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Downstream signal transductions are consequent of hormone-receptor interactions, and EDCs have been found to perturb both nuclear steroid receptors and cell surface membrane receptors (La Merrill et al., 2020)

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A study on genetic linkages between aberrant lipid metabolism and PD directly demonstrates that glucocerebrosidase and sphingomyelin phosphodiesterase 1 mutations enhance PD risk in humans, and that galactosylceramide beta hydrolase function loss increases -synuclein aggregation and accumulation in experimental murine models

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