Center for Advanced Biotechnology and Medicine , Piscataway, New Jersey 08854, United States.
Department of Biochemistry and Molecular Biology, Robert-Wood Johnson Medical School, Rutgers Biomedical Health Sciences , Piscataway, New Jersey 08854, United States.
J Proteome Res. 2017 Oct 6;16(10):3787-3804. doi: 10.1021/acs.jproteome.7b00460. Epub 2017 Aug 28.
Clinical trials have been conducted for the neuronal ceroid lipofuscinoses (NCLs), a group of neurodegenerative lysosomal diseases that primarily affect children. Whereas clinical rating systems will evaluate long-term efficacy, biomarkers to measure short-term response to treatment would be extremely valuable. To identify candidate biomarkers, we analyzed autopsy brain and matching CSF samples from controls and three genetically distinct NCLs due to deficiencies in palmitoyl protein thioesterase 1 (CLN1 disease), tripeptidyl peptidase 1 (CLN2 disease), and CLN3 protein (CLN3 disease). Proteomic and biochemical methods were used to analyze lysosomal proteins, and, in general, we find that changes in protein expression compared with control were most similar between CLN2 disease and CLN3 disease. This is consistent with previous observations of biochemical similarities between these diseases. We also conducted unbiased proteomic analyses of CSF and brain using isobaric labeling/quantitative mass spectrometry. Significant alterations in protein expression were identified in each NCL, including reduced STXBP1 in CLN1 disease brain. Given the confounding variable of post-mortem changes, additional validation is required, but this study provides a useful starting set of candidate NCL biomarkers for further evaluation.
已经开展了神经元蜡样脂褐质沉积症(NCLs)的临床试验,这是一组主要影响儿童的神经退行性溶酶体疾病。虽然临床评分系统将评估长期疗效,但测量短期治疗反应的生物标志物将非常有价值。为了确定候选生物标志物,我们分析了来自对照组和三种遗传上不同的 NCL 的尸检大脑和匹配的 CSF 样本,这些 NCL 是由于棕榈酰蛋白硫酯酶 1(CLN1 疾病)、三肽基肽酶 1(CLN2 疾病)和 CLN3 蛋白(CLN3 疾病)的缺乏引起的。我们使用蛋白质组学和生化方法来分析溶酶体蛋白,总的来说,我们发现与对照相比,CLN2 疾病和 CLN3 疾病之间的蛋白表达变化最为相似。这与这两种疾病之间以前观察到的生化相似性一致。我们还使用等压标记/定量质谱法对 CSF 和大脑进行了无偏的蛋白质组学分析。在每种 NCL 中都鉴定到了蛋白表达的显著改变,包括 CLN1 疾病大脑中的 STXBP1 减少。考虑到死后变化的混杂变量,需要进一步验证,但本研究为进一步评估提供了一组有用的 NCL 候选生物标志物。