Targeting Neuronal GPR65 With Delayed BTB09089 Treatment Improves Neurorehabilitation Following Ischemic Stroke.
Ru ChenMeng-Qi ZhangYu-Lu MiaoShu-Han ZhangYao ChengShao-Shuai WangJing YinCai-Hong YangHui-Feng ZhangLi TangYan LiYu ZhangYan-Ying FanPublished in: Stroke (2024)
Our findings indicated that delayed BTB09089 treatment improved neurological functional recovery and brain tissue repair poststroke through activating neuronal GRP65. GPR65 overexpression may be a potential strategy to expand the therapeutic time window of GPR65 agonists for neurorehabilitation after ischemic stroke.