Role of Alcohol Drinking in Alzheimer's Disease, Parkinson's Disease, and Amyotrophic Lateral Sclerosis
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...
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| Veröffentlicht in: | International journal of molecular sciences 2020-03, Vol.21 (7), p.2316 |
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| description | 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 (
) 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. |
| doi_str_mv | 10.3390/ijms21072316 |
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) 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.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms21072316</identifier><identifier>PMID: 32230811</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Alcohol Drinking - adverse effects ; Alcohol use ; alpha-Synuclein ; Alzheimer Disease - chemically induced ; Alzheimer Disease - metabolism ; Alzheimer's disease ; Amyloid beta-Peptides - toxicity ; Amyotrophic lateral sclerosis ; Amyotrophic Lateral Sclerosis - chemically induced ; Amyotrophic Lateral Sclerosis - metabolism ; Animals ; Brain - drug effects ; Brain - metabolism ; Brain damage ; Brain injury ; Brain research ; Cell Line ; Cognitive ability ; Cytochrome P450 ; Cytochromes P450 ; Dementia ; Disease ; Disease Progression ; Dopamine ; Drinking ; Drinking behavior ; Epidemiology ; Ethanol ; Ethanol - adverse effects ; Ethanol - toxicity ; Etiology ; Excitotoxicity ; Executive function ; Health risk assessment ; Hippocampus ; Humans ; Malnutrition ; Microbiota ; Neurodegenerative Diseases - chemically induced ; Neurons - drug effects ; Neurons - metabolism ; Neurotoxicity ; Older people ; Oxidative stress ; Oxidative Stress - drug effects ; Parkinson Disease - metabolism ; Parkinson's disease ; Pathogenesis ; Phosphorylation ; Population ; Population studies ; Review ; Risk Factors ; Studies ; Synuclein ; Tau protein ; β-Amyloid</subject><ispartof>International journal of molecular sciences, 2020-03, Vol.21 (7), p.2316</ispartof><rights>2020. This work is licensed under http://creativecommons.org/licenses/by/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2020 by the authors. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-665929755ddf9cae356d88384b82718a2ba3b2af43b09e956b6a21647710328c3</citedby><cites>FETCH-LOGICAL-c455t-665929755ddf9cae356d88384b82718a2ba3b2af43b09e956b6a21647710328c3</cites><orcidid>0000-0002-3954-3497</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7177420/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7177420/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32230811$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Peng, Bin</creatorcontrib><creatorcontrib>Yang, Qiang</creatorcontrib><creatorcontrib>B Joshi, Rachna</creatorcontrib><creatorcontrib>Liu, Yuancai</creatorcontrib><creatorcontrib>Akbar, Mohammed</creatorcontrib><creatorcontrib>Song, Byoung-Joon</creatorcontrib><creatorcontrib>Zhou, Shuanhu</creatorcontrib><creatorcontrib>Wang, Xin</creatorcontrib><title>Role of Alcohol Drinking in Alzheimer's Disease, Parkinson's Disease, and Amyotrophic Lateral Sclerosis</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>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 (
) 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.</description><subject>Alcohol Drinking - adverse effects</subject><subject>Alcohol use</subject><subject>alpha-Synuclein</subject><subject>Alzheimer Disease - chemically induced</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer's disease</subject><subject>Amyloid beta-Peptides - toxicity</subject><subject>Amyotrophic lateral sclerosis</subject><subject>Amyotrophic Lateral Sclerosis - chemically induced</subject><subject>Amyotrophic Lateral Sclerosis - metabolism</subject><subject>Animals</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>Brain damage</subject><subject>Brain injury</subject><subject>Brain research</subject><subject>Cell Line</subject><subject>Cognitive ability</subject><subject>Cytochrome P450</subject><subject>Cytochromes P450</subject><subject>Dementia</subject><subject>Disease</subject><subject>Disease