Unlocking the Inflammatory Clues of Parkinson’s Disease

Published on July 4, 2022

Picture this: you’re a superhero defending your brain from evil invaders. But sometimes, your immune system gets a little too excited and creates more problems than it solves. That’s what happens with neuroinflammation in Parkinson’s disease (PD). In this review, scientists dive into pre-clinical studies to discover the molecular pathways behind PD’s neuroinflammation. They find out that a protein called α-synuclein, known for its role in PD, can activate mast cells and contribute to the inflammation. They also uncover a common mechanism involving the NF-kB pathway that gets activated by neurotoxins and bacterial lipopolysaccharide (LPS). Additionally, they identify another culprit molecule, microsomal prostaglandin E synthase-1 (mPGES-1), in a specific PD model using 6-hydroxydopamine (6-OHDA). These discoveries shed light on how our immune responses can turn against us when they go haywire. So if you want to dig deeper into the intricate world of neuroinflammation in PD, check out the full research article!

Parkinson’s disease (PD), the second most common neurodegenerative disorder, is characterized by neuroinflammation, formation of Lewy bodies, and progressive loss of dopaminergic neurons in the substantia nigra of the brain. In this review, we summarize evidence obtained by animal studies demonstrating neuroinflammation as one of the central pathogenetic mechanisms of PD. We also focus on the protein factors that initiate the development of PD and other neurodegenerative diseases. Our targeted literature search identified 40 pre-clinical in vivo and in vitro studies written in English. Nuclear factor kappa B (NF-kB) pathway is demonstrated as a common mechanism engaged by neurotoxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 6-hydroxydopamine (6-OHDA), as well as the bacterial lipopolysaccharide (LPS). The α-synuclein protein, which plays a prominent role in PD neuropathology, may also contribute to neuroinflammation by activating mast cells. Meanwhile, 6-OHDA models of PD identify microsomal prostaglandin E synthase-1 (mPGES-1) as one of the contributors to neuroinflammatory processes in this model. Immune responses are used by the central nervous system to fight and remove pathogens; however, hyperactivated and prolonged immune responses can lead to a harmful neuroinflammatory state, which is one of the key mechanisms in the pathogenesis of PD.

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