Please use this identifier to cite or link to this item:
http://hdl.handle.net/10397/106241
DC Field | Value | Language |
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dc.contributor | Department of Food Science and Nutrition | en_US |
dc.creator | Zeng, XY | en_US |
dc.creator | Cheung, SKK | en_US |
dc.creator | Shi, MQ | en_US |
dc.creator | Or, PMY | en_US |
dc.creator | Li, ZN | en_US |
dc.creator | Liu, JYH | en_US |
dc.creator | Ho, WLH | en_US |
dc.creator | Liu, T | en_US |
dc.creator | Lu, K | en_US |
dc.creator | Rudd, JA | en_US |
dc.creator | Wang, YB | en_US |
dc.creator | Chan, AM | en_US |
dc.date.accessioned | 2024-05-03T00:45:58Z | - |
dc.date.available | 2024-05-03T00:45:58Z | - |
dc.identifier.issn | 1742-2094 | en_US |
dc.identifier.uri | http://hdl.handle.net/10397/106241 | - |
dc.language.iso | en | en_US |
dc.publisher | BioMed Central | en_US |
dc.rights | © The Author(s) 2023. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. | en_US |
dc.rights | The following publication Zeng, X., Cheung, S.K.K., Shi, M. et al. Astrocyte-specific knockout of YKL-40/Chi3l1 reduces Aβ burden and restores memory functions in 5xFAD mice. J Neuroinflammation 20, 290 (2023) is available at https://dx.doi.org/10.1186/s12974-023-02970-z. | en_US |
dc.subject | YKL-40 | en_US |
dc.subject | Astrocyte | en_US |
dc.subject | Amyloid-beta | en_US |
dc.subject | Alzheimer's disease | en_US |
dc.title | Astrocyte-specific knockout of YKL-40/<i>Chi3l1</i> reduces Aβ burden and restores memory functions in 5xFAD mice | en_US |
dc.type | Journal/Magazine Article | en_US |
dc.identifier.volume | 20 | en_US |
dc.identifier.doi | 10.1186/s12974-023-02970-z | en_US |
dcterms.abstract | Glial cell-mediated neuroinflammation and neuronal attrition are highly correlated with cognitive impairment in Alzheimer's disease. YKL-40 is a secreted astrocytic glycoprotein that serves as a diagnostic biomarker of Alzheimer's disease. High levels of YKL-40 are associated with either advanced Alzheimer's disease or the normal aging process. However, the functional role of YKL-40 in Alzheimer's disease development has not been firmly established. In a 5xFAD mouse model of Alzheimer's disease, we observed increased YKL-40 expression in the cerebrospinal fluid of 7-month-old mice and was correlated with activated astrocytes. In primary astrocytes, A beta 1-42 upregulated YKL-40 in a dose-dependent manner and was correlated with PI3-K signaling pathway activation. Furthermore, primary neurons treated with YKL-40 and/or A beta 1-42 resulted in significant synaptic degeneration, reduced dendritic complexity, and impaired electrical parameters. More importantly, astrocyte-specific knockout of YKL-40 over a period of 7 days in symptomatic 5xFAD mice could effectively reduce amyloid plaque deposition in multiple brain regions. This was also associated with attenuated glial activation, reduced neuronal attrition, and restored memory function. These biological phenotypes could be explained by enhanced uptake of A beta 1-42 peptides, increased rate of A beta 1-42 degradation and acidification of lysosomal compartment in YKL-40 knockout astrocytes. Our results provide new insights into the role of YKL-40 in Alzheimer's disease pathogenesis and demonstrate the potential of targeting this soluble biomarker to alleviate cognitive defects in symptomatic Alzheimer's disease patients. | en_US |
dcterms.accessRights | open access | en_US |
dcterms.bibliographicCitation | Journal of neuroinflammation, 2023, v. 20, 290 | en_US |
dcterms.isPartOf | Journal of neuroinflammation | en_US |
dcterms.issued | 2023 | - |
dc.identifier.isi | WOS:001112933500001 | - |
dc.identifier.artn | 290 | en_US |
dc.description.validate | 202405 bcrc | en_US |
dc.description.oa | Version of Record | en_US |
dc.identifier.FolderNumber | OA_Scopus/WOS | - |
dc.description.fundingSource | Others | en_US |
dc.description.fundingText | Natural Science Foundation of Shandong Province(Natural Science Foundation of Shandong Province) | en_US |
dc.description.pubStatus | Published | en_US |
dc.description.oaCategory | CC | en_US |
Appears in Collections: | Journal/Magazine Article |
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File | Description | Size | Format | |
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s12974-023-02970-z.pdf | 11.73 MB | Adobe PDF | View/Open |
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