• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

相似文献

1
The human visual cortex responds to gene therapy-mediated recovery of retinal function.人类视觉皮层对基因治疗介导的视网膜功能恢复有反应。
J Clin Invest. 2011 Jun;121(6):2160-8. doi: 10.1172/JCI57377. Epub 2011 May 23.
2
Three-year follow-up after unilateral subretinal delivery of adeno-associated virus in patients with Leber congenital Amaurosis type 2.2 型莱伯先天性黑矇患者单侧视网膜下注射腺相关病毒后的 3 年随访结果。
Ophthalmology. 2013 Jun;120(6):1283-91. doi: 10.1016/j.ophtha.2012.11.048. Epub 2013 Mar 6.
3
The Role of the Human Visual Cortex in Assessment of the Long-Term Durability of Retinal Gene Therapy in Follow-on RPE65 Clinical Trial Patients.人类视觉皮层在后续RPE65临床试验患者视网膜基因治疗长期疗效评估中的作用。
Ophthalmology. 2017 Jun;124(6):873-883. doi: 10.1016/j.ophtha.2017.01.029. Epub 2017 Feb 23.
4
Gene therapy for leber congenital amaurosis caused by RPE65 mutations: safety and efficacy in 15 children and adults followed up to 3 years.针对由RPE65基因突变引起的莱伯先天性黑蒙的基因治疗:15名儿童和成人的安全性和有效性,随访长达3年。
Arch Ophthalmol. 2012 Jan;130(1):9-24. doi: 10.1001/archophthalmol.2011.298. Epub 2011 Sep 12.
5
Gene therapy for Leber's congenital amaurosis is safe and effective through 1.5 years after vector administration.经载体给药 1.5 年后,莱伯先天性黑蒙的基因治疗是安全有效的。
Mol Ther. 2010 Mar;18(3):643-50. doi: 10.1038/mt.2009.277. Epub 2009 Dec 1.
6
Canine and human visual cortex intact and responsive despite early retinal blindness from RPE65 mutation.尽管因RPE65基因突变导致早期视网膜失明,但犬类和人类的视觉皮层仍保持完整且有反应。
PLoS Med. 2007 Jun;4(6):e230. doi: 10.1371/journal.pmed.0040230.
7
Age-dependent effects of RPE65 gene therapy for Leber's congenital amaurosis: a phase 1 dose-escalation trial.RPE65基因疗法治疗莱伯先天性黑蒙的年龄依赖性效应:一项1期剂量递增试验。
Lancet. 2009 Nov 7;374(9701):1597-605. doi: 10.1016/S0140-6736(09)61836-5. Epub 2009 Oct 23.
8
Safety and efficacy of gene transfer for Leber's congenital amaurosis.基因转移治疗莱伯先天性黑蒙的安全性和有效性。
N Engl J Med. 2008 May 22;358(21):2240-8. doi: 10.1056/NEJMoa0802315. Epub 2008 Apr 27.
9
Safety and Long-Term Efficacy of AAV4 Gene Therapy in Patients with RPE65 Leber Congenital Amaurosis.AAV4 基因治疗治疗 RPE65 型莱伯先天性黑矇患者的安全性和长期疗效。
Mol Ther. 2018 Jan 3;26(1):256-268. doi: 10.1016/j.ymthe.2017.09.014. Epub 2017 Sep 19.
10
Gene therapy rescues cone structure and function in the 3-month-old rd12 mouse: a model for midcourse RPE65 leber congenital amaurosis.基因治疗挽救 rd12 月龄小鼠的视锥结构和功能:一种 RPE65 莱伯先天性黑矇中途模型。
Invest Ophthalmol Vis Sci. 2011 Jan 5;52(1):7-15. doi: 10.1167/iovs.10-6138. Print 2011 Jan.

