Abstract
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.
Highlights
Introduction and Alcohol UseDual Effects and MechanismsAs the population ages, we need to pay more attention to age-related neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD) and Amyotrophic lateral sclerosis (ALS) [1]
This study suggests that an increased risk of dementia with greater alcohol intake was only associated with people carrying the APOE4 gene
Due to methodological limitations in most studies regarding the U-shaped relationship between alcohol consumption and cognitive function, in addition to other health risks and the social and economic burden associated with alcohol, it is not possible to assume that light-to-moderate consumption of alcohol is, protective toward dementia and/or cognitive decline; the WHO guidelines in 2019 do not favor a general recommendation of its use [43]
Summary
We need to pay more attention to age-related neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD) and Amyotrophic lateral sclerosis (ALS) [1] These neuronal diseases are chronic and progressive, decreasing the quality of life for both patients and their caregivers and bringing a heavy economic burden to society [2]. 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]. On the other hand, some studies show that moderate amounts of ethanol intake produce a neuroprotective effect. Dual Roles of Alcohol Intake in Alzheimer’s Disease (AD) Development and Progression
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