NeuralCipher Research overview
The text below is the source article’s original abstract under a verified reuse license. cc by
Abstract Background Parkinson's disease (PD) is a major neurodegenerative disorder after Alzheimer's disease, yet the molecular alterations driving its onset and progression remain only partly understood. Although mannose metabolism has been linked to nervous-system dysfunction, its contribution to PD has not been clearly defined. This work aimed to screen PD biomarkers related to mannose metabolism and to characterize their possible biological roles. Methods Bulk transcriptome datasets, single-cell RNA-sequencing data, and clinical validation samples were analyzed together. Candidate biomarkers were filtered through WGCNA, differential expression analysis, machine-learning algorithms, and external validation. Functional enrichment, immune-cell deconvolution, drug/compound prediction, and molecular docking were used to infer biomarker-related mechanisms. Single-cell analyses further evaluated cell-specific expression patterns and intercellular communication, and RT-qPCR was performed for experimental confirmation. Results The WGCNA procedure defined 684 genes in mannose metabolism-associated modules, while differential expression analysis detected 808 altered genes. After sequential screening, SELENBP1, AK3, and C9orf41 were retained as biomarkers. They were enriched in 67, 46, and 63 pathways, respectively, including oxidative phosphorylation. Immune analysis showed significant differences in M0 macrophages, monocytes, and activated natural killer (NK) cells between groups. Docking predicted binding energies of -6.4, -7.1, and − 10.5 kcal/mol for SELENBP1-bisphenol A, AK3-bisphenol A, and C9orf41-doxorubicin, respectively. Six cell populations were annotated, and CD8 T cells and CD4 T cells showed relatively high biomarker expression and were selected as key cells. B cell-to-CD8 T cell and B cell-to-granulocyte-macrophage progenitor (GMP) communication was observed only in PD samples. RT-qPCR confirmed significant downregulation of SELENBP1, AK3, and C9orf41 in PD samples. Conclusion SELENBP1, AK3, and C9orf41 were screened as PD-related mannose metabolism biomarkers and may provide candidate molecules for future mechanistic research and translational validation.
Scientific assessment
Research question
Assess the question within the original study’s scope.
Methods & sample
Check the source article for study design and sample details.
Key findings
An editorially approved findings summary is not yet published for this record.
Limitations
Generalizability, bias and clinical meaning require separate assessment.
Methods, samples and clinical conclusions are not inferred from bibliographic metadata.