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Review Article

YKL-40 and LAMPs as possible markers in neuroinflammation and autophagy during central nervous system infections

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Article: 2360541 | Received 18 Mar 2024, Accepted 22 May 2024, Published online: 03 Jun 2024
 

Abstract

Central nervous system infections continue to be a public health concern owing to the high mortality and the significant neurological sequelae among survivors. The diverse etiology with overlapping clinical and laboratory abnormalities makes the management of such patients challenging. Neuroinflammation plays an essential role in triggering oxidative stress and autophagy dysregulation. Impaired autophagy may lead to abnormal protein aggregation resulting in neurodegeneration. YKL-40 is a secreted glycoprotein, involved in several diseases accompanied by inflammation. The lysosome-associated membrane proteins (LAMPs) 1 and 2 exhibit diverse expression levels in a range of cell processes (including autophagy) and clinical conditions but the complete picture of their biological function is still unknown. This review highlights the role of YKL-40 and LAMPs in central nervous system infections. We suggest that these biomolecules might have a promising value as biomarkers or targets for therapy and could provide additional evidence for inflammatory activity in different neurological diseases.

Acknowledgment

The authors thank Valentina Mihaylova for the help in the design of the figure.

Author contributions

All the authors contributed to the data research, writing, editing, and reviewing of the manuscript. All authors have read and agreed to the final version of the manuscript.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

Data is available from the corresponding author upon request.

Additional information

Funding

This study was funded by the European Union-NextGenerationEU, through the National Recovery and Resilience Plan of the Republic of Bulgaria, project № BG-RRP-2.004-0007-C01 and by MU-Plovdiv project № 02/2022.