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Author Spotlight: Exploring Non-Motor Symptoms in Parkinson's Disease
Published on: September 22, 2023
Dysbiosis in Parkinson's disease might be triggered by certain antibiotics
Gábor Ternák1, Dániel Kuti2, Krisztina J Kovács3
1University of Pécs, Faculty of Medicine, Chair of Migration Health, Pécs, Szigeti út 12, Pécs 7624, Hungary.
Abstract:
Parkinson's disease (PD) is a neurodegenerative amyloid disorder with debilitating motor symptoms due to the loss of dopamine-synthesizing, basal ganglia-projecting neurons in the substantia nigra. An interesting feature of the disease is that most of PD patients have gastrointestinal problems and bacterial dysbiosis, years before the full expression of motor symptoms. We hypothesized that antibiotic consumption might be a contributing factor of gut microbiome dysbiosis in PD, favoring curli-producing Enterobacteria. Curli is a bacterial α-synuclein (αSyn) which is deposited first in the enteric nervous system and amyloid deposits are propagated in a prion like manner to the central nervous system. In addition, antibiotics result in a low-grade systemic inflammation, which also contributes to damage of neurons in enteric- and central nervous system. To support our hypothesis, by comparing PD prevalence change with antibiotic consumption data in EU countries, we found significant positive correlation between use narrow spectrum penicillin + penicillinase resistant penicillin and increased prevalence of the disease.
Insights
Antibiotic use, particularly specific penicillins, may contribute to Parkinson's disease (PD) by causing gut dysbiosis and inflammation. This gut microbiome imbalance may promote the spread of amyloid aggregates implicated in PD pathogenesis.
Area of Science:
- Neuroscience
- Microbiology
- Epidemiology
Background:
- Parkinson's disease (PD) is a neurodegenerative disorder characterized by motor symptoms resulting from neuronal loss.
- Gastrointestinal issues and bacterial dysbiosis are common in PD patients years before motor symptom onset.
- Gut microbiome alterations may precede and potentially contribute to PD pathogenesis.
Purpose of the Study:
- To investigate the hypothesis that antibiotic consumption contributes to gut dysbiosis in Parkinson's disease.
- To explore the role of antibiotics in promoting curli-producing Enterobacteria and subsequent amyloid propagation.
- To examine the correlation between antibiotic use and PD prevalence in European countries.
Main Methods:
- Comparative analysis of PD prevalence data and antibiotic consumption statistics across EU countries.
- Focus on the association between specific antibiotic classes (narrow-spectrum penicillin + penicillinase-resistant penicillin) and PD prevalence.
- Literature review on the role of bacterial amyloid curli and systemic inflammation in neurodegeneration.
Main Results:
- A significant positive correlation was observed between the consumption of narrow-spectrum penicillin and penicillinase-resistant penicillin and increased PD prevalence.
- Antibiotic use can induce systemic inflammation and gut microbiome dysbiosis.
- Curli, a bacterial amyloid, may play a role in the prion-like spread of alpha-synuclein pathology from the gut to the central nervous system.
Conclusions:
- Antibiotic consumption, specifically certain penicillins, is potentially linked to an increased prevalence of Parkinson's disease.
- Gut dysbiosis induced by antibiotics may facilitate the development and progression of PD.
- Further research is warranted to elucidate the precise mechanisms linking antibiotic exposure, gut microbiome, and Parkinson's disease.
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