Gjumrakch Aliev
GALLY International Biomedical Research Consulting LLC., USA
Title: Mitochondrial Lesions as an Earlier hallmark for Liver and Brain Neuronal Damage During the Chronic Ethanol Self Administration in Cynomolgus Monkeys: New Challenge for Treatment Strategy
Biography
Biography: Gjumrakch Aliev
Abstract
Alcoholism is the third leading cause of preventable death in the United States and caused several neurological diseases. Aside from promoting cardiomyopathies, chronic alcohol consumption is associated with an increased risk of dementia, the development of liver or pancreas failure, and cancers of the oral cavity and pharynx. Although a J-shaped curve for all cause mortality has been identified for average alcohol consumption, irregular heavy drinking also carries significantly greater risks for cardiovascular and neurological disease. Alcohol induced cardiovascular and neurological diseases has a complex multigenic etiology. Significant variations in the response to chronic alcohol consumption may be related to unique genotypes that modify the metabolic response to ethanol. Future studies to further characterize the role of different genotypes will help identify those genotypes are more susceptible to chronic alcohol consumption.
Mitochondria are important for providing cellular energy ATP through the oxidative phosphorylation pathway. They are also critical in regulating many cellular functions including the fatty acid oxidation, the metabolism of glutamate and urea, the antioxidant defense, and the apoptosis pathway. Mitochondria are an important source of reactive oxygen species (ROS) leaked from the electron transport chain while they are susceptible to oxidative damage, leading to mitochondrial dysfunction and tissue injury. Several studies suggested that alcoholism causes impaired mitochondrial function leads to many types of neurodegenerative diseases.
Alcoholism may result in severe neurological deficits and cognitive impairments. Neuropathy and neurocognitive deficits are common among chronic alcohol users, which are believed to be associated with mitochondrial dysfunction in the brain especially cerebellum, cortex as well as liver. The specific type of brain mitochondrial ultrastructural lesions that are adversely affected by alcohol abuse has not been studied. Increasing evidence indicates that chronic alcoholism appears to be linked to oxidative damage and aging. However, the precise connection between chronic alcoholism and oxidative damage is unclear and is under investigation. Our recent gene expression analysis revealed that genes related to oxidative phosphorylation and longevity were down-regulated in the ethanol-fed monkeys, suggesting that alcohol may accelerate aging in monkeys by damaging their mitochondria