Dysbiosis significantly elevates the probability of altered affective function in Alzheimer disease (AD)
Language English Country United States Media print-electronic
Document type Journal Article, Review
PubMed
40414630
DOI
10.1016/bs.irn.2025.04.005
PII: S0074-7742(25)00020-0
Knihovny.cz E-resources
- Keywords
- Gut microbiota, Insulin resistance, Neurodegenerative disorders, Oxidative stress, Probiotics,
- MeSH
- Alzheimer Disease * microbiology metabolism physiopathology MeSH
- Dysbiosis * complications metabolism MeSH
- Humans MeSH
- Probiotics therapeutic use MeSH
- Gastrointestinal Microbiome * physiology MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
Changes in the makeup of gut microbiota are linked to many neuropsychiatric diseases. Although the exact connection between gut dysbiosis and brain dysfunction is not yet fully understood, but recent data suggests that gut dysbiosis may contribute to the development of Alzheimer's disease (AD) by promoting neuroinflammation, insulin resistance, oxidative stress, and amyloid-beta (Aβ) aggregation. Gut dysbiosis in animal models is primarily characterized by an elevated ratio of Firmicutes/Bacteroidetes which may lead to the accumulation of amyloid precursor protein (APP) in the intestine, in the early stages of AD. Probiotics play a significant role in preventing against the symptoms of AD by restoring gut-brain homeostasis. This chapter provides an overview of the gut microbiota and its dysregulation in etiology of AD. Moreover, novel insights into alteration of the composition of gut microbiota as a preventive or therapeutic approach to AD are discussed.
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