Progression</subject><subject>Dopamine</subject><subject>Drinking</subject><subject>Drinking behavior</subject><subject>Epidemiology</subject><subject>Ethanol</subject><subject>Ethanol - adverse effects</subject><subject>Ethanol - toxicity</subject><subject>Etiology</subject><subject>Excitotoxicity</subject><subject>Executive function</subject><subject>Health risk assessment</subject><subject>Hippocampus</subject><subject>Humans</subject><subject>Malnutrition</subject><subject>Microbiota</subject><subject>Neurodegenerative Diseases - chemically induced</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neurotoxicity</subject><subject>Older people</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Parkinson Disease - metabolism</subject><subject>Parkinson's disease</subject><subject>Pathogenesis</subject><subject>Phosphorylation</subject><subject>Population</subject><subject>Population studies</subject><subject>Review</subject><subject>Risk Factors</subject><subject>Studies</subject><subject>Synuclein</subject><subject>Tau protein</subject><subject>β-Amyloid</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpVUV1LwzAUDaK4OX3zWQI--LJqPpqmeRHG5hcMFD-eQ9qma2bbzKQT5q83sin16V7OOZx7LgeAU4wuKRXoyiwbTzDihOJkDwxxTEiEUML3e_sAHHm_RIhQwsQhGFBCKEoxHoLFs601tCWc1LmtbA1nzrTvpl1A0wbsq9Km0e7Cw5nxWnk9hk_KBd7btg-qtoCTZmM7Z1eVyeFcddqpGr7ktXbWG38MDkpVe32ymyPwdnvzOr2P5o93D9PJPMpjxrooSZgggjNWFKXIlaYsKdKUpnGWEo5TRTJFM6LKmGZIaMGSLFEEJzHnGFGS5nQErre-q3XW6CLXbRdyyJUzjXIbaZWR_5nWVHJhPyXHnMcEBYPznYGzH2vtO7m0a9eGzJLQlCGOqWBBNd6q8vCdd7r8u4CR_KlF9msJ8rN-qj_xbw_0G4vqiK8</recordid><startdate>20200327</startdate><enddate>20200327</enddate><creator>Peng, Bin</creator><creator>Yang, Qiang</creator><creator>B Joshi, Rachna</creator><creator>Liu, Yuancai</creator><creator>Akbar, Mohammed</creator><creator>Song, Byoung-Joon</creator><creator>Zhou, Shuanhu</creator><creator>Wang, Xin</creator><general>MDPI AG</general><general>MDPI</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-3954-3497</orcidid></search><sort><creationdate>20200327</creationdate><title>Role of Alcohol Drinking in Alzheimer's Disease, Parkinson's Disease, and Amyotrophic Lateral Sclerosis</title><author>Peng, Bin ; Yang, Qiang ; B Joshi, Rachna ; Liu, Yuancai ; Akbar, Mohammed ; Song, Byoung-Joon ; Zhou, Shuanhu ; Wang, Xin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-665929755ddf9cae356d88384b82718a2ba3b2af43b09e956b6a21647710328c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Alcohol Drinking - 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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 (
) 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.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>32230811</pmid><doi>10.3390/ijms21072316</doi><orcidid>https://orcid.org/0000-0002-3954-3497</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | International journal of molecular sciences, 2020-03, Vol.21 (7), p.2316 |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Alcohol Drinking - adverse effects Alcohol use alpha-Synuclein Alzheimer Disease - chemically induced Alzheimer Disease - metabolism Alzheimer's disease Amyloid beta-Peptides - toxicity Amyotrophic lateral sclerosis Amyotrophic Lateral Sclerosis - chemically induced Amyotrophic Lateral Sclerosis - metabolism Animals Brain - drug effects Brain - metabolism Brain damage Brain injury Brain research Cell Line Cognitive ability Cytochrome P450 Cytochromes P450 Dementia Disease Disease Progression Dopamine Drinking Drinking behavior Epidemiology Ethanol Ethanol - adverse effects Ethanol - toxicity Etiology Excitotoxicity Executive function Health risk assessment Hippocampus Humans Malnutrition Microbiota Neurodegenerative Diseases - chemically induced Neurons - drug effects Neurons - metabolism Neurotoxicity Older people Oxidative stress Oxidative Stress - drug effects Parkinson Disease - metabolism Parkinson's disease Pathogenesis Phosphorylation Population Population studies Review Risk Factors Studies Synuclein Tau protein β-Amyloid |
| title | Role of Alcohol Drinking in Alzheimer's Disease, Parkinson's Disease, and Amyotrophic Lateral Sclerosis |
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