Wennström Malin, Surova Yulia, Hall Sara, Nilsson Christer, Minthon Lennart, Hansson Oskar, Nielsen Henrietta M
Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.
Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden; Department of Neurology, Skåne University Hospital, Lund, Sweden.
PLoS One. 2015 Aug 13;10(8):e0135458. doi: 10.1371/journal.pone.0135458. eCollection 2015.
A major difference in the revised diagnostic criteria for Alzheimer's disease (AD) is the incorporation of biomarkers to support a clinical diagnosis and allow the identification of preclinical AD due to AD neuropathological processes. However, AD-specific fluid biomarkers which specifically distinguish clinical AD dementia from other dementia disorders are still missing. Here we aimed to evaluate the disease-specificity of increased YKL-40 levels in cerebrospinal fluid (CSF) from AD patients with mild to moderate dementia (n = 49) versus Parkinson's disease (PD) (n = 61) and dementia with Lewy bodies (DLB) patients (n = 36), and non-demented controls (n = 44). Second we aimed to investigate whether altered YKL-40 levels are associated with CSF levels of other inflammation-associated molecules. When correcting for age, AD patients exhibited 21.3%, 27.7% and 38.8% higher YKL-40 levels compared to non-demented controls (p = 0.0283), DLB (p = 0.0027) and PD patients (p<0.0001). The AD-associated increase in YKL-40 was not associated with CSF P-tau, T-tau or Aβ42. No relationship between increased YKL-40 and levels of the astrocytic marker glial-fibrillary acidic protein (GFAP), interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1) and interferon gamma-induced protein 10 (IP-10) could be identified. Our results confirm previous reports of an age-associated increased in CSF YKL-40 levels and further demonstrate increased CSF YKL-40 in AD patients versus non-demented controls and patients with DLB or PD. The increase in YKL-40 levels in the AD patients was unrelated to the established CSF AD biomarkers and the inflammatory markers GFAP, MCP-1, IP-10 and IL-8, proposing YKL-40 as a marker of yet to be identified AD-related pathological processes.
阿尔茨海默病(AD)修订诊断标准的一个主要差异是纳入了生物标志物,以支持临床诊断,并能够识别由AD神经病理过程导致的临床前AD。然而,能够特异性区分临床AD痴呆与其他痴呆症的AD特异性体液生物标志物仍然缺失。在此,我们旨在评估轻度至中度痴呆的AD患者(n = 49)与帕金森病(PD)患者(n = 61)、路易体痴呆(DLB)患者(n = 36)以及非痴呆对照者(n = 44)脑脊液(CSF)中YKL-40水平升高的疾病特异性。其次,我们旨在研究YKL-40水平的改变是否与其他炎症相关分子的CSF水平有关。在校正年龄后,与非痴呆对照者(p = 0.0283)、DLB患者(p = 0.0027)和PD患者(p<0.0001)相比,AD患者的YKL-40水平分别高出21.3%、27.7%和38.8%。AD患者中YKL-40的升高与CSF中的磷酸化tau蛋白(P-tau)、总tau蛋白(T-tau)或淀粉样β蛋白42(Aβ42)无关。未发现YKL-40升高与星形胶质细胞标志物胶质纤维酸性蛋白(GFAP)、白细胞介素-8(IL-8)、单核细胞趋化蛋白-1(MCP-1)和干扰素γ诱导蛋白10(IP-10)水平之间存在关联。我们的结果证实了先前关于CSF中YKL-40水平随年龄增加的报道,并进一步表明与非痴呆对照者以及DLB或PD患者相比,AD患者的CSF中YKL-40升高。AD患者中YKL-40水平的升高与既定的CSF AD生物标志物以及炎症标志物GFAP、MCP-1、IP-10和IL-8无关,提示YKL-40是尚未明确的AD相关病理过程的标志物。