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Cytokine expression levels in ALS: A potential link between inflammation and BMAA-triggered protein misfolding
Nara Michaelson1, Dominic Facciponte2, Walter Bradley3
1Dartmouth-Hitchcock Medical Center, Lebanon, NH, USA; Geisel School of Medicine at Dartmouth, Hanover, NH, USA.
Abstract:
Recently, it has been shown that proinflammatory cytokines play a complex and important role in the pathogenesis of many neurological disorders, including amyotrophic lateral sclerosis (ALS). To help facilitate future discoveries and more effective treatment strategies, we highlight the role that both innate and adaptive immune systems play in ALS and summarize the main observations that relate to cytokine expression levels in this disease. Furthermore, we propose a mechanism by which a known neurotoxin, β-N-methylamino-l-alanine (BMAA), may trigger this cytokine expression profile through motor neuron protein misfolding and subsequent NLRP3 (nucleotide-binding domain (NOD)-like receptor protein 3) inflammasome activation.
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