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1
Combination brain and systemic injections of AAV provide maximal functional and survival benefits in the Niemann-Pick mouse.在尼曼-匹克病小鼠模型中,联合进行脑部和全身的腺相关病毒(AAV)注射可带来最大的功能改善和生存益处。
Proc Natl Acad Sci U S A. 2007 May 29;104(22):9505-10. doi: 10.1073/pnas.0703509104. Epub 2007 May 21.
2
Gene transfer of human acid sphingomyelinase corrects neuropathology and motor deficits in a mouse model of Niemann-Pick type A disease.人类酸性鞘磷脂酶的基因转移可纠正A型尼曼-匹克病小鼠模型中的神经病理学和运动缺陷。
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3
AAV vector-mediated correction of brain pathology in a mouse model of Niemann-Pick A disease.腺相关病毒载体介导的尼曼-匹克病A型小鼠模型脑病理改变的校正
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4
Safety study of adeno-associated virus serotype 2-mediated human acid sphingomyelinase expression in the nonhuman primate brain.腺相关病毒血清型 2 介导的人酸性鞘磷脂酶在非人灵长类动物脑内表达的安全性研究。
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Merits of combination cortical, subcortical, and cerebellar injections for the treatment of Niemann-Pick disease type A.联合皮质、皮质下和小脑注射治疗 A 型尼曼-匹克病的优点。
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6
Toward gene therapy for Niemann-Pick disease (NPD): separation of retrovirally corrected and noncorrected NPD fibroblasts using a novel fluorescent sphingomyelin.迈向尼曼-匹克病(NPD)的基因治疗:使用新型荧光鞘磷脂分离经逆转录病毒校正和未校正的NPD成纤维细胞。
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Intracerebral transplantation of adult mouse neural progenitor cells into the Niemann-Pick-A mouse leads to a marked decrease in lysosomal storage pathology.将成年小鼠神经祖细胞脑内移植到尼曼-皮克A型小鼠体内会导致溶酶体贮积病理显著减轻。
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Adeno-associated viral vector serotype 9-based gene therapy for Niemann-Pick disease type A.腺相关病毒血清型 9 为基础的基因治疗尼曼-匹克病 A 型。
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Intracerebral transplantation of mesenchymal stem cells into acid sphingomyelinase-deficient mice delays the onset of neurological abnormalities and extends their life span.将间充质干细胞脑内移植到酸性鞘磷脂酶缺陷小鼠中可延迟神经异常的发作并延长其寿命。
J Clin Invest. 2002 May;109(9):1183-91. doi: 10.1172/JCI14862.
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Retroviral-mediated transfer of the human acid sphingomyelinase cDNA: correction of the metabolic defect in cultured Niemann-Pick disease cells.逆转录病毒介导的人酸性鞘磷脂酶cDNA转移:纠正培养的尼曼-匹克病细胞中的代谢缺陷。
Proc Natl Acad Sci U S A. 1992 Apr 15;89(8):3227-31. doi: 10.1073/pnas.89.8.3227.

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Adeno-associated viral vector serotype 9-based gene therapy for Niemann-Pick disease type A.腺相关病毒血清型 9 为基础的基因治疗尼曼-匹克病 A 型。
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Trehalose reduces retinal degeneration, neuroinflammation and storage burden caused by a lysosomal hydrolase deficiency.海藻糖可减轻溶酶体水解酶缺乏引起的视网膜变性、神经炎症和储存负担。
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Low-dose Gene Therapy Reduces the Frequency of Enzyme Replacement Therapy in a Mouse Model of Lysosomal Storage Disease.低剂量基因疗法降低溶酶体贮积病小鼠模型中酶替代疗法的频率。
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本文引用的文献

