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Diet in Parkinson’s Disease: Critical Role for the Microbiome
Open accessAbstract
Background. Parkinson’s disease (PD) is the most common movement disorder affecting up to 1% of the population above the age of 60 and 4–5% of those above the age of 85. Little progress has been made on efforts to prevent disease development or halt disease progression. Diet has emerged as a potential factor that may prevent the development or slow the progression of PD. In this review, we discuss evidence for a role for the intestinal microbiome in PD and how diet-associated changes in the microbiome may be a viable approach to prevent or modify disease progression. Methods. We reviewed studies demonstrating that dietary components/foods were related to risk for PD. We reviewed evidence for the dysregulated intestinal microbiome in PD patients including abnormal shifts in the intestinal microbiota composition (i.e., dysbiosis) characterized by a loss of short chain fatty acid (SCFA) bacteria and increased lipopolysaccharide (LPS) bacteria. We also examined several candidate mechanisms by which the microbiota can influence PD including the NLRP3 inflammasome, insulin resistance, mitochondrial function, vagal nerve signaling. Results. The PD-associated microbiome is associated with decreased production of SCFA and increased LPS and it is believed that these changes may contribute to the development or exacerbation of PD. Diet robustly impacts the intestinal microbiome and the Western diet is associated with increased risk for PD whereas the Mediterranean diet (including high intake of dietary fiber) decreases PD risk. Mechanistically this may be the consequence of changes in the relative abundance of SCFA-producing or LPS-containing bacteria in the intestinal microbiome with effects on intestinal barrier function, endotoxemia (i.e., systemic LPS), NLRP3 inflammasome activation, insulin resistance, and mitochondrial dysfunction, and the production of factors such as glucagon like peptide 1 (GLP-1) and brain derived neurotrophic factor (BDNF) as well as intestinal gluconeogenesis. Conclusions. This review summarizes a model of microbiota-gut-brain-axis regulation of neuroinflammation in PD including several new mechanisms. We conclude with the need for clinical trials in PD patients to test this model for beneficial effects of Mediterranean based high fiber diets.
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“The high-fat, low-fiber Western diet has been associated with an increased risk of Parkinson’s disease.”
From Mediterranean Diet as an Antioxidant: The Impact on Metabolic Health and Overall Wellbeing (2021) · cites this paper as [112]
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Metadata
- Authors
- Jackson, A., Forsyth, C. B., Shaikh, M., Voigt, R. M., Engen, P. A., Ramirez, V., & Keshavarzian, A.
- Affiliations
- Rush University Medical Center (US)
- Corresponding author
- Keshavarzian, Ali
- Venue
- Frontiers in Neurology
- Publisher
- Frontiers Media SA
- Published
- 2019-12-10
- Volume
- 10
- Pages
- 1245-1245
- ISSN
- 1664-2295 (ISSN-L)
- PMC
- PMC6915094
- OpenAlex
- W2995752611
- Cited by
- 145
- References
- 328
- Citations by year
- 2026: 16 · 2025: 22 · 2024: 21 · 2023: 17 · 2022: 35 · 2021: 18 · 2020: 13 · 2019: 1
- FWCI
- 1.48
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Neurology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- U.S. Department of Defense
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Nutritional Studies and Diet
- Keywords
- Parkinson's disease, diet, gut microbiota, dysbiosis, short-chain fatty acids, lipopolysaccharide, Western diet, Mediterranean diet, dietary fiber, NLRP3 inflammasome, insulin resistance, mitochondrial dysfunction, microbiota-gut-brain axis, neuroinflammation, endotoxemia, intestinal barrier function, glucagon-like peptide-1, brain-derived neurotrophic factor, intestinal gluconeogenesis
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