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Published on: July 14, 2010
Inflammation-induced impairment of synaptic plasticity accelerates atherosclerosis co-depression disease: insights
Yulong Zhao1, Qiang Luo1, Peng Ren1
1School of Rehabilitation Medicine, Gannan Medical University, Ganzhou, 341000, Jiangxi, China.
Insights
This study identifies potential biomarkers for atherosclerosis (AS) and depression co-occurrence. Inflammation-induced synaptic damage is a key mechanism in AS co-depression, offering new diagnostic and treatment avenues.
Area of Science:
- Cardiovascular Research
- Neuroscience
- Biomarker Discovery
Background:
- Atherosclerosis (AS) is a precursor to cardiovascular diseases and frequently co-occurs with depression.
- The complex mechanisms of this comorbidity present clinical treatment challenges.
- This study investigates biomarkers and mechanisms in atherosclerosis co-depression.
Purpose of the Study:
- To identify potential biomarkers for atherosclerosis (AS) comorbid with depression.
- To elucidate the underlying molecular mechanisms driving AS co-depression.
- To validate findings through integrated bioinformatic and experimental approaches.
Main Methods:
- Differential gene expression analysis and protein-protein interaction networks were performed on AS and depression datasets.
- Gene Ontology and KEGG pathway analyses identified enriched biological processes.
- An animal model of AS with depression was established for comprehensive physiological and behavioral assessments, including RNA sequencing and synaptic analysis.
Main Results:
- Thirty genes were co-differentially expressed between AS and depression.
- Shank2, MDGA2, and S100B emerged as potential diagnostic markers.
- Animal models showed elevated lipids, atherosclerotic plaques, depressive behaviors, reduced Shank2 expression, and impaired synaptic plasticity, linked to inflammation.
Conclusions:
- Seven candidate biomarkers for AS co-depression were identified.
- Inflammation-induced synaptic damage is a critical mechanism in AS co-depression.
- Findings provide novel insights for diagnosing and treating AS co-depression disorders.
Background:
Atherosclerosis (AS) serves as the pathological foundation for numerous cardiovascular and cerebrovascular diseases and is highly comorbid with depression. The mechanisms underlying this co-morbidity are exceptionally complex, posing significant challenges to effective clinical treatment. Consequently, our study aims to explore the potential biomarkers and mechanisms involved in developing atherosclerosis co-depression disease.
Methods:
We performed differential expression analysis, protein-protein interaction analysis, Gene Ontology (GO) function enrichment analysis, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis on co-differentiated genes using AS and depression-related datasets from the GEO database. Potential biomarkers were identified through ROC curve analysis. To evaluate the effectiveness of the model, we established an animal model of AS comorbid with depressive disorder and performed a series of assessments, including the sugar-water preference test, open field test, tail suspension test, lipid profile analysis, and pathological examination of aortic sections. Additionally, RNA sequencing analysis of brain tissue, Golgi staining, and detection of synaptic function-related proteins were performed in AS comorbid depressed mice. Finally, in vitro cellular experiments were conducted to further validate the molecular targets and underlying mechanisms.
Results:
We identified 968 differentially expressed genes associated with AS and 472 differentially expressed genes associated with depression, with 30 genes co-differentially expressed. Protein-protein interaction (PPI) analysis revealed that CCR5, CCR2, NPY, and OPRM1 were strongly associated with AS co-depression, while ROC analysis indicated that Shank2, MDGA2, and S100B were diagnostic markers for AS with depression. Differentially expressed genes were closely associated with the chemokine signaling pathway, neuroactive ligand-receptor interaction, cytokine-cytokine receptor interaction, and taste transduction. Animal studies demonstrated that ApoE-/- mice exhibited elevated lipids, atherosclerotic plaques, and depressive behaviors. RNA sequencing revealed that 30 genes were differentially expressed in the high-fat combined bind (HFB) group, with inflammatory pathways also activated in the brain. Shank2 expression was decreased in the hippocampus and prefrontal cortex, and Golgi staining revealed impaired synaptic plasticity. Cellular experiments demonstrated that IL-1β could induce a decrease in Shank2 expression.
Conclusion:
Our study identified seven candidate AS co-depression biomarkers and verified that inflammation-induced damage to synaptic plastic rows is an important mechanism of AS co-depression, providing new insights into the diagnosis and treatment of AS co-depression disorders.
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