The Link between Gut Dysbiosis and Neuroinflammation in Parkinson’s Disease

• Published in: Neuroscience 2020-04, Vol.432, p.160-173
• Main Authors: Baizabal-Carvallo, José Fidel, Alonso-Juarez, Marlene
• Format: Article
• Language: English
• Subjects: alpha-Synuclein - metabolism; butyrate; Dysbiosis; Gastrointestinal Microbiome; Humans; lipopolysaccaride; microbiota; microglia; Parkinson Disease; Parkinson’s disease; Substantia Nigra - metabolism
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/j.neuroscience.2020.02.030

•Patients with Parkinson’s disease have inflammation and intestinal dysbiosis.•Dysbiosis may contribute to increased intestinal and BBB permeability in PD patients.•Bacterial endotoxins may enhance the systemic and CNS inflammation in PD.•Toxins from the GI tract may accelerate degeneration and contribute to dyskinesia.•Modification of dysbiosis may provide benefit in PD, but studies are lacking. Parkinson’s disease (PD) is the second most common neurodegenerative disorder. Despite its high frequency the etiology is still unclear; several lines of evidence show that an inflammatory process is implicated in the pathogenesis of this disorder; where activation of brain microglia plays a central role in the damage of dopaminergic neurons of the substantia nigra. Such inflammation has been attributed to the toxic effect of aggregated α-synuclein; however, evidence also implicates an altered gut microbiota (dysbiosis) through the systemic release of endotoxins such as lipopolysaccharide and other metabolic products. This exposure may be enhanced by increased permeability of the intestinal (“leaky gut”) and the blood brain barrier; enhancing the entrance of microbiota-produced substances into the central nervous system. In this manuscript, we explore the evidence from clinical and basic science implicating microglia activation by gut dysbiosis and how this phenomenon may impact in the symptomatology and progression of PD.