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Estrogens and parkinson disease

Neuroprotective, symptomatic, neither, or both?

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Abstract

Parkinson disease is a neurodegenerative disorder caused by substantia nigra dopamine cell death and is characterized by bradykinesia, rigidity, rest tremor, and postural instability. Epidemiologic and clinical studies have suggested that gender and estrogen play a role in modulating Parkinson disease. The etiology of the estrogenic effect is unclear—it may be neuroprotective, symptomatic, or both. Retrospective studies suggest a possible neuroprotective role. Interventional studies have suggested a positive modulatory role or no role at all. While it is difficult to establish whether there is a true neuroprotective benefit of estrogen in the setting of even mild symptomatic benefit, laboratory data suggest such a neuroprotective role. Estrogen may act as an antiapoptotic agent, an antioxidant, or a neurotrophic modulating agent, promoting crosstalk with neurotrophic factors. The selective estrogen receptor modulators (SERMs) may also confer neuroprotection. However, prior to establishing the role of estrogen in Parkinson disease, additional study, including of the SERMs, is warranted.

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Authors and Affiliations

  1. Department of Neurology, Albert Einstein College of Medicine and Beth Israel Medical Center, New York, NY

    Rachel Saunders-Pullman MD, MPH

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  1. Rachel Saunders-Pullman MD, MPH
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Correspondence to Rachel Saunders-Pullman MD, MPH.

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Saunders-Pullman, R. Estrogens and parkinson disease. Endocr 21, 81–87 (2003). https://doi.org/10.1385/ENDO:21:1:81

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  • DOI: https://doi.org/10.1385/ENDO:21:1:81

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