引用本文的文献

1
Characterizing Inner Retinal Changes in End-Stage Inherited Retinal Diseases That Might be Suitable for Optogenetic Therapies.表征终末期遗传性视网膜疾病中可能适用于光遗传学疗法的视网膜内层变化。
Transl Vis Sci Technol. 2025 Jun 2;14(6):2. doi: 10.1167/tvst.14.6.2.
2
Clinical and genetic features of achromatopsia in preschool children: novel insights into retinal architecture and therapeutic window for clinical trials.学龄前儿童色盲的临床和遗传特征:对视网膜结构及临床试验治疗窗口期的新见解
Front Med (Lausanne). 2025 Apr 2;12:1560556. doi: 10.3389/fmed.2025.1560556. eCollection 2025.
3
Improvements induced by retinal gene therapy with voretigene neparvovec depend on visual cortical hemispheric dominance mechanisms.用voretigene neparvovec进行视网膜基因治疗所带来的改善取决于视觉皮层半球优势机制。
Commun Med (Lond). 2025 Apr 9;5(1):107. doi: 10.1038/s43856-025-00820-y.
4
Interim safety and efficacy of gene therapy for RLBP1-associated retinal dystrophy: a phase 1/2 trial.RLBP1 相关性视网膜营养不良的基因治疗的 1/2 期临床试验:临时安全性和疗效。
Nat Commun. 2024 Sep 10;15(1):7438. doi: 10.1038/s41467-024-51575-4.
5
Partial rescue of the full-field electroretinogram in patients with RPE65-related retinal dystrophy following gene augmentation therapy with voretigene neparvovec-rzyl.经 voretigene neparvovec-rzyl 基因增强疗法治疗后,RPE65 相关视网膜营养不良患者全视野视网膜电图得到部分挽救。
Doc Ophthalmol. 2024 Oct;149(2):63-75. doi: 10.1007/s10633-024-09987-6. Epub 2024 Aug 14.
6
Pattern-reversal visual evoked potentials in prosthetic vision and simulated visual reduction.人工视觉和模拟视觉减退中的模式反转视觉诱发电位。
BMJ Open Ophthalmol. 2024 Aug 5;9(1):e001705. doi: 10.1136/bmjophth-2024-001705.
7
Gene replacement therapy in Bietti crystalline corneoretinal dystrophy: an open-label, single-arm, exploratory trial.贝蒂氏结晶状角膜视网膜营养不良的基因替代疗法:一项开放标签、单臂探索性试验。
Signal Transduct Target Ther. 2024 Apr 24;9(1):95. doi: 10.1038/s41392-024-01806-3.
8
Voretigene neparvovec for inherited retinal dystrophy due to RPE65 mutations: a scoping review of eligibility and treatment challenges from clinical trials to real practice.用于 RPE65 突变引起的遗传性视网膜营养不良的 voretigene neparvovec:从临床试验到实际实践的资格和治疗挑战的范围审查。
Eye (Lond). 2024 Sep;38(13):2504-2515. doi: 10.1038/s41433-024-03065-6. Epub 2024 Apr 16.
9
Central visual pathways affected by degenerative retinal disease before and after gene therapy.基因治疗前后退行性视网膜疾病对中心视觉通路的影响。
Brain. 2024 Sep 3;147(9):3234-3246. doi: 10.1093/brain/awae096.
10
Safety and Efficacy of Adeno-Associated Viral Gene Therapy in Patients With Retinal Degeneration: A Systematic Review and Meta-Analysis.腺相关病毒基因治疗在视网膜变性患者中的安全性和疗效:系统评价和荟萃分析。
Transl Vis Sci Technol. 2023 Nov 1;12(11):24. doi: 10.1167/tvst.12.11.24.

