SRC-1 Knockout Exerts No Effect on Amyloid β Deposition in APP/PS1 Mice

Frontiers in Aging Neuroscience

Jin-Yi Yang¹  Yu-Hui Yuan²  Dan-Dan Zhu³  Qi-Fa Li³  Rong Jiang³  Bin Wang³  Michael Ntim³  Qiong Wu³  Shao Li³  Xue-Fei Wu³  Xuan Zhang⁴  Na Li⁴ 

[1] Department of Urology, Affiliated Dalian Friendship Hospital of Dalian Medical University, Dalian, China;Institute of Cancer Stem Cell, Dalian Medical University, Dalian, China;Liaoning Provincial Key Laboratory of Cerebral Diseases, Department of Physiology, College of Basic Medical Sciences, Dalian Medical University, Dalian, China;National-Local Joint Engineering Research Center for Drug-Research and Development (R and D) of Neurodegenerative Diseases, Dalian Medical University, Dalian, China;

关键词: steroid receptor coactivator 1;    Alzheimer’s disease;    amyloid-β;    synapse;    glia;   

DOI  :  10.3389/fnagi.2020.00145

来源: DOAJ

【 摘 要 】

Steroid receptor coactivator 1 (SRC-1) is the key coactivator because of its transcriptional activity. Previous studies have shown that SRC-1 is abundant in the hippocampus and has been implicated in cognition. SRC-1 is also related to some major risk factors for Alzheimer’s disease (AD), such as a decline in estrogen and aging, however, whether SRC-1 is involved in the pathogenesis of AD remains unclear. In this study, we established SRC-1 knockout in AD mice by cross breeding SRC-1−/− mutant mice with APP/PS1 transgenic mice, and investigated the expression of some synaptic proteins, the amyloid β (Aβ) deposition, and activation of astrocytes and microglia in the hippocampus of APP/PS1×SRC-1−/− mice. The results showed that SRC-1 knockout neither affects the Aβ plaque and activation of glia, nor changes the expression of synaptic proteins in AD model mice. The above results suggest that the complete deletion of SRC-1 in the embryo exerts no effect on the pathogenesis of APP/PS1 mice. Nevertheless, this study could not eliminate the possible role of SRC-1 in the development of AD due to the lack of observation of other events in AD such as tau hyperphosphorylation and the limitation of the animal model employed.

【 授权许可】

Unknown