17β-HSD10-IN-4

C57BL/6 (B6) APPswe/PSEN1dE9 (APP/PS1) transgenic (male, 6 months old)^[1]

10 mg/kg

i.p.; daily; 14 days

Improved spatial learning and memory, with treated mice spending 29 seconds in the target quadrant during the Morris water maze probe trial, demonstrating reduced escape latency, increased platform crossings, and goal-directed swimming trajectories.
Reduced cerebral reactive oxygen species (ROS) levels by 24% and increased ATP content by 76% in APP/PS1 mouse brain cells; suppressed cytochrome c release to near wild-type levels.
Reduced cortical phosphorylated Tau (p-Tau) levels by 32% and cortical p-Tau/Tau ratio by 18%; reduced hippocampal p-Tau levels by 18% and hippocampal p-Tau/Tau ratio by 11%; reduced CDK5 overexpression by 13% in the cortex and 7% in the hippocampus.
Increased cortical brain-derived neurotrophic factor (BDNF) levels by 58% compared to untreated APP/PS1 mice, restoring levels to near wild-type values.
Reduced cerebral Aβ plaque load by approximately two-thirds (plaque burden was one-third of that in untreated APP/PS1 mice).
Showed no significant change in 17β-HSD10 protein expression relative to untreated APP/PS1 mice.