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Gut permeability and microbiota in parkinson’s disease: Role of depression, tryptophan catabolites, oxidative and nitrosative stress and melatonergic pathways

Version 2 2024-06-03, 19:27
Version 1 2017-02-15, 12:29
journal contribution
posted on 2024-06-03, 19:27 authored by G Anderson, M Seo, Michael BerkMichael Berk, AF Carvalho, M Maes
BACKGROUND: Increased gut permeability (leaky gut) and alterations in gut microbiota are now widely accepted as relevant to the etiology, course and treatment of many neuropsychiatric disorders, including Parkinson disease (PD). Although a wide array of data on the biological underpinnings of PD has not yet been linked to such gut-associated changes, increased gut permeability and dysregulated microbiota alter many pathways germane to PD. METHODS: In this article we review and integrate these wider biological changes in PD, including increased oxidative and nitrosative stress, immune-inflammatory processes, tryptophan catabolites and alterations in serotoninergic and melatoninergic pathways. RESULTS: These wider biological changes in PD are compatible with alterations in gut permeability and changes in gut microbiota. By driving tryptophan down the kynurenine pathway, pro-inflammatory cytokines and chronic stress-driven activation of the hypothalamic-pituitary-adrenal axis decrease the availability of serotonin as a precursor for activation of the melatonergic pathways. CONCLUSION: Decreased local melatonin synthesis in glia, gut, neuronal and immune cells is likely to be important to the etiology, course and management of PD.

History

Journal

Current Pharmaceutical Design

Volume

22

Pagination

6142-6151

Location

United Arab Emirates

ISSN

1381-6128

eISSN

1873-4286

Language

English

Publication classification

C Journal article, C1 Refereed article in a scholarly journal

Copyright notice

2016, Bentham Science Publishers

Issue

40

Publisher

BENTHAM SCIENCE PUBL LTD