Go with your Gut: How inflammation can speed up Motor Dysfunction in Alpha‑Synuclein Mutant Mice Sonita Mohammadi
Parkinson's Disease (PD) is a neurodegenerative disorder that causes motor symptoms bradykinesia, rigidity, and tremor (de Lau & Breteler, 2006) PD prevalence increases with age and affects 1% of the population over the age of 60 (de Lau & Breteler, 2006). No cure exists and pharmacological therapies are available to diminish the symptoms of the disease. Recent studies suggest gut microbiota can lead to the formation of alpha-synuclein in the enteric nervous system (ENS) and can travel via the vagus nerve to the central nervous system (CNS) (Fitzgerald et al., 2019). Alpha-synuclein is an important factor of Lewy body’s production that comes from in the loss of dopaminergic neurons in the substantia nigra as a cause of PD (Pickrell et al., 2015). Studies are trying to prevent Lewy body development by focusing on alpha-synuclein aggregates (Pickrell et al., 2015). The initial paper by Kishimoto et al., (2019) explored the role of chronic mild gut inflammation and how it plays a role in hastening the onset of motor dysfunction in PD mice (Kishimoto et al., 2019). In their animal model, Parkinson's disease (PD) mice treated with dextran sodium sulfate (DSS) in their water for 12 weeks and observed that the onset of motor disorder sped up (Kishimoto et al., 2019). The PD mutant DSS- treated mice exhibited motor dysfunction considerably earlier than their control group (Kishimoto et al., 2019). This study concluded that a chronic mild increase in gut inflammation speeds up the onset of motor dysfunction in PD. Key words: Parkinson’s disease, inflammation, alpha-synuclein, Enteric neurons, Neuroinflammation
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