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dc.contributor.authorBranigan, G.L.
dc.contributor.authorTorrandell-Haro, G.
dc.contributor.authorChen, S.
dc.contributor.authorShang, Y.
dc.contributor.authorPerez-Miller, S.
dc.contributor.authorMao, Z.
dc.contributor.authorPadilla-Rodriguez, M.
dc.contributor.authorCortes-Flores, H.
dc.contributor.authorVitali, F.
dc.contributor.authorBrinton, R.D.
dc.date.accessioned2024-03-22T01:37:32Z
dc.date.available2024-03-22T01:37:32Z
dc.date.issued2023-10-24
dc.identifier.citationBranigan, 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).
dc.identifier.issn2589-0042
dc.identifier.doi10.1016/j.isci.2023.108316
dc.identifier.urihttp://hdl.handle.net/10150/671439
dc.description.abstractWorldwide, 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 Authors
dc.language.isoen
dc.publisherElsevier Inc.
dc.rights© 2023 The Authors. This is an open access article under the CC BY-NC-ND license.
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectCancer
dc.subjectNeurology
dc.subjectTherapy
dc.titleBreast cancer therapies reduce risk of Alzheimer's disease and promote estrogenic pathways and action in brain
dc.typeArticle
dc.typetext
dc.contributor.departmentCenter for Innovation in Brain Science, University of Arizona
dc.contributor.departmentDepartment of Pharmacology, University of Arizona College of Medicine
dc.contributor.departmentMedical Scientist Training Program, University of Arizona, College of Medicine
dc.contributor.departmentCenter of Bioinformatics and Biostatistics, University of Arizona College of Medicine
dc.contributor.departmentDepartment of Neurology, University of Arizona College of Medicine
dc.identifier.journaliScience
dc.description.noteOpen access journal
dc.description.collectioninformationThis 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.
dc.eprint.versionFinal Published Version
dc.source.journaltitleiScience
refterms.dateFOA2024-03-22T01:37:32Z


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© 2023 The Authors. This is an open access article under the CC BY-NC-ND license.
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.