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These potential therapies exert specific effects by targeting abnormal -syn aggregation, correcting brain iron dyshomeostasis, modulating cellular signaling pathways, among other mechanisms, and have demonstrated significant neuroprotective effects in preclinical studies (Table 2)

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Estrogens signal through myriad pathways, including genomic mechanisms mediated by two nuclear receptors (ER and ER) that recruit various co-regulatory proteins and induce transcription at estrogen response elements (EREs), in addition to other promoters by tethering to transcription factors (e.g., AP-1 and NF-B)