Protein aggregation causes alpha-synuclein (α-syn) to change from its original physiological role to a pathological state, which is a potential pathogenic mechanism in Parkinson’s disease (PD). Chiral l/d-Cu_xCo_yS supraparticles (l/d-SPs) with a circular dichroism value of 35 mdeg at 805 nm were fabricated using a simple wet-chemical method. The l/d-SPs prevented the α-syn monomers from forming fibrils and triggered the α-syn fibrils to turn into monomers under 808 nm near-infrared (NIR) light. In living MN9D cells, d-SPs reduced cellular damage, neuronal functional deficits, and neuron loss caused by α-syn fibrils after NIR spectroscopy treatment within 10 min to prevent α-syn aggregation. Significantly, the reactive oxygen species produced by d-SPs were 1.42 times higher than those produced by l-SPs. In vivo experiments showed that d-SPs had a protective effect on neuron damage caused by α-syn aggregate deposition, reduced the symptoms in a mouse model of PD, and restored cognitive ability. After NIR light treatment, the amount of α-syn in a mouse model of PD decreased by more than 67.5%. At the same time, d-SPs gradually decomposed into small nanoparticles within 60 days and were excreted through the blood–brain barrier. This discovery paves the way for the treatment of neurodegenerative diseases using chiral SPs under NIR light irradiation.

蛋白质聚集导致α-突触核蛋白（α-syn）从其原始生理作用转变为病理状态，这是帕金森病（PD）的潜在致病机制。使用简单的湿化学方法制造了在 805 nm 处圆二色性值为 35 mdeg 的手性l / d -Cu _x Co _y S超粒子（l / d -SPs）。所述升/ d -SPS从原纤形成防止α-syn时单体和引发α-syn时的原纤维变成单体下的近红外（NIR）光808纳米。在活的 MN9D 细胞中，d-SP 在 10 分钟内通过 NIR 光谱处理后减少了由 α-syn 原纤维引起的细胞损伤、神经元功能缺陷和神经元丢失，以防止 α-syn 聚集。值得注意的是，d -SPs产生的活性氧比l -SPs产生的活性氧高 1.42 倍。体内实验表明d- SPs对α-syn聚集体沉积引起的神经元损伤具有保护作用，减轻PD小鼠模型的症状，恢复认知能力。近红外光处理后，PD小鼠模型中α-syn的含量下降了67.5%以上。同时，d-SPs 在 60 天内逐渐分解成小的纳米颗粒，并通过血脑屏障排出体外。这一发现为在近红外光照射下使用手性 SP 治疗神经退行性疾病铺平了道路。