ArticleInternational journal of molecular sciences2023
YKL-40 and the Cellular Metabolic Profile in Parkinson's Disease.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 13 citations in OpenAlex.
- Review
- Association of Clinical Severity in Autism Spectrum Disorder with Biomolecules Involved in Lipid Metabolism, Inflammation and miRNAs.Biomolecules · 2026Article
- Tracing neuroinflammation in neurodegeneration: insights from a scoping review on biofluid biomarkers.Brain communications · 2026Review
- Elevated CHI3L1 as a Potential Biomarker of Cognitive Dysfunction in Anti-NMDAR Encephalitis: Evidence From Clinical Results and Mice Model.CNS neuroscience & therapeutics · 2026Article
- Regional homogeneity differences in resting-state fMRI between Parkinson's disease and multiple system atrophy-parkinsonian type.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- CHI3L1: An Emerging Player in Neuroinflammation and Neurodegeneration.Molecular neurobiology · 2025Review
- The silent saboteur: oxidative stress and the path to cognitive dysfunction.Neurodegenerative disease management · 2025Review
- Correlation of inflammatory markers with depression and sleep disorders accompanying the prodromal stage of Parkinson's disease.World journal of psychiatry · 2025Review
- Heparin-binding of the human chitinase-like protein YKL-40 is allosterically modified by chitin oligosaccharides.Biochemistry and biophysics reports · 2025Article
- Chitinase-3 Like-Protein-1 Signature in Neurological Disorders: Emphasis on Stroke.Journal of molecular neuroscience : MN · 2025Review
- Chitinase-3-like-1: a multifaceted player in neuroinflammation and degenerative pathologies with therapeutic implications.Molecular neurodegeneration · 2025Review
- Early diagnosis of Parkinson's disease: biomarker study.Frontiers in aging neuroscience · 2025Review
- Inflammatory Effects and Regulatory Mechanisms of Chitinase-3-like-1 in Multiple Human Body Systems: A Comprehensive Review.International journal of molecular sciences · 2024Review
- Blood DNA methylomic signatures associated with CSF biomarkers of Alzheimer's disease in the EMIF-AD study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Pink1/Parkin deficiency alters circulating lymphocyte populations and increases platelet-T cell aggregates in rats.Research square · 2024Article
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Authors and funding
4 authors at 2 institutions in 1 country.
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Abstract
Parkinson's disease (PD) is the second most common neurodegenerative disease worldwide. A growing body of evidence suggests that mitochondrial dysfunction and inflammation play a crucial role as a pathogenetic mechanism in PD. The glycoprotein YKL-40 (CHI3L1) is a potential biomarker involved in inflammation and tumor processes. The aim of the present study was to investigate the metabolic profile of PBMCs from PD patients and to search for a possible relationship between cellular bioenergetics and YKL-40. The study included 18 naïve PD patients and an age-matched control group (HC, n = 7). Patients were diagnosed according to the MDS-PD, the UPDRS, and the Hoen-Yahr scales. Mitochondrial activity was measured by a metabolic analyzer on isolated PBMCs from PD patients. Gene (qPCR) and protein (ELISA) expression levels of YKL40 were investigated. New data are reported revealing changes in the mitochondrial activity and YKL-40 levels in PD patients. Bioenergetic parameters showed increased respiratory reserve capacity in PD compared to HC. The protein levels of YKL-40 were threefold higher in PD. We found a correlation between the YKL-40 protein levels and basal respiration and between YKL-40 and ATP production. These observations suggest an interplay between YKL-40 and mitochondrial function in PD. We assume that the YKL-40 gene and protein levels in combination with changes in mitochondrial function might serve as an additional tool to monitor the clinical course of PD.
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