Key genes and pathways in asparagine metabolism in Alzheimer’s Disease: a bioinformatics approach DOI Creative Commons
Xiaoqian Lan,

Guangli Feng,

Qing Li

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown

Published: April 28, 2025

Abstract Background Asparagine (Asn) metabolism is essential for maintaining cellular homeostasis and supporting neuronal energy demands. Recent studies have suggested its dysregulation may contribute to Alzheimer’s disease (AD) pathogenesis; however, the specific genes regulatory mechanisms involved remain incompletely understood. Methods Four publicly available microarray datasets (GSE5281, GSE29378, GSE36980, GSE138260) were utilized investigate with differential expression between control AD samples. metabolism-related (AMGs) retrieved from GeneCards database, their intersection DEGs yielded candidate asparagine differentially expressed (AMG-DEGs). Functional enrichment analysis (Gene Set Enrichment Analysis, Gene Ontology Kyoto Encyclopedia of Genes Genomes), protein–protein interaction (PPI) network analysis, centrality scoring identified hub genes. Regulatory investigated through construction competing endogenous RNA transcription factor networks. Potential therapeutic compounds predicted via drug–gene evaluated using molecular docking simulations. Results Thirty-nine AMG-DEGs found be enriched in neurodevelopmental, synaptic transmission, inflammatory signaling pathways. PPI screening revealed seven ( HPRT1 , GAD2 TUBB3 GFAP CD44 CCL2 NFKBIA ). highlighted miRNAs, long non-coding RNAs, factors modulation. Drug Bathocuproine disulfonate, DL-Mevalonic acid, Phenethyl isothiocyanate as promising strong binding affinities proteins. Conclusion This study comprehensively maps reveals a set elements potentially progression. The provide foundation further experimental validation development novel metabolism-targeted strategies treatment.

Language: Английский

Evaluation of the Anti-Alzheimer Activity of Lycium barbarum Polysaccharide in Aβ1–42-Induced Neurotoxicity in Rat Model DOI Creative Commons

Qingxin Lu,

Y. Gloria Meng,

H. C. Feng

et al.

Current Issues in Molecular Biology, Journal Year: 2025, Volume and Issue: 47(4), P. 226 - 226

Published: March 26, 2025

As a common neurodegenerative disorder, Alzheimer’s disease (AD) manifests as progressive memory loss, cognitive deficits, and dementia in older adults. the basis of traditional Chinese medicinal herb Goji berries, Lycium barbarum polysaccharide (LBP) has been proven to exhibit multiple pharmacological activities, including antioxidant, neuroprotective, anti-inflammatory effects. Evidence supports that LBP can enhance function holds promise counteracting AD. In order determine neuroprotective effects LBP, this study was conducted on an AD rat model induced by intracerebroventricular injection Aβ1–42 peptides. From 24 h after induction until end behavioral experiment, rats were orally administered (150 300 mg/kg) once day. Neurobehavioral parameters evaluated starting 1 week administration. After tests, euthanized, whole brain cortex isolated detect variations histopathology biochemical parameters. significantly reversed impairments, assessed through Y-maze, Passive Avoidance Test (PAT), Morris water maze (MWM) test, respectively. Furthermore, not only attenuated NFκB, TNF-α, IL-1β, IL-6, AChE, oxidative/nitrosative stress levels but also increased IL-4, IL-10, ACh ChAT activity cortex. HE staining exhibited neuroprotection LBP. Our findings imply may improve mechanisms is potential anti-AD compound.

Language: Английский

Citations

0
Key genes and pathways in asparagine metabolism in Alzheimer’s Disease: a bioinformatics approach DOI Creative Commons
Xiaoqian Lan,

Guangli Feng,

Qing Li

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown

Published: April 28, 2025

Abstract Background Asparagine (Asn) metabolism is essential for maintaining cellular homeostasis and supporting neuronal energy demands. Recent studies have suggested its dysregulation may contribute to Alzheimer’s disease (AD) pathogenesis; however, the specific genes regulatory mechanisms involved remain incompletely understood. Methods Four publicly available microarray datasets (GSE5281, GSE29378, GSE36980, GSE138260) were utilized investigate with differential expression between control AD samples. metabolism-related (AMGs) retrieved from GeneCards database, their intersection DEGs yielded candidate asparagine differentially expressed (AMG-DEGs). Functional enrichment analysis (Gene Set Enrichment Analysis, Gene Ontology Kyoto Encyclopedia of Genes Genomes), protein–protein interaction (PPI) network analysis, centrality scoring identified hub genes. Regulatory investigated through construction competing endogenous RNA transcription factor networks. Potential therapeutic compounds predicted via drug–gene evaluated using molecular docking simulations. Results Thirty-nine AMG-DEGs found be enriched in neurodevelopmental, synaptic transmission, inflammatory signaling pathways. PPI screening revealed seven ( HPRT1 , GAD2 TUBB3 GFAP CD44 CCL2 NFKBIA ). highlighted miRNAs, long non-coding RNAs, factors modulation. Drug Bathocuproine disulfonate, DL-Mevalonic acid, Phenethyl isothiocyanate as promising strong binding affinities proteins. Conclusion This study comprehensively maps reveals a set elements potentially progression. The provide foundation further experimental validation development novel metabolism-targeted strategies treatment.

Language: Английский

Citations

0