Nilsson Johanna, Gobom Johan, Sjödin Simon, Brinkmalm Gunnar, Ashton Nicholas J, Svensson Johan, Johansson Per, Portelius Erik, Zetterberg Henrik, Blennow Kaj, Brinkmalm Ann
Institute of Neuroscience and Physiology The Sahlgrenska Academy at the University of Gothenburg Mölndal Sweden.
Clinical Neurochemistry Laboratory Sahlgrenska University Hospital Mölndal Sweden.
Alzheimers Dement (Amst). 2021 May 1;13(1):e12179. doi: 10.1002/dad2.12179. eCollection 2021.
Synaptic dysfunction and degeneration is one of the earliest events in Alzheimer's disease (AD) and the best correlate of cognitive decline. Thus, identification and validation of biomarkers reflecting synaptic degeneration to be used as prognostic biomarkers are greatly needed.
Solid-phase extraction and parallel reaction monitoring mass spectrometry were used to quantify 17 synaptic proteins in CSF, in two cross-sectional studies including AD (n = 52) and controls (n = 37).
Increased concentrations of beta-synuclein, gamma-synuclein, neurogranin, phosphatidylethanolamine-binding protein 1, and 14-3-3 proteins were observed in AD patients compared to controls, while neuronal pentraxin-2 and neuronal pentraxin receptor were decreased.
We have established a method with a novel panel of synaptic proteins as biomarkers of synaptic dysfunction. The results indicate that several of the proteins included in the panel may serve as synaptic biomarkers for AD.
突触功能障碍和退化是阿尔茨海默病(AD)最早出现的事件之一,也是认知能力下降的最佳关联因素。因此,迫切需要识别和验证反映突触退化的生物标志物,以用作预后生物标志物。
在两项横断面研究中,包括AD患者(n = 52)和对照组(n = 37),采用固相萃取和平行反应监测质谱法定量脑脊液中的17种突触蛋白。
与对照组相比,AD患者脑脊液中β-突触核蛋白、γ-突触核蛋白、神经颗粒素、磷脂酰乙醇胺结合蛋白1和14-3-3蛋白的浓度升高,而神经元五聚体蛋白2和神经元五聚体蛋白受体降低。
我们建立了一种以一组新型突触蛋白作为突触功能障碍生物标志物的方法。结果表明,该组中包含的几种蛋白质可能作为AD的突触生物标志物。