Department of Pharmacy, Center for Drug Research, Ludwig-Maximilians-Universität München, Munich, Germany.
Physiological Genomics, BioMedical Center, Ludwig-Maximilians-Universität München, Planegg/Martinsried, Germany.
Cell Mol Life Sci. 2022 Feb 23;79(3):148. doi: 10.1007/s00018-022-04161-0.
Patients with progressive neurodegenerative disorder retinitis pigmentosa (RP) are diagnosed in the midst of ongoing retinal degeneration and remodeling. Here, we used a Pde6b-deficient RP gene therapy mouse model to test whether treatment at late disease stages can halt photoreceptor degeneration and degradative remodeling, while sustaining constructive remodeling and restoring function. We demonstrated that when fewer than 13% of rods remain, our genetic rescue halts photoreceptor degeneration, electroretinography (ERG) functional decline and inner retinal remodeling. In addition, in a water maze test, the performance of mice treated at 16 weeks of age or earlier was indistinguishable from wild type. In contrast, no efficacy was apparent in mice treated at 24 weeks of age, suggesting the photoreceptors had reached a point of no return. Further, remodeling in the retinal pigment epithelium (RPE) and retinal vasculature was not halted at 16 or 24 weeks of age, although there appeared to be some slowing of blood vessel degradation. These data suggest a novel working model in which restoration of clinically significant visual function requires only modest threshold numbers of resilient photoreceptors, halting of destructive remodeling and sustained constructive remodeling. These novel findings define the potential and limitations of RP treatment and suggest possible nonphotoreceptor targets for gene therapy optimization.
患有进行性神经退行性疾病色素性视网膜炎 (RP) 的患者在持续的视网膜变性和重塑过程中被诊断出来。在这里,我们使用 Pde6b 缺陷型 RP 基因治疗小鼠模型来测试在疾病晚期治疗是否可以阻止光感受器变性和退化性重塑,同时维持建设性重塑并恢复功能。我们证明,当杆状细胞少于 13%时,我们的基因治疗可以阻止光感受器变性、视网膜电图 (ERG) 功能下降和内视网膜重塑。此外,在水迷宫测试中,在 16 周龄或更早接受治疗的小鼠的表现与野生型无异。相比之下,在 24 周龄时接受治疗的小鼠则没有明显的效果,这表明光感受器已经达到了无法恢复的地步。此外,在 16 或 24 周龄时,视网膜色素上皮 (RPE) 和视网膜血管的重塑并未停止,尽管血管退化似乎有所减缓。这些数据表明了一种新的工作模式,即恢复具有临床意义的视觉功能仅需要少量有弹性的光感受器即可,同时需要阻止破坏性重塑并维持建设性重塑。这些新发现定义了 RP 治疗的潜力和局限性,并提示了基因治疗优化的可能的非光感受器靶标。