Chronic Neurologic Effects of Alcohol

Hammoud, Nadia; Jimenez-Shahed, Joohi

doi:10.1016/j.cld.2018.09.010

Cited by 62 publications

(45 citation statements)

References 52 publications

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“…After drinking, alcohol can cause brief euphoria, then progresses to respiratory depression and coma in a dose-dependent manner [21]. Moreover, chronic alcohol intake leads to increased glutamate-induced excitotoxicity, oxidative stress [22] and permanent neuronal damage associated with malnutrition, such as dementia with decreased cognitive and executive function, cerebellar degeneration with impaired motor skills and/or ataxia, polyneuropathy and Wernicke and Korsakoff syndromes [23]. Ethanol also negatively affects the availability of nerve growth factor and brain-derived neurotrophic factor, resulting in impaired intracellular signaling pathways [23].…”

Section: Introduction and Alcohol Use: Dual Effects And Mechanismsmentioning

confidence: 99%

“…However, on the other hand, some studies show that moderate amounts of ethanol intake produce a neuroprotective effect. In addition, alcohol can increase insulin sensitivity [24], growth factor and brain-derived neurotrophic factor, resulting in impaired intracellular signaling pathways [23]. However, on the other hand, some studies show that moderate amounts of ethanol intake produce a neuroprotective effect.…”

Section: Introduction and Alcohol Use: Dual Effects And Mechanismsmentioning

confidence: 99%

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Role of Alcohol Drinking in Alzheimer’s Disease, Parkinson’s Disease, and Amyotrophic Lateral Sclerosis

Peng

Yang²,

Joshi

et al. 2020

IJMS

103

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Neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS), increase as the population ages around the world. Environmental factors also play an important role in most cases. Alcohol consumption exists extensively and it acts as one of the environmental factors that promotes these neurodegenerative diseases. The brain is a major target for the actions of alcohol, and heavy alcohol consumption has long been associated with brain damage. Chronic alcohol intake leads to elevated glutamate-induced excitotoxicity, oxidative stress and permanent neuronal damage associated with malnutrition. The relationship and contributing mechanisms of alcohol with these three diseases are different. Epidemiological studies have reported a reduction in the prevalence of Alzheimer’s disease in individuals who drink low amounts of alcohol; low or moderate concentrations of ethanol protect against β-amyloid (Aβ) toxicity in hippocampal neurons; and excessive amounts of ethanol increase accumulation of Aβ and Tau phosphorylation. Alcohol has been suggested to be either protective of, or not associated with, PD. However, experimental animal studies indicate that chronic heavy alcohol consumption may have dopamine neurotoxic effects through the induction of Cytochrome P450 2E1 (CYP2E1) and an increase in the amount of α-Synuclein (αSYN) relevant to PD. The findings on the association between alcohol consumption and ALS are inconsistent; a recent population-based study suggests that alcohol drinking seems to not influence the risk of developing ALS. Additional research is needed to clarify the potential etiological involvement of alcohol intake in causing or resulting in major neurodegenerative diseases, which will eventually lead to potential therapeutics against these alcoholic neurodegenerative diseases.

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Section: Introduction and Alcohol Use: Dual Effects And Mechanismsmentioning

confidence: 99%

Section: Introduction and Alcohol Use: Dual Effects And Mechanismsmentioning

confidence: 99%

Role of Alcohol Drinking in Alzheimer’s Disease, Parkinson’s Disease, and Amyotrophic Lateral Sclerosis

Peng

Yang²,

Joshi

et al. 2020

IJMS

103

View full text Add to dashboard Cite

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“…Brain damage is also more severe in chronic alcoholics with cirrhosis of the liver (Zahr et al, ), which may be due to higher doses of EtOH reaching the brain (Harper, ). Chronic alcoholic exposure alters the blood–brain barrier such that there is increased diffusion of alcohol into the brain as well as increased exposure to systemic inflammatory molecules, such as cytokines, resulting in neuroinflammation (Hammoud and Jimenez‐Shahed, ). Further, hepatic dysfunction results in an increase in neurotoxic metabolites such as ammonia and the development of hepatic encephalopathy (reviewed in Davis and Bajaj, ; Hammoud and Jimenez‐Shahed, ).…”

