Bioinformatics Applied to Neuroscience

This research topic explores the role of autophagy, immunity, and RNA methylation modification in various neurological diseases, such as intracerebral hemorrhage, ischemic stroke, Parkinson's Disease, Alzheimer's Disease, and major depressive disorder. It also investigates the role of CCT2, m7G modification, and circRNAs in these diseases.

• Bioinformatics methods identified four key autophagy genes associated with intracerebral hemorrhage and explored their mechanisms.
• Hub genes and pathways related to the pathogenesis of ischemic stroke and major depressive disorder were identified, with innate immunity activated and acquired immunity suppressed in both disorders.
• Immune-related genes were strongly related to Parkinson's Disease and could be used to distinguish between PD and normal samples.
• CCT2 was found to be significantly and positively associated with multiple pathways linked to autophagy and negatively associated with neuronal death.
• Five key m7G-related genes were identified that could accurately predict clinical risk of Ischemic Stroke.
• Three circRNAs were identified as potential biomarkers for diagnosing intracerebral hemorrhage.
• Differentially expressed circRNAs derived from circulating exosomes in spinal cord injury rats were investigated.
• Four characteristic genes and potential therapeutic drugs were identified for ischemic stroke.
• A ceRNA regulatory network composed of circRNAs, miRNAs, and mRNAs was established to identify potential biomarkers and therapeutic targets for postoperative cognitive dysfunction.
• Seven CR-related immune biomarkers were identified and four genes were screened as candidate immune biomarkers with good predictive power.
• A novel diagnostic model for Alzheimer's Disease was established using artificial neural networks.
• Machine learning algorithms were used to construct a diagnostic model for major depressive disorder.
• Differentially expressed genes, PCD-related ceRNA regulatory networks, and key regulatory axes were identified for cerebral ischemia/reperfusion injury.
• No causal relationship between C-reactive protein levels and