YKL-40 and neuron-specific enolase in neurodegeneration and neuroinflammation

被引:34
|
作者
Dichev, Valentin [1 ,2 ]
Kazakova, Maria [1 ,2 ]
Sarafian, Victoria [1 ,2 ]
机构
[1] Med Univ Plovdiv, Dept Med Biol, Plovdiv 400, Bulgaria
[2] Med Univ Plovdiv, Res Inst, Plovdiv 4000, Bulgaria
关键词
biomarkers; inflammation; neuronal degeneration; CEREBROSPINAL-FLUID BIOMARKERS; HUMAN CARTILAGE GLYCOPROTEIN; MESSENGER-RNA EXPRESSION; MYELIN BASIC-PROTEIN; NORMAL HUMAN-TISSUES; ALZHEIMERS-DISEASE; GAMMA-ENOLASE; HUMAN-SERUM; CHITINASE; NSE;
D O I
10.1515/revneuro-2019-0100
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Neurodegenerative diseases comprise a large number of disorders with high impact on human health. Neurodegenerative processes are caused by various etiological factors and differ in their clinical presentation. Neuroinflammation is widely discussed as both a cause and a consequence in the manifestation of these disorders. The interplay between the two entities is considered as a major contributor to the ongoing disease progression. An attentive search and implementation of new and reliable markers specific for the processes of inflammation and degeneration is still needed. YKL-40 is a secreted glycoprotein produced by activated glial cells during neuroinflammation. Neuron-specific enolase (NSE), expressed mainly by neuronal cells, is a long-standing marker for neuronal damage. The aim of this review is to summarize, darify, and evaluate the potential significance and relationship between YKL-40 and NSE as biomarkers in the monitoring and prognosis of a set of neurological diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and multiple sclerosis. YKL-40 appears to be a more reliable biomarker in neurological diseases than NSE. The more prominent expression pattern of YKL-40 could be explained with the more obvious involvement of glial cells in pathological processes accompanying each neurodegenerative disease, whereas reduced NSE levels are likely related to low metabolic activity and increased death of neurons.
引用
收藏
页码:539 / 553
页数:15
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