1
Correction of the Biochemical and Functional Deficits in Fabry Mice Following AAV8-mediated Hepatic Expression of α-galactosidase A.腺相关病毒8型介导的α-半乳糖苷酶A在肝脏表达后对法布里病小鼠生化和功能缺陷的纠正
Mol Ther. 2007 Mar;15(3):492-500. doi: 10.1038/sj.mt.6300066. Epub 2016 Dec 8.
2
Correction of the biochemical and functional deficits in fabry mice following AAV8-mediated hepatic expression of alpha-galactosidase A.AAV8介导的α-半乳糖苷酶A在肝脏中表达后法布里小鼠生化和功能缺陷的纠正
Mol Ther. 2007 Mar;15(3):492-500. doi: 10.1038/sj.mt.6300066. Epub 2006 Dec 26.
3
Central nervous system-directed AAV2/5-mediated gene therapy synergizes with bone marrow transplantation in the murine model of globoid-cell leukodystrophy.在球状细胞脑白质营养不良的小鼠模型中,中枢神经系统定向的腺相关病毒2/5介导的基因治疗与骨髓移植具有协同作用。
Mol Ther. 2007 Jan;15(1):44-52. doi: 10.1038/sj.mt.6300026.
4
Enhanced efficacy of an AAV vector encoding chimeric, highly secreted acid alpha-glucosidase in glycogen storage disease type II.编码嵌合型、高分泌性酸性α-葡萄糖苷酶的腺相关病毒载体在II型糖原贮积病中的疗效增强
Mol Ther. 2006 Dec;14(6):822-30. doi: 10.1016/j.ymthe.2006.08.001. Epub 2006 Sep 20.
5
Gene therapy of the brain in the dog model of Hurler's syndrome.在黏多糖贮积症I型狗模型中的脑基因治疗。
Ann Neurol. 2006 Aug;60(2):204-13. doi: 10.1002/ana.20870.
6
Early, sustained efficacy of adeno-associated virus vector-mediated gene therapy in glycogen storage disease type Ia.腺相关病毒载体介导的基因疗法对Ia型糖原贮积病的早期持续疗效
Gene Ther. 2006 Sep;13(17):1281-9. doi: 10.1038/sj.gt.3302774. Epub 2006 May 4.
7
Gene therapy for lysosomal storage diseases.溶酶体贮积症的基因治疗
Mol Ther. 2006 May;13(5):839-49. doi: 10.1016/j.ymthe.2006.01.006. Epub 2006 Mar 20.
8
AAV8-mediated expression of glucocerebrosidase ameliorates the storage pathology in the visceral organs of a mouse model of Gaucher disease.腺相关病毒8型介导的葡萄糖脑苷脂酶表达改善了戈谢病小鼠模型内脏器官中的储存病理。
J Gene Med. 2006 Jun;8(6):719-29. doi: 10.1002/jgm.901.
9
Intracranial delivery of CLN2 reduces brain pathology in a mouse model of classical late infantile neuronal ceroid lipofuscinosis.在经典型晚发性婴儿神经元蜡样脂褐质沉积症小鼠模型中,向颅内递送CLN2可减轻脑部病变。
J Neurosci. 2006 Feb 1;26(5):1334-42. doi: 10.1523/JNEUROSCI.2676-05.2006.
10
Gene transfer of human acid sphingomyelinase corrects neuropathology and motor deficits in a mouse model of Niemann-Pick type A disease.人类酸性鞘磷脂酶的基因转移可纠正A型尼曼-匹克病小鼠模型中的神经病理学和运动缺陷。
Proc Natl Acad Sci U S A. 2005 Dec 6;102(49):17822-7. doi: 10.1073/pnas.0509062102. Epub 2005 Nov 21.

在尼曼-匹克病小鼠模型中,联合进行脑部和全身的腺相关病毒(AAV)注射可带来最大的功能改善和生存益处。

Combination brain and systemic injections of AAV provide maximal functional and survival benefits in the Niemann-Pick mouse.

作者信息

Passini Marco A, Bu Jie, Fidler Jonathan A, Ziegler Robin J, Foley Joseph W, Dodge James C, Yang Wendy W, Clarke Jennifer, Taksir Tatyana V, Griffiths Denise A, Zhao Michael A, O'Riordan Catherine R, Schuchman Edward H, Shihabuddin Lamya S, Cheng Seng H

机构信息

Genzyme Corporation, Framingham, MA 01701, USA.

出版信息

Proc Natl Acad Sci U S A. 2007 May 29;104(22):9505-10. doi: 10.1073/pnas.0703509104. Epub 2007 May 21.

DOI:10.1073/pnas.0703509104
PMID:17517638
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1874225/
Abstract

Niemann-Pick disease (NPD) is caused by the loss of acid sphingomyelinase (ASM) activity, which results in widespread accumulation of undegraded lipids in cells of the viscera and CNS. In this study, we tested the effect of combination brain and systemic injections of recombinant adeno-associated viral vectors encoding human ASM (hASM) in a mouse model of NPD. Animals treated by combination therapy exhibited high levels of hASM in the viscera and brain, which resulted in near-complete correction of storage throughout the body. This global reversal of pathology translated to normal weight gain and superior recovery of motor and cognitive functions compared to animals treated by either brain or systemic injection alone. Furthermore, animals in the combination group did not generate antibodies to hASM, demonstrating the first application of systemic-mediated tolerization to improve the efficacy of brain injections. All of the animals treated by combination therapy survived in good health to an investigator-selected 54 weeks, whereas the median lifespans of the systemic-alone, brain-alone, or untreated ASM knockout groups were 47, 48, and 34 weeks, respectively. These data demonstrate that combination therapy is a promising therapeutic modality for treating NPD and suggest a potential strategy for treating disease indications that cause both visceral and CNS pathologies.

摘要

尼曼-皮克病(NPD)是由酸性鞘磷脂酶(ASM)活性丧失引起的,这导致在内脏和中枢神经系统细胞中未降解脂质广泛积累。在本研究中,我们在NPD小鼠模型中测试了联合脑内和全身注射编码人ASM(hASM)的重组腺相关病毒载体的效果。接受联合治疗的动物在内脏和脑中表现出高水平的hASM,这导致全身储存几乎完全得到纠正。与单独接受脑内或全身注射治疗的动物相比,这种病理状态的全面逆转转化为正常体重增加以及运动和认知功能的更好恢复。此外,联合组动物未产生针对hASM的抗体,这证明了全身介导的免疫耐受在提高脑内注射疗效方面的首次应用。所有接受联合治疗的动物均健康存活至研究者选定的54周,而单独全身注射、单独脑内注射或未治疗的ASM基因敲除组的中位寿命分别为47周、48周和34周。这些数据表明联合治疗是治疗NPD的一种有前景的治疗方式,并为治疗导致内脏和中枢神经系统病变的疾病指征提出了一种潜在策略。