本文引用的文献

1
From retinotopy to recognition: fMRI in human visual cortex.从视网膜定位到识别:人类视觉皮层的 fMRI 研究。
Trends Cogn Sci. 1998 May 1;2(5):174-83. doi: 10.1016/s1364-6613(98)01171-1.
2
Lighting a candle in the dark: advances in genetics and gene therapy of recessive retinal dystrophies.在黑暗中点燃蜡烛:隐性视网膜营养不良的遗传学和基因治疗进展。
J Clin Invest. 2010 Sep;120(9):3042-53. doi: 10.1172/JCI42258. Epub 2010 Sep 1.
3
Molecular anthropology meets genetic medicine to treat blindness in the North African Jewish population: human gene therapy initiated in Israel.分子人类学与基因医学相遇,为北非犹太人群体治疗失明:以色列启动人类基因治疗。
Hum Gene Ther. 2010 Dec;21(12):1749-57. doi: 10.1089/hum.2010.047. Epub 2010 Nov 3.
4
Task-dependent V1 responses in human retinitis pigmentosa.人类视网膜色素变性中与任务相关的V1反应。
Invest Ophthalmol Vis Sci. 2010 Oct;51(10):5356-64. doi: 10.1167/iovs.09-4775. Epub 2010 May 5.
5
Cortical maps and white matter tracts following long period of visual deprivation and retinal image restoration.长期视觉剥夺和视网膜像恢复后的皮质图谱和白质束。
Neuron. 2010 Jan 14;65(1):21-31. doi: 10.1016/j.neuron.2009.12.006.
6
Gene therapy for Leber's congenital amaurosis is safe and effective through 1.5 years after vector administration.经载体给药 1.5 年后,莱伯先天性黑蒙的基因治疗是安全有效的。
Mol Ther. 2010 Mar;18(3):643-50. doi: 10.1038/mt.2009.277. Epub 2009 Dec 1.
7
Age-dependent effects of RPE65 gene therapy for Leber's congenital amaurosis: a phase 1 dose-escalation trial.RPE65基因疗法治疗莱伯先天性黑蒙的年龄依赖性效应:一项1期剂量递增试验。
Lancet. 2009 Nov 7;374(9701):1597-605. doi: 10.1016/S0140-6736(09)61836-5. Epub 2009 Oct 23.
8
Defining the residual vision in leber congenital amaurosis caused by RPE65 mutations.定义由RPE65基因突变引起的莱伯先天性黑蒙中的残余视力。
Invest Ophthalmol Vis Sci. 2009 May;50(5):2368-75. doi: 10.1167/iovs.08-2696. Epub 2008 Dec 30.
9
Human gene therapy for RPE65 isomerase deficiency activates the retinoid cycle of vision but with slow rod kinetics.针对RPE65异构酶缺乏症的人类基因疗法可激活视觉的视黄醛循环,但视杆动力学缓慢。
Proc Natl Acad Sci U S A. 2008 Sep 30;105(39):15112-7. doi: 10.1073/pnas.0807027105. Epub 2008 Sep 22.
10
Treatment of leber congenital amaurosis due to RPE65 mutations by ocular subretinal injection of adeno-associated virus gene vector: short-term results of a phase I trial.通过眼内视网膜下注射腺相关病毒基因载体治疗由RPE65基因突变引起的莱伯先天性黑蒙:I期试验的短期结果
Hum Gene Ther. 2008 Oct;19(10):979-90. doi: 10.1089/hum.2008.107.

人类视觉皮层对基因治疗介导的视网膜功能恢复有反应。

The human visual cortex responds to gene therapy-mediated recovery of retinal function.

机构信息

Diffusion Tensor Image Analyses and Brain Morphometry Center, Department of Radiology, Children's Hospital of Philadelphia (CHOP), Philadelphia, Pennsylvania 19104, USA.

出版信息

J Clin Invest. 2011 Jun;121(6):2160-8. doi: 10.1172/JCI57377. Epub 2011 May 23.

DOI:10.1172/JCI57377
PMID:21606598
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3104779/
Abstract

Leber congenital amaurosis (LCA) is a rare degenerative eye disease, linked to mutations in at least 14 genes. A recent gene therapy trial in patients with LCA2, who have mutations in RPE65, demonstrated that subretinal injection of an adeno-associated virus (AAV) carrying the normal cDNA of that gene (AAV2-hRPE65v2) could markedly improve vision. However, it remains unclear how the visual cortex responds to recovery of retinal function after prolonged sensory deprivation. Here, 3 of the gene therapy trial subjects, treated at ages 8, 9, and 35 years, underwent functional MRI within 2 years of unilateral injection of AAV2-hRPE65v2. All subjects showed increased cortical activation in response to high- and medium-contrast stimuli after exposure to the treated compared with the untreated eye. Furthermore, we observed a correlation between the visual field maps and the distribution of cortical activations for the treated eyes. These data suggest that despite severe and long-term visual impairment, treated LCA2 patients have intact and responsive visual pathways. In addition, these data suggest that gene therapy resulted in not only sustained and improved visual ability, but also enhanced contrast sensitivity.

摘要

Leber 先天性黑蒙(LCA)是一种罕见的退行性眼病,与至少 14 个基因的突变有关。最近一项针对 LCA2 患者(其 RPE65 发生突变)的基因治疗试验表明,将携带该正常基因 cDNA 的腺相关病毒(AAV)注射到视网膜下(AAV2-hRPE65v2)可以显著改善视力。然而,目前尚不清楚视觉皮层在长期感觉剥夺后对视网膜功能恢复的反应如何。在此,3 名基因治疗试验受试者在接受 AAV2-hRPE65v2 单侧注射后 2 年内接受了功能磁共振成像检查。所有受试者在接受治疗的眼睛暴露于高对比度和中对比度刺激后,大脑皮层的激活反应均增加。此外,我们还观察到治疗眼的视野图与大脑皮层激活分布之间存在相关性。这些数据表明,尽管存在严重和长期的视力障碍,但接受治疗的 LCA2 患者仍具有完整且有反应的视觉通路。此外,这些数据表明,基因治疗不仅带来了持续和改善的视觉能力,还提高了对比度敏感度。