Tortelli Brett, Fujiwara Hideji, Bagel Jessica H, Zhang Jessie, Sidhu Rohini, Jiang Xuntian, Yanjanin Nicole M, Shankar Roopa Kanakatti, Carillo-Carasco Nuria, Heiss John, Ottinger Elizabeth, Porter Forbes D, Schaffer Jean E, Vite Charles H, Ory Daniel S
Diabetic Cardiovascular Disease Center and Department of Medicine, Washington University School of Medicine, 660 S. Euclid Avenue, St. Louis, MO 63110, USA.
Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Hum Mol Genet. 2014 Nov 15;23(22):6022-33. doi: 10.1093/hmg/ddu331. Epub 2014 Jun 25.
Niemann-Pick C1 (NPC1) disease is a rare, neurodegenerative lysosomal cholesterol storage disorder, typified by progressive cognitive and motor function impairment. Affected individuals usually succumb to the disease in adolescence. 2-Hydroxypropyl-β-cyclodextrin (HP-β-CD) has emerged as a promising intervention that reduces lipid storage and prolongs survival in NPC1 disease animal models. A barrier to the development of HP-β-CD and other treatments for NPC disease has been the lack of validated biochemical measures to evaluate efficacy. Here we explored whether cholesterol homeostatic responses resulting from HP-β-CD-mediated redistribution of sequestered lysosomal cholesterol could provide biomarkers to monitor treatment. Upon direct CNS delivery of HP-β-CD, we found increases in plasma 24(S)-HC in two independent NPC1 disease animal models, findings that were confirmed in human NPC1 subjects receiving HP-β-CD. Since circulating 24(S)-HC is almost exclusively CNS-derived, the increase in plasma 24(S)-HC provides a peripheral, non-invasive measure of the CNS effect of HP-β-CD. Our findings suggest that plasma 24(S)-HC, along with the other cholesterol-derived markers examined in this study, can serve as biomarkers that will accelerate development of therapeutics for NPC1 disease.
尼曼-皮克C1型(NPC1)病是一种罕见的神经退行性溶酶体胆固醇贮积症,以进行性认知和运动功能损害为典型特征。受影响个体通常在青春期死于该病。2-羟丙基-β-环糊精(HP-β-CD)已成为一种有前景的干预措施,可减少NPC1病动物模型中的脂质贮积并延长生存期。HP-β-CD及其他NPC病治疗方法研发的一个障碍是缺乏用于评估疗效的经过验证的生化指标。在此,我们探讨了HP-β-CD介导的隔离溶酶体胆固醇重新分布所产生的胆固醇稳态反应是否能够提供用于监测治疗的生物标志物。在将HP-β-CD直接递送至中枢神经系统后,我们在两个独立的NPC1病动物模型中发现血浆24(S)-羟基胆固醇(24(S)-HC)升高,这一发现也在接受HP-β-CD治疗的NPC1病人类受试者中得到证实。由于循环中的24(S)-HC几乎完全源自中枢神经系统,血浆24(S)-HC的升高提供了一种对HP-β-CD中枢神经系统效应的外周、非侵入性测量方法。我们的研究结果表明,血浆24(S)-HC以及本研究中检测的其他胆固醇衍生标志物可作为生物标志物,加速NPC1病治疗药物的研发。