Pablo Hervella, Maria Luz Alonso-Alonso, Ana Sampedro-Viana, Manuel Rodríguez-Yáñez, Iria López-Dequidt, José M Pumar, Alberto Ouro, Daniel Romaus-Sanjurjo, Francisco Campos, Tomás Sobrino, José Castillo, Yago Leira, Ramón Iglesias-Rey
{"title":"皮层下和大脑深部小血管疾病的不同血液生物标志物。","authors":"Pablo Hervella, Maria Luz Alonso-Alonso, Ana Sampedro-Viana, Manuel Rodríguez-Yáñez, Iria López-Dequidt, José M Pumar, Alberto Ouro, Daniel Romaus-Sanjurjo, Francisco Campos, Tomás Sobrino, José Castillo, Yago Leira, Ramón Iglesias-Rey","doi":"10.1177/17562864241243274","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Cerebral small vessel disease is the most common cause of lacunar strokes (LS). Understanding LS pathogenesis is vital for predicting disease severity, prognosis, and developing therapies.</p><p><strong>Objectives: </strong>To research molecular profiles that differentiate LS in deep brain structures from those in subcortical white matter.</p><p><strong>Design: </strong>Prospective case-control study involving 120 patients with imaging-confirmed LS and a 120 control group.</p><p><strong>Methods: </strong>We examined the relationship between Alzheimer's disease biomarkers [amyloid beta (Aβ<sub>1-40</sub>, Aβ<sub>1-42</sub>)], serum inflammatory marker (interleukin-6, IL-6), and endothelial dysfunction markers [soluble tumor necrosis factor-like weak inducer of apoptosis, and pentraxin-3 (sTWEAK, PTX3)] with respect to LS occurring in deep brain structures and subcortical white matter. In addition, we investigated links between LS, leukoaraiosis presence (white matter hyperintensities, WMHs), and functional outcomes at 3 months. Poor outcome was defined as a modified Rankin scale >2 at 3 months.</p><p><strong>Results: </strong>Significant differences were observed in levels of IL-6, PTX3, and sTWEAK between patients with deep lacunar infarcts and those with recent small subcortical infarcts (20.8 <i>versus</i> 15.6 pg/mL, <i>p</i> < 0.001; 7221.3 <i>versus</i> 4624.4 pg/mL, <i>p</i> < 0.0001; 2528.5 <i>versus</i> 1660.5 pg/mL, <i>p</i> = 0.001). Patients with poor outcomes at 3 months displayed notably higher concentrations of these biomarkers compared to those with good outcomes. By contrast, Aβ<sub>1-40</sub> and Aβ<sub>1-42</sub> were significantly lower in patients with deep LS (<i>p</i> < 0.0001). Aβ<sub>1-42</sub> levels were significantly higher in patients with LS in subcortical white matter who had poor outcomes. WMH severity only showed a significant association with deep LS and correlated with sTWEAK (<i>p</i> < 0.0001).</p><p><strong>Conclusion: </strong>The pathophysiological mechanisms of lacunar infarcts in deep brain structures seem different from those in the subcortical white matter. As a result, specific therapeutic and preventive strategies should be explored.</p>","PeriodicalId":22980,"journal":{"name":"Therapeutic Advances in Neurological Disorders","volume":"17 ","pages":"17562864241243274"},"PeriodicalIF":4.7000,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11143814/pdf/","citationCount":"0","resultStr":"{\"title\":\"Differential blood-based biomarkers of subcortical and deep brain small vessel disease.\",\"authors\":\"Pablo Hervella, Maria Luz Alonso-Alonso, Ana Sampedro-Viana, Manuel Rodríguez-Yáñez, Iria López-Dequidt, José M Pumar, Alberto Ouro, Daniel Romaus-Sanjurjo, Francisco Campos, Tomás Sobrino, José Castillo, Yago Leira, Ramón Iglesias-Rey\",\"doi\":\"10.1177/17562864241243274\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Cerebral small vessel disease is the most common cause of lacunar strokes (LS). Understanding LS pathogenesis is vital for predicting disease severity, prognosis, and developing therapies.</p><p><strong>Objectives: </strong>To research molecular profiles that differentiate LS in deep brain structures from those in subcortical white matter.</p><p><strong>Design: </strong>Prospective case-control study involving 120 patients with imaging-confirmed LS and a 120 control group.</p><p><strong>Methods: </strong>We examined the relationship between Alzheimer's disease biomarkers [amyloid beta (Aβ<sub>1-40</sub>, Aβ<sub>1-42</sub>)], serum inflammatory marker (interleukin-6, IL-6), and endothelial dysfunction markers [soluble tumor necrosis factor-like weak inducer of apoptosis, and pentraxin-3 (sTWEAK, PTX3)] with respect to LS occurring in deep brain structures and subcortical white matter. In addition, we investigated links between LS, leukoaraiosis presence (white matter hyperintensities, WMHs), and functional outcomes at 3 months. Poor outcome was defined as a modified Rankin scale >2 at 3 months.