Breast cancer therapies reduce risk of Alzheimer's disease and promote estrogenic pathways and action in brain
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Affiliation
Center for Innovation in Brain Science, University of ArizonaDepartment of Pharmacology, University of Arizona College of Medicine
Medical Scientist Training Program, University of Arizona, College of Medicine
Center of Bioinformatics and Biostatistics, University of Arizona College of Medicine
Department of Neurology, University of Arizona College of Medicine
Issue Date
2023-10-24Metadata
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Elsevier Inc.Citation
Branigan, G. L., Torrandell-Haro, G., Chen, S., Shang, Y., Perez-Miller, S., Mao, Z., ... & Brinton, R. D. (2023). Breast cancer therapies reduce risk of Alzheimer’s disease and promote estrogenic pathways and action in brain. Iscience, 26(11).Journal
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© 2023 The Authors. This is an open access article under the CC BY-NC-ND license.Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
Worldwide, an ever-increasing number of women are prescribed estrogen-modulating therapies (EMTs) for the treatment of breast cancer. In parallel, aging of the global population of women will contribute to risk of both breast cancer and Alzheimer's disease. To address the impact of anti-estrogen therapies on risk of Alzheimer's and neural function, we conducted medical informatic and molecular pharmacology analyses to determine the impact of EMTs on risk of Alzheimer's followed by determination of EMT estrogenic mechanisms of action in neurons. Collectively, these data provide both clinical and mechanistic data indicating that select EMTs exert estrogenic agonist action in neural tissue that are associated with reduced risk of Alzheimer's disease while simultaneously acting as effective estrogen receptor antagonists in breast. © 2023 The AuthorsNote
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2589-0042Version
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Except where otherwise noted, this item's license is described as © 2023 The Authors. This is an open access article under the CC BY-NC-ND license.