{"title":"中风后抑郁网络自发重组的机制。","authors":"Yirong Fang, Xian Chao, Zeyu Lu, Hongmei Huang, Ran Shi, Dawei Yin, Hao Chen, Yanan Lu, Jinjing Wang, Peng Wang, Xinfeng Liu, Wen Sun","doi":"10.1016/j.nicl.2024.103723","DOIUrl":null,"url":null,"abstract":"<p><p>Exploring the causal relationship between focal brain lesions and post-stroke depression (PSD) can provide therapeutic insights. However, a gap exists between causal and therapeutic information. Exploring post-stroke brain repair processes post-stroke could bridge this gap. We defined a depression network using the normative connectome and investigated the predictive capacity of lesion-induced network damage on depressive symptoms in discovery cohort of 96 patients, at baseline and six months post-stroke. Stepwise functional connectivity (SFC) was used to examine topological changes in the depression network over time to identify patterns of network reorganization. The predictive value of reorganization information was evaluated for follow-up symptoms in discovery and validation cohort 1 (22 worsening PSD patients) as well as for treatment responsiveness in validation cohort 2 (23 antidepressant-treated patients). We evaluated the consistency of significant reorganization areas with neuromodulation targets. Spatial correlations of network reorganization patterns with gene expression and neurotransmitter maps were analyzed. The predictive power of network damage for symptoms diminished at follow-up compared to baseline (Δadjusted R<sup>2</sup> = -0.070, p < 0.001). Reorganization information effectively predicted symptoms at follow-up in the discovery cohort (adjust R<sup>2</sup> = 0.217, 95 %CI: 0.010 to 0.431), as well as symptom exacerbation (r = 0.421, p = 0.033) and treatment responsiveness (r = 0.587, p = 0.012) in the validation cohorts. Regions undergoing significant reorganization overlapped with neuromodulatory targets known to be effective in treating depression. The reorganization of the depression network was associated with immune-inflammatory responses gene expressions and gamma-aminobutyric acid. Our findings may yield important insights into the repair mechanisms of PSD and provide a critical context for developing post-stroke treatment strategies.</p>","PeriodicalId":54359,"journal":{"name":"Neuroimage-Clinical","volume":"45 ","pages":"103723"},"PeriodicalIF":3.4000,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11699604/pdf/","citationCount":"0","resultStr":"{\"title\":\"Mechanisms underlying the spontaneous reorganization of depression network after stroke.\",\"authors\":\"Yirong Fang, Xian Chao, Zeyu Lu, Hongmei Huang, Ran Shi, Dawei Yin, Hao Chen, Yanan Lu, Jinjing Wang, Peng Wang, Xinfeng Liu, Wen Sun\",\"doi\":\"10.1016/j.nicl.2024.103723\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Exploring the causal relationship between focal brain lesions and post-stroke depression (PSD) can provide therapeutic insights. However, a gap exists between causal and therapeutic information. Exploring post-stroke brain repair processes post-stroke could bridge this gap. We defined a depression network using the normative connectome and investigated the predictive capacity of lesion-induced network damage on depressive symptoms in discovery cohort of 96 patients, at baseline and six months post-stroke. Stepwise functional connectivity (SFC) was used to examine topological changes in the depression network over time to identify patterns of network reorganization. The predictive value of reorganization information was evaluated for follow-up symptoms in discovery and validation cohort 1 (22 worsening PSD patients) as well as for treatment responsiveness in validation cohort 2 (23 antidepressant-treated patients). We evaluated the consistency of significant reorganization areas with neuromodulation targets. Spatial correlations of network reorganization patterns with gene expression and neurotransmitter maps were analyzed. The predictive power of network damage for symptoms diminished at follow-up compared to baseline (Δadjusted R<sup>2</sup> = -0.070, p < 0.001). Reorganization information effectively predicted symptoms at follow-up in the discovery cohort (adjust R<sup>2</sup> = 0.217, 95 %CI: 0.010 to 0.431), as well as symptom exacerbation (r = 0.421, p = 0.033) and treatment responsiveness (r = 0.587, p = 0.012) in the validation cohorts. Regions undergoing significant reorganization overlapped with neuromodulatory targets known to be effective in treating depression. The reorganization of the depression network was associated with immune-inflammatory responses gene expressions and gamma-aminobutyric acid. Our findings may yield important insights into the repair mechanisms of PSD and provide a critical context for developing post-stroke treatment strategies.</p>\",\"PeriodicalId\":54359,\"journal\":{\"name\":\"Neuroimage-Clinical\",\"volume\":\"45 \",\"pages\":\"103723\"},\"PeriodicalIF\":3.4000,\"publicationDate\":\"2024-12-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11699604/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neuroimage-Clinical\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1016/j.nicl.2024.103723\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"NEUROIMAGING\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuroimage-Clinical","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.nicl.2024.103723","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"NEUROIMAGING","Score":null,"Total":0}
Mechanisms underlying the spontaneous reorganization of depression network after stroke.
Exploring the causal relationship between focal brain lesions and post-stroke depression (PSD) can provide therapeutic insights. However, a gap exists between causal and therapeutic information. Exploring post-stroke brain repair processes post-stroke could bridge this gap. We defined a depression network using the normative connectome and investigated the predictive capacity of lesion-induced network damage on depressive symptoms in discovery cohort of 96 patients, at baseline and six months post-stroke. Stepwise functional connectivity (SFC) was used to examine topological changes in the depression network over time to identify patterns of network reorganization. The predictive value of reorganization information was evaluated for follow-up symptoms in discovery and validation cohort 1 (22 worsening PSD patients) as well as for treatment responsiveness in validation cohort 2 (23 antidepressant-treated patients). We evaluated the consistency of significant reorganization areas with neuromodulation targets. Spatial correlations of network reorganization patterns with gene expression and neurotransmitter maps were analyzed. The predictive power of network damage for symptoms diminished at follow-up compared to baseline (Δadjusted R2 = -0.070, p < 0.001). Reorganization information effectively predicted symptoms at follow-up in the discovery cohort (adjust R2 = 0.217, 95 %CI: 0.010 to 0.431), as well as symptom exacerbation (r = 0.421, p = 0.033) and treatment responsiveness (r = 0.587, p = 0.012) in the validation cohorts. Regions undergoing significant reorganization overlapped with neuromodulatory targets known to be effective in treating depression. The reorganization of the depression network was associated with immune-inflammatory responses gene expressions and gamma-aminobutyric acid. Our findings may yield important insights into the repair mechanisms of PSD and provide a critical context for developing post-stroke treatment strategies.
期刊介绍：
NeuroImage: Clinical, a journal of diseases, disorders and syndromes involving the Nervous System, provides a vehicle for communicating important advances in the study of abnormal structure-function relationships of the human nervous system based on imaging.
The focus of NeuroImage: Clinical is on defining changes to the brain associated with primary neurologic and psychiatric diseases and disorders of the nervous system as well as behavioral syndromes and developmental conditions. The main criterion for judging papers is the extent of scientific advancement in the understanding of the pathophysiologic mechanisms of diseases and disorders, in identification of functional models that link clinical signs and symptoms with brain function and in the creation of image based tools applicable to a broad range of clinical needs including diagnosis, monitoring and tracking of illness, predicting therapeutic response and development of new treatments. Papers dealing with structure and function in animal models will also be considered if they reveal mechanisms that can be readily translated to human conditions.
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