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The Impact of Estradiol on Neurogenesis and Cognitive Functions in Alzheimer's Disease.

Authors
  • Sahab-Negah, Sajad1, 2, 3
  • Hajali, Vahid1, 2
  • Moradi, Hamid Reza4
  • Gorji, Ali5, 6, 7, 8, 9
  • 1 Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. , (Iran)
  • 2 Department of Neuroscience, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. , (Iran)
  • 3 Shefa Neuroscience Research Center, Khatam Alanbia Hospital, Tehran, Iran. , (Iran)
  • 4 Histology and Embryology Group, Basic Science Department, Faculty of Veterinary Medicine, Shiraz University, Shiraz, Iran. , (Iran)
  • 5 Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. [email protected] , (Iran)
  • 6 Department of Neuroscience, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. [email protected] , (Iran)
  • 7 Shefa Neuroscience Research Center, Khatam Alanbia Hospital, Tehran, Iran. [email protected] , (Iran)
  • 8 Department of Neurosurgery and Department of Neurology, Westfälische Wilhelms-Universität Münster, Münster, Germany. [email protected] , (Germany)
  • 9 Epilepsy Research Center, Westfälische Wilhelms-Universität Münster, Domagkstr. 11, Münster, Germany. [email protected] , (Germany)
Type
Published Article
Journal
Cellular and Molecular Neurobiology
Publisher
Springer-Verlag
Publication Date
Apr 01, 2020
Volume
40
Issue
3
Pages
283–299
Identifiers
DOI: 10.1007/s10571-019-00733-0
PMID: 31502112
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Alzheimer's disease (AD) is described as cognitive and memory impairments with a sex-related epidemiological profile, affecting two times more women than men. There is emerging evidence that alternations in the hippocampal neurogenesis occur at the early stage of AD. Therapies that may effectively slow, stop, or regenerate the dying neurons in AD are being extensively investigated in the last few decades, but none has yet been found to be effective. The regulation of endogenous neurogenesis is one of the main therapeutic targets for AD. Mounting evidence indicates that the neurosteroid estradiol (17β-estradiol) plays a supporting role in neurogenesis, neuronal activity, and synaptic plasticity of AD. This effect may provide preventive and/or therapeutic approaches for AD. In this article, we discuss the molecular mechanism of potential estradiol modulatory action on endogenous neurogenesis, synaptic plasticity, and cognitive function in AD.

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