The critical period for neuroprotection by estrogen replacement therapy and the potential underlying mechanisms.

The critical period for neuroprotection by estrogen replacement therapy and the potential underlying mechanisms. Curr Neuropharmacol. 2020 Jan 23;: Authors: Guo H, Liu M, Zhang L, Wang L, Hou W, Ma Y, Ma Y Abstract 17β-Estradiol (estradiol or E2) is a steroid hormone that has been broadly applied as a neuroprotective therapeutic for a variety of neurodegenerative and cerebrovascular disorders such as ischemic stroke, Alzheimer's disease, and Parkinson's disease. Several laboratory and clinical studies have reported that estrogen replacement therapy (ERT) had no effect against these diseases in elderly postmenopausal women, and at worst, increased their risk of onset and mortality. This review focuses on the growing body of data from in vitro and animal models characterizing the potential underlying mechanisms and signaling pathways that govern successful neuroprotection by ERT, including the roles of E2 receptors in mediating neuroprotection, E2 genomic regulation of apoptosis-related pathways, membrane-bound receptor-mediated non-genomic signaling pathways, and the antioxidant mechanisms of E2. Also discussed is current evidence for a critical period of effective treatment with estrogen following natural or surgical menopause and the outcomes of E2 administration within the advantageous time period. The known mechanisms governing the duration of the critical period include depletion of E2 receptors, the switch to a ketogenic metabo...
Source: Current Neuropharmacology - Category: Drugs & Pharmacology Authors: Tags: Curr Neuropharmacol Source Type: research