Premature menopause and risk of neurological disease: Basic mechanisms and clinical implications

Erin L. Scott, Quan guang Zhang, Ratna K. Vadlamudi, Darrell W. Brann

Research output: Contribution to journalReview article

18 Scopus citations

Abstract

Since basic scientific studies in the 1990s revealed dramatic gender differences in neurological damage from cerebral ischemia, significant evidence has accumulated for a neuroprotective role of ovarian-derived 17β-Estradiol (E2). Intriguingly, observational studies have further suggested that early and prolonged loss of ovarian E2 (premature menopause) leads to a doubled lifetime risk for dementia and a fivefold increased risk of mortality from neurological disorders, but some controversy remains. Here, we briefly summarize and analyze clinical cohort studies assessing the detrimental neurological outcomes of premature menopause. Furthermore, we discuss current basic science studies elucidating the molecular mechanisms underlying the enhanced risk of neurological disease in prematurely menopausal women and the "window of opportunity" for estrogen benefit. Finally, we highlight four critical issues in the field that require collaboration between basic scientists and clinicians for successful resolution, with the ultimate goal of maintaining optimal neurological health in prematurely menopausal women.

Original languageEnglish (US)
Pages (from-to)2-6
Number of pages5
JournalMolecular and Cellular Endocrinology
Volume389
Issue number1-2
DOIs
StatePublished - May 25 2014

Keywords

  • Dementia
  • Estradiol
  • Estrogen
  • Menopause
  • Neurological disease

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology

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