</p><p><strong>Results: </strong>Significant differences were observed in levels of IL-6, PTX3, and sTWEAK between patients with deep lacunar infarcts and those with recent small subcortical infarcts (20.8 <i>versus</i> 15.6 pg/mL, <i>p</i> < 0.001; 7221.3 <i>versus</i> 4624.4 pg/mL, <i>p</i> < 0.0001; 2528.5 <i>versus</i> 1660.5 pg/mL, <i>p</i> = 0.001). Patients with poor outcomes at 3 months displayed notably higher concentrations of these biomarkers compared to those with good outcomes. By contrast, Aβ<sub>1-40</sub> and Aβ<sub>1-42</sub> were significantly lower in patients with deep LS (<i>p</i> < 0.0001). Aβ<sub>1-42</sub> levels were significantly higher in patients with LS in subcortical white matter who had poor outcomes. WMH severity only showed a significant association with deep LS and correlated with sTWEAK (<i>p</i> < 0.0001).</p><p><strong>Conclusion: </strong>The pathophysiological mechanisms of lacunar infarcts in deep brain structures seem different from those in the subcortical white matter. As a result, specific therapeutic and preventive strategies should be explored.</p>\",\"PeriodicalId\":22980,\"journal\":{\"name\":\"Therapeutic Advances in Neurological Disorders\",\"volume\":\"17 \",\"pages\":\"17562864241243274\"},\"PeriodicalIF\":4.7000,\"publicationDate\":\"2024-05-31\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11143814/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Therapeutic Advances in Neurological Disorders\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1177/17562864241243274\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q1\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Therapeutic Advances in Neurological Disorders","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1177/17562864241243274","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
Differential blood-based biomarkers of subcortical and deep brain small vessel disease.
Background: Cerebral small vessel disease is the most common cause of lacunar strokes (LS). Understanding LS pathogenesis is vital for predicting disease severity, prognosis, and developing therapies.
Objectives: To research molecular profiles that differentiate LS in deep brain structures from those in subcortical white matter.
Design: Prospective case-control study involving 120 patients with imaging-confirmed LS and a 120 control group.
Methods: We examined the relationship between Alzheimer's disease biomarkers [amyloid beta (Aβ1-40, Aβ1-42)], serum inflammatory marker (interleukin-6, IL-6), and endothelial dysfunction markers [soluble tumor necrosis factor-like weak inducer of apoptosis, and pentraxin-3 (sTWEAK, PTX3)] with respect to LS occurring in deep brain structures and subcortical white matter. In addition, we investigated links between LS, leukoaraiosis presence (white matter hyperintensities, WMHs), and functional outcomes at 3 months. Poor outcome was defined as a modified Rankin scale >2 at 3 months.
Results: Significant differences were observed in levels of IL-6, PTX3, and sTWEAK between patients with deep lacunar infarcts and those with recent small subcortical infarcts (20.8 versus 15.6 pg/mL, p < 0.001; 7221.3 versus 4624.4 pg/mL, p < 0.0001; 2528.5 versus 1660.5 pg/mL, p = 0.001). Patients with poor outcomes at 3 months displayed notably higher concentrations of these biomarkers compared to those with good outcomes. By contrast, Aβ1-40 and Aβ1-42 were significantly lower in patients with deep LS (p < 0.0001). Aβ1-42 levels were significantly higher in patients with LS in subcortical white matter who had poor outcomes. WMH severity only showed a significant association with deep LS and correlated with sTWEAK (p < 0.0001).
Conclusion: The pathophysiological mechanisms of lacunar infarcts in deep brain structures seem different from those in the subcortical white matter. As a result, specific therapeutic and preventive strategies should be explored.
期刊介绍：
Therapeutic Advances in Neurological Disorders is a peer-reviewed, open access journal delivering the highest quality articles, reviews, and scholarly comment on pioneering efforts and innovative studies across all areas of neurology. The journal has a strong clinical and pharmacological focus and is aimed at clinicians and researchers in neurology, providing a forum in print and online for publishing the highest quality articles in this area.
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