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Interestingly, external iron supplementation has been shown to inhibit M1 polarization by downregulating proinflammatory mediators and iNOS expression through STAT1 inhibition, without impairing phagocytic capacityM1 (108)

This protein is misfolded and accumulates to form Lewy bodies (van Ham et al., 2009), and other mechanisms such as oxidative stress, mitochondrial dysfunction, disrupted axonal transport, glutamate neurotoxicity, cellular senescence, and neuroinflammation are included in its pathogenesis (Poewe et al., 2017)