YKL-40 (Chitinase 3-like I) is expressed in a subset of astrocytes in Alzheimer’s disease and other tauopathies
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BACKGROUND: The innate immune system is known to be involved early in the pathogenesis of Alzheimer's disease (AD) and other neurodegenerative disorders. The inflammatory response in the central nervous system can be measured postmortem or through a series of inflammatory mediator surrogates. YKL-40 (also named Chitinase-3-like I) has been frequently investigated in body fluids as a surrogate marker of neuroinflammation in AD and other neurological disorders. However, the expression pattern of YKL-40 in the human brain with neurodegenerative pathology remains poorly investigated. Our aim was to study the cellular expression pattern of YKL-40 in the brain of patients with clinical and neuropathological criteria for AD (n = 11); three non-AD tauopathies: Pick's disease (PiD; n = 8), corticobasal degeneration (CBD; n = 8) and progressive supranuclear palsy (PSP; n = 9) and a group of neurologically healthy controls (n = 6). METHODS: Semiquantitative neuropathological evaluation and quantitative confocal triple immunofluorescence studies were performed. An in-house algorithm was used to detect and quantify pathology burden of random regions of interest on a full tissue-section scan. Kruskal-Wallis and Dunn's multiple comparison tests were performed for colocalization and quantification analyses. RESULTS: We found that brain YKL-40 immunoreactivity was observed in a subset of astrocytes in all four diseases and in controls. There was a strong colocalization between YKL-40 and the astroglial marker GFAP but not with neuronal nor microglial markers. Intriguingly, YKL-40-positive astrocytes were tau-negative in PSP, CBD and PiD. The number of YKL-40-positive astrocytes was increased in tauopathies compared with that in controls. A positive correlation was found between YKL-40 and tau immunoreactivities. CONCLUSIONS: This study confirms that YKL-40 is expressed by a subset of astrocytes in AD and other tauopathies. YKL-40 expression is elevated in several neurodegenerative conditions and correlates with tau pathology.
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YKL-40 is mainly expressed by astrocytes, but also by microglia, often in close vicinity to senile plaques and neurofibrillary tangles.
“YKL-40 is mainly expressed by astrocytes, but also by microglia, often in close vicinity to senile plaques and neurofibrillary tangles [15–17].”
From Cerebrospinal fluid levels of the neurotrophic factor neuroleukin are increased in early Alzheimer’s disease, but not in cerebral amyloid angiopathy (2021) · cites this paper as [16]
The Results report that 75–85% of YKL-40 immunoreactivity colocalized with an astroglial marker, supporting the astrocyte portion of the claim. But the Results found no colocalization with a microglial marker, and the Discussion says the authors did not detect YKL-40 in microglia. The paper does not establish that YKL-40-positive cells are often close to senile plaques or neurofibrillary tangles; it describes the astrocytes as mainly isolated. (LLM, conf=0.88)
Experimental — accuracy not yet measuredYKL-40 is a secreted glycoprotein that in the CNS is expressed by microglia and astrocytes and is considered one of the most promising biomarkers of neuroinflammation in AD.
“YKL-40 is a secreted glycoprotein that in the CNS is expressed by microglia and astrocytes19,20 and is considered one of the most promising biomarkers of neuroinflammation in AD.”
From CSF biomarkers of neuroinflammation and cerebrovascular dysfunction in early Alzheimer disease (2018) · cites this paper as [20]
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References 48 · Cited by 158
- Authors
- Querol-Vilaseca, M., Colom-Cadena, M., Pegueroles, J., San Martín-Paniello, C., Clarimon, J., Belbin, O., Fortea, J., & Lleó, A.
- Affiliations
- Universitat Autònoma de Barcelona (ES)
- Corresponding author
- Lleó, Alberto
- Venue
- Journal of Neuroinflammation
- Published
- 2017-06-09
- Volume
- 14
- Issue
- 1
- Pages
- 118-118
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC5466718
- OpenAlex
- W2624641603
- Cited by
- 158
- References
- 48
- Citations by year
- 2026: 17 · 2025: 11 · 2024: 17 · 2023: 12 · 2022: 25 · 2021: 25 · 2020: 21 · 2019: 21 · 2018: 8 · 2017: 1
- FWCI
- 10.32
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Dipòsit Digital de Documents de la UAB (Universitat Autònoma de Barcelona) (submittedVersion, cc-by)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Fondo de Investigación Sanitario, Instituto de Salud Carlos III (PI14/1561)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- YKL-40, astrocytes, Alzheimer's disease, tauopathy, Pick's disease, corticobasal degeneration, progressive supranuclear palsy, neuroinflammation, tau pathology, glial fibrillary acidic protein, innate immune response, neurodegeneration
- MeSH terms
- Chitinase-3-Like Protein 1, Alzheimer Disease, Astrocytes, Brain, Humans, Gene Expression Regulation, Enzymologic, Tauopathies
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