|星空彩票电脑版
%A ZHONG Ming, SHEN Li-Xia %T
Study of the Mechanism of Estrogen on Neuroprotective Effect%0 Journal Article %D 2015 %J ACTA NEUROPHARMACOLOGICA %R %P 54-64 %V 5 %N 2 %U {http://actanp.hebeinu.edu.cn/CN/abstract/article_244.shtml} %8 2015-04-26 %X Alzheimer’s disease(AD) is a neurodegenerative disease of the central nervous system, which is characterized by deposition of amyloid beta(Aβ) and neurofibrillary tangles and the incidence of women significantly higher than men. The studies have shown that the occurrence and development of AD are closely associated with the declining estrogen levels, however, the mechanism underlying estrogen’s neuroprotective effect is not fully clarified. The study found that when estrogen bind to its receptor, it can regulate the activity of Trx-1 and Ask-1, inhibit the cytosolic translocation of Death domain associate protein(Daxx), block the Ask-1/JNK signal transduction pathway to exert against oxidative stress and apoptosis; Estrogen organizes ER to activate MAPK/ERK signaling pathway to promote the non-amyloidogenic pathway of Amyloid precursor protein(APP) which is prevent the formation of Aβ; In addition, the research also found that the activated estrogen receptors interaction with caveolin proteins to activate metabotropic glutamate receptors(mGluRs) which induces cAMP-response element binding protein(CREB) phosphorylation; It mediates second messenger to protect against glutamate excitotoxicity so as to exert neuroprotective effect. In this review, the potential mechanisms of estrogen’s neuroprotective effect are reviewed, in order to provide theoretical basis for the prevention and treatment of AD.