The Impact of Alcohol-Induced Dysbiosis on Diseases and Disorders of the Central Nervous System.
Addiction
Alzheimer’s disease
Microbiota
Neuroinflammation
Parkinson’s disease
QIAGEN Ingenuity Pathway Analysis
Journal
Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology
ISSN: 1557-1904
Titre abrégé: J Neuroimmune Pharmacol
Pays: United States
ID NLM: 101256586
Informations de publication
Date de publication:
06 2022
06 2022
Historique:
received:
11
06
2021
accepted:
11
11
2021
pubmed:
30
11
2021
medline:
15
12
2022
entrez:
29
11
2021
Statut:
ppublish
Résumé
The human digestive tract contains a diverse and abundant microbiota that is important for health. Excessive alcohol use can disrupt the balance of these microbes (known as dysbiosis), leading to elevated blood endotoxin levels and systemic inflammation. Using QIAGEN Ingenuity Pathway Analysis (IPA) bioinformatics tool, we have confirmed that peripheral endotoxin (lipopolysaccharide) mediates various cytokines to enhance the neuroinflammation signaling pathway. The literature has identified alcohol-mediated neuroinflammation as a possible risk factor for the onset and progression of neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD), and psychiatric disorders such as addiction to alcohol and other drugs. In this review, we discuss alcohol-use-induced dysbiosis in the gut and other body parts as a causal factor in the progression of Central Nervous System (CNS) diseases including neurodegenerative disease and possibly alcohol use disorder.
Identifiants
pubmed: 34843074
doi: 10.1007/s11481-021-10033-4
pii: 10.1007/s11481-021-10033-4
doi:
Types de publication
Journal Article
Review
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
131-151Subventions
Organisme : NIDA NIH HHS
ID : DA046258
Pays : United States
Organisme : NIAAA NIH HHS
ID : AA026071
Pays : United States
Informations de copyright
© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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