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

Abstract

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 beta(A beta) deposition, and activation of astrocytes and microglia in the hippocampus of APP/PSI x SRC-1(-/-) mice. The results showed that SRC-1 knockout neither affects the A beta 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.