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Gut permeability and microbiota in Parkinson's disease: role of depression, tryptophan catabolites, oxidative and nitrosative stress and melatonergic pathways

Anderson, G., Seo, M., Berk, M., Carvalho, A.F. and Maes, M. 2016, Gut permeability and microbiota in Parkinson's disease: role of depression, tryptophan catabolites, oxidative and nitrosative stress and melatonergic pathways, Current pharmaceutical design, vol. 22, no. 40, pp. 6142-6151, doi: 10.2174/138161282266616090.

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Title Gut permeability and microbiota in Parkinson's disease: role of depression, tryptophan catabolites, oxidative and nitrosative stress and melatonergic pathways
Author(s) Anderson, G.
Seo, M.
Berk, M.ORCID iD for Berk, M. orcid.org/0000-0002-5554-6946
Carvalho, A.F.
Maes, M.
Journal name Current pharmaceutical design
Volume number 22
Issue number 40
Start page 6142
End page 6151
Total pages 10
Publisher Bentham Science Publishers
Place of publication Bussum, The Netherlands
Publication date 2016
ISSN 1873-4286
Keyword(s) Parkinson disease
gut microbiota
gut permeability
leaky gut
melatonin
alpha 7 nicotinic
tryptophan catabolites
Summary 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.
Language eng
DOI 10.2174/138161282266616090
Field of Research 110999 Neurosciences not elsewhere classified
1115 Pharmacology And Pharmaceutical Sciences
Socio Economic Objective 920111 Nervous System and Disorders
HERDC Research category C1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2016, Bentham Science Publishers
Persistent URL http://hdl.handle.net/10536/DRO/DU:30091301

Document type: Journal Article
Collection: School of Medicine
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