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Damage-associated molecular patterns (DAMPs) released by injured neurons, such as pathological proteins, extracellular ATP, and high mobility group box 1 protein (HMGB1), can activate pattern recognition receptors on the glial cell surface, triggering neuroinflammation ( In conclusion, neuroinflammation serves as a critical bridge connecting peripheral pathology and central symptoms in MG, while age-related factors significantly influence MG onset and progression through immunosenescence, neuromuscular junction degeneration, and activation of the neuroinflammation-oxidative stress-mitochondrial dysfunction axis

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There is, however, compelling evidence to support a mode of action for tumour induction based on metabolism of chloroform by the target cell population, followed by cytotoxicity of oxidative metabolites and regenerative cell proliferation