期刊
CELLULAR AND MOLECULAR NEUROBIOLOGY
卷 40, 期 3, 页码 283-299出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10571-019-00733-0
关键词
Neurodegeneration; Dementia; Hormone; Neurogenesis; Cell therapy; Brain
资金
- Deutscher Akademischer Austauschdienst [57403633] Funding Source: Medline
- Iran National Science Foundation [-] Funding Source: Medline
- National Institute for Medical Research Development [964650] Funding Source: Medline
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 (17 beta-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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