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Intestinal Inflammation and Parkinson's Disease.

ABSTRACT: Parkinson's disease (PD) is the second most common neurodegenerative disease which significantly influences the life quality of patients. The protein α-synuclein plays an important driving role in PD occurrence and development. Braak's hypothesis suggests that α-synuclein is produced in intestine, and then spreads into the central nervous system through the vagus nerve. The abnormal expression of α-synuclein has been found in inflammatory bowel disease (IBD). Intestinal inflammation and intestinal dysbiosis have been involved in the occurrence and development of PD. The present review aimed to summarize recent advancements in studies focusing on intestinal inflammation and PD, especially the mechanisms through which link intestinal inflammation and PD. The intestinal dysfunctions such as constipation have been introduced as non-motor manifestations of PD. The possible linkages between IBD and PD, including genetic overlaps, inflammatory responses, intestinal permeability, and intestinal dysbiosis, are mainly discussed. Although it is not confirmed whether PD starts from intestine, intestinal dysfunction may affect intestinal microenvironment to influence central nervous system, including the α-synuclein pathologies and systematic inflammation. It is expected to develop some new strategies in the diagnosis and treatment of PD from the aspect of intestine. It may also become an exciting direction to find better ways to regulate the composition of gut microorganism to treat PD.

SUBMITTER: Li Y

PROVIDER: S-EPMC8612622 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Parkinson's disease (PD) is a common degenerative disease of the central nervous system. Although some drugs can alleviate the progress of PD, their long-term use will lead to complications, so it is still necessary to find new drugs to delay or cure PD effectively. In view of the difficulty in developing new drugs, it is imperative to discover new functions of existing compounds that could be used to treat PD. In this study, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was used to induce PD symptoms in a mouse model. Subsequently, these mice were treated with the antibiotic ceftriaxone. Ceftriaxone alleviated the behavioural and neuropathological changes induced by MPTP, downregulated the expression of glial fibrillary acidic protein (GFAP) and ionised calcium-binding adapter molecule 1 (Iba1) as markers of astroglia and microglia, respectively, and reduced the expression of neuroinflammation-related Toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), and phosphorylated nuclear factor kappa-B (p-NF-κB)/NF-κB in the brain of PD mice. In addition, ceftriaxone reduced the abundance of pathogenic bacteria of the genus Proteus and increased the abundance of probiotic Akkermansia. Finally, ceftriaxone treatment increased the expression of the tight junction proteins zona occludens-1(ZO-1) and occludin in the colon, decreased the expression of the inflammation-related proteins TLR4, MyD88, and NF-κB in the colon, and decreased the serum concentration of the proinflammatory cytokines interleukin-1β (IL-1β), IL-6, and tumour necrosis factor-α (TNF-α). These results indicate that ceftriaxone had a neuroprotective effect on MPTP-induced PD mice, and its neuroprotective effect could be through regulating inflammation and intestinal microbiota. While we showed that ceftriaxone exerts a neuroprotective effect in an MPTP-induced PD mouse model, our findings are limited to the short-term effects of ceftriaxone. Additional work using transgenic mice is required to determine the long-term effects of ceftriaxone. In addition, the dose and frequency of ceftriaxone use should be evaluated.

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Intestinal Inflammation and Parkinson's Disease.

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