition of alcoholic neuropathy. </jats:sec