Intermediate-term spatial memory was impaired in SOD1 <sup>G93A</sup> females, whereas long-term spatial memory deficits as well as lower acoustic startle response, and prepulse inhibition were identified in SOD1 <sup>G93A</sup> mice of both sexes compared with respective controls.
Our analyses indicated that luteoline had a significant effect on decreasing the contents of ROS and MDA, elevating the activity of SOD, and ultimately improving spatial learning and memory deficits of mice.
Here, we show that Sod1 deficiency in an amyloid precursor protein-overexpressing mouse model (AD mouse, Tg2576) accelerated Aβ oligomerization and memory impairment as compared with control AD mouse and that these phenomena were basically mediated by oxidative damage.