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Cited by 156Alcohol Consumption and Health EffectsAlzheimer's disease research and treatmentsAlcoholism and Thiamine Deficiency

The DOI matches its Crossref record; 137 of the 138 references it cites were found in a registry or an index.

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

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Peng, Bin, Yang, Qiang, B Joshi, Rachna, Liu, Yuancai, Akbar, Mohammed, Song, Byoung-Joon, Zhou, Shuanhu, Wang, Xin·2020·International Journal of Molecular Sciences
DOI 10.3390/ijms21072316PMC PMC7177420
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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.

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Figure 1 The harmful effects and mechanisms of alcohol. Chronic and excessive alcohol consumption alters gut microbiota, increases intestinal permeability (leaky gut) and causes brain damage. Lipopolysaccharide (LPS) and peptidoglycan (PGN) from the gut lumen to the systemic circulation are recognized by toll-like receptors (TLRs) expressed by immune cells and induce structural plasticity changes such as ionized calcium-binding adapter molecule 1 (IBA1) and glial fibrillary acidic protein (GFAP), as well as an inflammatory response by the nuclear factor-ĸB (NF-ĸB) pathway. The inflammatory cytokines and mediators, such as interleukin 4 (IL-4), IL-10, reactive oxygen species (ROS), inducible NO synthase (iNOS), IL-1β, IL-6, tumor necrosis factor (TNF)-α, C-C Motif Chemokine Ligand 2 (CCL2) and cyclooxygenase-2 (COX-2) may result in altered neuronal functions and angiogenesis.
Figure 1 The harmful effects and mechanisms of alcohol. Chronic and excessive alcohol consumption alters gut microbiota, increases intestinal permeability (leaky gut) and causes brain damage. Lipopolysaccharide (LPS) and peptidoglycan (PGN) from the gut lumen to the systemic circulation are recognized by toll-like receptors (TLRs) expressed by immune cells and induce structural plasticity changes such as ionized calcium-binding adapter molecule 1 (IBA1) and glial fibrillary acidic protein (GFAP), as well as an inflammatory response by the nuclear factor-ĸB (NF-ĸB) pathway. The inflammatory cytokines and mediators, such as interleukin 4 (IL-4), IL-10, reactive oxygen species (ROS), inducible NO synthase (iNOS), IL-1β, IL-6, tumor necrosis factor (TNF)-α, C-C Motif Chemokine Ligand 2 (CCL2) and cyclooxygenase-2 (COX-2) may result in altered neuronal functions and angiogenesis.CC BY · PubMed Central
Figure 2 Dual roles of alcohol drinking in Alzheimer’s disease (AD), Parkinson’s disease (PD) and Amyotrophic lateral sclerosis (ALS). In AD, low or moderate concentrations of ethanol protect against the damage induced by Aβ. Excessive amounts of ethanol increase accumulation of Aβ and Tau phosphorylation [35]. In PD, most studies show that alcohol decreases levels of DA and increases the levels of αSYN. One study suggested that the high drinking alko alcohol (AA) rats showed lower stimulated DA levels and more efficient DA re-uptake in the nucleus accumbens core than the low drinking non-alcohol (ANA) rats did. In the same structure, AA rats also had significantly higher levels of α-syn. No differences were found in the effects of two different doses of ethanol (0.1 and 3.0 g/kg) [42]. A meta-analysis concluded that beer, but not wine and liquor, probably protected against PD [36]. In ALS, red wine extract intake was reported to prolong the lifespan of mSOD1-transgenic mice and protected neurons from apoptosis in vitro. There is a dysfunction of the glutamatergic excitatory system in ALS, and chronic alcohol intake involves changes in glutamatergic transmission. The association between alcohol and ALS is still unclear. Abbreviations: Aβ: β-amyloid; DA: Dopamine; mSOD1: Mutated SOD1.
Figure 2 Dual roles of alcohol drinking in Alzheimer’s disease (AD), Parkinson’s disease (PD) and Amyotrophic lateral sclerosis (ALS). In AD, low or moderate concentrations of ethanol protect against the damage induced by Aβ. Excessive amounts of ethanol increase accumulation of Aβ and Tau phosphorylation [35]. In PD, most studies show that alcohol decreases levels of DA and increases the levels of αSYN. One study suggested that the high drinking alko alcohol (AA) rats showed lower stimulated DA levels and more efficient DA re-uptake in the nucleus accumbens core than the low drinking non-alcohol (ANA) rats did. In the same structure, AA rats also had significantly higher levels of α-syn. No differences were found in the effects of two different doses of ethanol (0.1 and 3.0 g/kg) [42]. A meta-analysis concluded that beer, but not wine and liquor, probably protected against PD [36]. In ALS, red wine extract intake was reported to prolong the lifespan of mSOD1-transgenic mice and protected neurons from apoptosis in vitro. There is a dysfunction of the glutamatergic excitatory system in ALS, and chronic alcohol intake involves changes in glutamatergic transmission. The association between alcohol and ALS is still unclear. Abbreviations: Aβ: β-amyloid; DA: Dopamine; mSOD1: Mutated SOD1.CC BY · PubMed Central

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Metadata

Authors
Peng, B., Yang, Q., B Joshi, R., Liu, Y., Akbar, M., Song, B.-J., Zhou, S., & Wang, X.
Affiliations
  • Brigham and Women's Hospital (US)
  • Hubei Provincial Key Lab for Quality and Safety of Traditional Chinese Medicine Health Food, Jing Brand Research Institute, Daye 435100, China
  • Departments of Neurosurgery, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA
  • National Institutes of Health (US)
Corresponding author
  • Zhou, Shuanhu
  • Wang, Xin
ORCID
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2020-03-27
Volume
21
Issue
7
Pages
2316
ISSN
1422-0067 (ISSN-L)
DOI
10.3390/ijms21072316
PMC
PMC7177420
OpenAlex
W3013624048
Cited by
156
References
138
Citations by year
2026: 13 · 2025: 38 · 2024: 34 · 2023: 30 · 2022: 24 · 2021: 15 · 2020: 2
FWCI
2.72
Type
journal article
Language
en
Open access
Licence
Locations
  • International Journal of Molecular Sciences (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Brigham and Women's Hospital
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Clinical Neurology › Alcoholism and Thiamine Deficiency
Keywords
alcohol consumption, neurodegenerative diseases, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, ethanol, amyloid-beta, tau phosphorylation, excitotoxicity, oxidative stress, dopamine neurotoxicity, CYP2E1, alpha-synuclein, environmental risk factors
MeSH terms
Alcohol Drinking, Ethanol, Alzheimer Disease, Amyotrophic Lateral Sclerosis, Animals, Brain, Cell Line, Humans, Neurons, Parkinson Disease, Risk Factors, Amyloid beta-Peptides, Oxidative Stress, Disease Progression, Neurodegenerative Diseases, alpha-Synuclein

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