粘多糖病Ⅱ型
酶替代疗法
遗传增强
亨特综合征
粘多糖病
医学
神经学
神经病理学
溶酶体贮存病
跨细胞
桑德霍夫病
基因传递
病毒载体
血脑屏障
中枢神经系统
神经科学
生物信息学
免疫学
周围神经病变
鞘脂
腺相关病毒
小RNA
I型粘多糖病
病理
神经化学
药理学
疾病
基因
内科学
作者
Xiu Jin,Qin Ye,Xiaoyi Wu,Jing Su,Li Song,Jiamei Fu,Xu Qiuxia,Min Luo,Fanfei Liu,Chengda Ren,Ming Hu,M H Liu,Yifan An,Qiqi Li,Manjun Li,Yang Yang
出处
期刊:Neurotherapeutics
[Springer Science+Business Media]
日期:2025-09-23
卷期号:22 (6): e00741-e00741
被引量:1
标识
DOI:10.1016/j.neurot.2025.e00741
摘要
Mucopolysaccharidosis type II (MPS II) is a neurodegenerative lysosomal storage disorder (LSD) caused by inherited mutations in the iduronate-2-sulfatase (IDS) gene. Approximately two-thirds of patients exhibit severe central nervous system (CNS) involvement and cognitive impairment, which remain unaddressed by conventional enzyme replacement therapy (ERT) due to the inability of wild-type IDS to cross the blood-brain barrier (BBB). To overcome this limitation, we engineered a brain-penetrant IDS variant, eBT-IDS4, which retained enzymatic activity and demonstrated enhanced BBB transcytosis in vitro. We then evaluated a liver-directed gene therapy approach using an adeno-associated virus 8 (AAV8) vector encoding eBT-IDS4 under the control of a liver-specific promoter (LSP) in an adult MPS II mouse model. Intravenous administration of AAV8.LSP.IVS2.eBT-IDS4 resulted in sustained supraphysiological IDS activity and normalization of glycosaminoglycan (GAG) levels in peripheral tissues. Notably, this strategy achieved 89 % of wild-type IDS activity in the brain, leading to complete correction of neuropathology and reversal of cognitive deficits in 8-month-old MPS II mice. These findings support a promising, minimally invasive gene therapy strategy for treating MPS II and other neurodegenerative LSDs.
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