Section: Discussionmentioning

confidence: 99%

“…Chronic alcoholic exposure alters the blood–brain barrier such that there is increased diffusion of alcohol into the brain as well as increased exposure to systemic inflammatory molecules, such as cytokines, resulting in neuroinflammation (Hammoud and Jimenez‐Shahed, ). Further, hepatic dysfunction results in an increase in neurotoxic metabolites such as ammonia and the development of hepatic encephalopathy (reviewed in Davis and Bajaj, ; Hammoud and Jimenez‐Shahed, ). Although individuals with a history of hepatic encephalopathy were excluded from this study, the indirect effects of neurotoxic metabolites on the brain may occur in advance of such a diagnosis (Davis and Bajaj, ).…”

Section: Discussionmentioning

confidence: 99%

Sex Differences in the Expression of the α5 Subunit of the GABA_A Receptor in Alcoholics with and without Cirrhosis of the Liver

Janeczek

Colson

Dodd

et al. 2020

Alcoholism Clin & Exp Res

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Background: Alcohol exposure alters the expression of a large number of genes, resulting in neuronal adaptions and neuronal loss, but the underlying mechanisms are largely unknown. miRNAs are gene repressors that are abundant in the brain. A recent study identified~35 miRNAs that are up-regulated in the prefrontal cortex of human alcoholics and predicted to target genes that are down-regulated in the same region. Although interactions between alcohol-responsive miRNAs and their target genes have been predicted, few studies have validated these predictions.Methods: We measured the expression of GABA A a5 mRNA in the prefrontal and motor cortices of human alcoholics and matched controls using real-time PCR. The expression of miR-203 was measured in a subset of these cases. The predicted interaction of miR-203 and GABRA5 was validated for miR-203 using a luciferase reporter assay.Results: In both frontal and motor cortices, the expression of GABA A a5 was significantly lower in cirrhotic alcoholics compared with controls. Further, the pattern of expression between the groups was significantly different between males and females. The expression of miR-203 was higher in the prefrontal cortex of cirrhotic alcoholics compared with controls and uncomplicated alcoholics. These differences were particularly marked in female cases. Cotransfection of GABRA5 with miR-203 in HEK293T cells reduced luciferase reporter activity.Conclusion: There are sex differences in the expression of GABA A a5 and miR-203 in the brain of human alcoholics which are particularly marked in alcoholics with cirrhosis of the liver. Further, miR-203 may mediate the changes in expression of this GABA A receptor isoform that is brought about by alcohol exposure.

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“…Алкогольная полинейропатия (АП) -неврологическое заболевание, характеризующееся нарушением функций множества периферических нервов вследствие токсического воздействия алкоголя и его метаболитов на нервные волокна и последующего нарушения обменных процессов в них. Эта нозология выделена как отдельное заболевание и кодируется в МКБ-10 как G62.1 [8,13,19]. По отношению к другим полинейропатиям доля алкогольного поражения составляет 36% [4].…”

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Alcoholic polyneuropathy: ways of diagnostics and therapy

2019

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The article is devoted to the analysis of the pathogenetic mechanisms of the formation of alcoholic lesions of the peripheral nervous system. Various clinical forms of alcoholic polyneuropathy are considered, ways to diagnose using modern instrumental and laboratory methods are proposed. The authors analyze the main ways of forming a therapeutic strategy, consider groups of drugs used to treat alcoholic polyneuropathy. The data of own clinical experience of using the preparation of thioctic acid are given.

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Chronic Neurologic Effects of Alcohol

Cited by 62 publications

References 52 publications

Role of Alcohol Drinking in Alzheimer’s Disease, Parkinson’s Disease, and Amyotrophic Lateral Sclerosis

Role of Alcohol Drinking in Alzheimer’s Disease, Parkinson’s Disease, and Amyotrophic Lateral Sclerosis

Sex Differences in the Expression of the α5 Subunit of the GABA_A Receptor in Alcoholics with and without Cirrhosis of the Liver

Alcoholic polyneuropathy: ways of diagnostics and therapy

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Chronic Neurologic Effects of Alcohol

Cited by 62 publications

References 52 publications

Role of Alcohol Drinking in Alzheimer’s Disease, Parkinson’s Disease, and Amyotrophic Lateral Sclerosis

Role of Alcohol Drinking in Alzheimer’s Disease, Parkinson’s Disease, and Amyotrophic Lateral Sclerosis

Sex Differences in the Expression of the α5 Subunit of the GABAA Receptor in Alcoholics with and without Cirrhosis of the Liver

Alcoholic polyneuropathy: ways of diagnostics and therapy

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Product

Resources

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Sex Differences in the Expression of the α5 Subunit of the GABA_A Receptor in Alcoholics with and without Cirrhosis of the Liver