RESUMO
This study delivers a thorough analysis of long non-coding RNAs (lncRNAs) in regulating programmed cell death (PCD), vital for neurodegenerative diseases like Alzheimer's disease (AD) and Parkinson's disease (PD). We propose a new framework PCDLnc, and identified 20 significant lncRNAs, including HEIH, SNHG15, and SNHG5, associated with PCD gene sets, which were known for roles in proliferation and apoptosis in neurodegenerative diseases. By using GREAT software, we identified regulatory functions of top lncRNAs in different neurodegenerative diseases. Moreover, lncRNAs cis-regulated mRNAs linked to neurodegeneration, including JAK2, AKT1, EGFR, CDC42, SNCA, and ADIPOQ, highlighting their therapeutic potential in neurodegenerative diseases. A further exploration into the differential expression of mRNA identified by PCDLnc revealed a role in apoptosis, ferroptosis and autophagy. Additionally, protein-protein interaction (PPI) network analysis exposed abnormal interactions among key genes, despite their consistent expression levels between disease and normal samples. The randomforest model effectively distinguished between disease samples, indicating a high level of accuracy. Shared gene subsets in AD and PD might serve as potential biomarkers, along with disease-specific gene sets. Besides, we also found the strong relationship between AD and immune infiltration. This research highlights the role of lncRNAs and their associated genes in PCD in neurodegenerative diseases, offering potential therapeutic targets and diagnostic markers for future study and clinical application.
Assuntos
Doença de Alzheimer , Apoptose , Doença de Parkinson , RNA Longo não Codificante , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Doença de Alzheimer/genética , Doença de Alzheimer/patologia , Doença de Alzheimer/metabolismo , Doença de Parkinson/genética , Doença de Parkinson/patologia , Doença de Parkinson/metabolismo , Humanos , Apoptose/genética , Redes Reguladoras de Genes , Mapas de Interação de Proteínas/genética , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Ferroptose/genética , Regulação da Expressão Gênica , Autofagia/genéticaRESUMO
Objective: This study aims to investigate the relationship and mechanisms of action among academic stress, academic anxiety, academic self-efficacy, and academic burnout among adolescents. Methods: A study of 929 Chinese adolescents (53.71% males, mean age = 11.94 years, SD = 0.77) was conducted using the Study Stress Questionnaire, Academic Anxiety Subscale, Junior Middle School Students' Learning Weariness Scale, and the Academic Self-efficacy Questionnaire. Results: â Academic stress was significantly and positively correlated with academic anxiety and academic burnout, and significantly and negatively correlated with academic self-efficacy. â¡Academic anxiety partially mediated the relationship between academic stress and academic burnout. â¢Academic self-efficacy significantly moderated the direct effect of academic stress on academic burnout, and higher academic self-efficacy could buffer the negative effect of academic stress. â£Academic self-efficacy significantly moderated the second half of the mediated model's path (academic anxiety â academic burnout), that is, low academic self-efficacy amplified the risk effect of academic anxiety on academic burnout. Conclusion: Academic anxiety partially mediates the relationship between academic stress and academic burnout, and this mediating role is moderated by academic self-efficacy.