Introduction: Neuroinflammation is a common pathophysiological mechanism in neurodegenerative diseases (ND). Cerebrospinal fluid (CSF) YKL-40 has recently been candidated as a neuroinflammatory biomarker of ND.

Areas covered: We provide an update on the role of CSF YKL-40 as a pathophysiological biomarker of ND. YKL-40 may discriminate Alzheimer’s disease (AD) from controls and may predict the progression from the early preclinical to the late dementia stage. In genetic AD, YKL-40 increases decades before the clinical onset. It does not seem a specific biomarker of a certain ND although sporadic Creutzfeldt–Jacob disease shows the highest YKL-40 concentrations. YKL-40 may discriminate between amyotrophic lateral sclerosis (ALS) and ALS-mimics. YKL-40 is potentially associated with the rate of ALS progression. YKL-40 correlates with biomarkers of neuronal injury, large axonal damage and synaptic disruption in various ND. It is not associated with the presence of the APOE-ε4 allele whereas possibly linked to aging, female sex, Hispanic ethnicity and some genetic variants of the chitinase-3-like 1 locus.

Expert opinion: There is growing evidence expanding the relevance of CSF YKL-40 as a pathophysiological biomarker for ND. Patients showing high YKL-40 levels might benefit from targeted clinical trials that use compounds acting against neuroinflammatory mechanisms, independently of the initial clinical diagnosis of ND.

简介：神经炎症是神经退行性疾病（ND）的常见病理生理机制。脑脊液（CSF）YKL-40最近已被选为ND的神经炎症生物标志物。

涵盖的领域：我们提供有关CSF YKL-40作为ND病理生理生物标记物的作用的最新信息。YKL-40可以将阿尔茨海默氏病（AD）与对照区分开，并可以预测从临床前早期到痴呆晚期的进展。在遗传性AD中，YKL-40在临床发作之前增加了数十年。尽管零星的克雅氏病显示出最高的YKL-40浓度，但它似乎不是某种ND的特定生物标记。YKL-40可以区分肌萎缩性侧索硬化症（ALS）和ALS模仿物。YKL-40可能与ALS进展的速度有关。YKL-40与各种ND中神经元损伤，大轴突损伤和突触破坏的生物标志物相关。它与APOE的存在无关-ε4等位基因可能与衰老，女性，西班牙裔种族和几丁质酶3样1基因座的某些遗传变异有关。

专家意见：越来越多的证据证明CSF YKL-40作为ND的病理生理生物标志物的重要性。表现出高YKL-40水平的患者可能会受益于使用针对神经炎症机制的化合物的靶向临床试验，而与ND的最初临床诊断无关。