Harnessing Synaptic Vesicle Release and Recycling Mechanism for Molecule Delivery to Neurons

Karen KL Yee, Junichi Kumamoto, Daijiro Inomata, Naoki Suzuki, Ryuhei Harada, Norihiro Yumoto
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Abstract

Neurodegenerative clinical trials often fail due to insufficient drug doses in reaching targeted cells and the unintended delivery to non-targeted cells. This study demonstrates an alternative neuron-selective drug delivery system, which utilizes the synaptic vesicle release and recycling mechanism (SVRM) by antibody shuttles targeting synaptic vesicle transmembrane proteins for molecule delivery. Using Synaptotagmin-2 (SYT2), we exemplify that intravenously administered anti-SYT2 antibodies localize to neuromuscular junctions, undergo uptake, and retrograde transport to ChAT-positive motor neurons (MNs) in the spinal cord and brainstem. The delivery of anti-microtubule agent and Malat1 gapmer antisense oligonucleotide to MNs with anti-SYT2 antibodies induces axon degeneration and reduction of Malat1 RNA expression, respectively. This approach circumvents the blood-spinal cord barrier, enabling selective delivery of therapeutic molecules to neurons while minimizing effects in non-targeted cells. Thus harnessing SVRM presents a promising strategy for enhancing drug concentrations in neurons and improving treatment efficacy for neurodegenerative diseases.
利用突触小泡释放和再循环机制向神经元输送分子
神经退行性疾病的临床试验往往因药物剂量不足无法到达靶细胞以及药物意外输送到非靶细胞而失败。本研究展示了另一种神经元选择性给药系统,它利用突触小泡释放和再循环机制(SVRM),通过抗体穿梭器靶向突触小泡跨膜蛋白进行分子给药。我们利用突触表蛋白-2(SYT2)举例说明了静脉注射抗SYT2抗体可定位到神经肌肉接头、被摄取并逆向运输到脊髓和脑干中ChAT阳性的运动神经元(MNs)。用抗SYT2抗体向运动神经元输送抗微管剂和Malat1 gapmer反义寡核苷酸,可分别诱导轴突变性和减少Malat1 RNA的表达。这种方法可绕过血液-脊髓屏障,将治疗分子选择性地输送到神经元,同时将对非靶向细胞的影响降至最低。因此,利用 SVRM 是提高神经元内药物浓度和改善神经退行性疾病治疗效果的一种有前途的策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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