KCa3.1 constitutes a pharmacological target for astrogliosis associated with Alzheimer's disease
详细信息 查看全文
- 作者：Mengni Yia ; 1 ; Panpan Yub ; 1 ; Qin Lua ; Herbert M. Gellerc ; Zhihua Yua ; yuzhihua@shsmu.edu.cn" class="auth_mail" title="E-mail the corresponding author ; Hongzhuan Chena ; hongzhuan_chen@hotmail.com" class="auth_mail" title="E-mail the corresponding author
- 关键词：Astrogliosis ; Alzheimer's disease ; GFAP ; Mouse ; Culture
- 刊名：Molecular and Cellular Neuroscience
- 出版年：2016
- 出版时间：October 2016
- 年：2016
- 卷：76
- 期：Complete
- 页码：21-32
- 全文大小：2974 K
文摘
- •
KCa3.1 expression was increased in reactive astrocytes as well as neurons in the brains of both SAMP8 mice and Alzheimer’s disease patients.
- •
10">Blockade or deletion of KCa3.1 reduced the activation of glia cells and rescued the memory loss in SAMP8 mice.
- •
15">KCa3.1 involved in Aβ oligomer-induced astrogliosis by regulating Ca2 + influx.