PDF(Pubmed)
Abstract：
UNASSIGNED: 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.
UNASSIGNED: To research molecular profiles that differentiate LS in deep brain structures from those in subcortical white matter.
UNASSIGNED: Prospective case-control study involving 120 patients with imaging-confirmed LS and a 120 control group.
UNASSIGNED: 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.
UNASSIGNED: 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).
UNASSIGNED: 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.
UNASSIGNED: To research molecular profiles that differentiate LS in deep brain structures from those in subcortical white matter.
UNASSIGNED: Prospective case-control study involving 120 patients with imaging-confirmed LS and a 120 control group.
UNASSIGNED: 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.
UNASSIGNED: 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).
UNASSIGNED: 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.
摘要：
■脑小血管病是腔隙性中风（LS）的最常见原因。了解LS发病机制对于预测疾病严重程度至关重要，预后,并开发治疗方法。
■研究将脑深部结构中的LS与皮质下白质中的LS区分开的分子谱。
■前瞻性病例对照研究，包括120例经影像学证实的LS患者和120例对照组。
■我们检查了阿尔茨海默病生物标志物[淀粉样β（Aβ1-40，Aβ1-42）]之间的关系，血清炎症标志物（白细胞介素-6，IL-6），和内皮功能障碍标志物[可溶性肿瘤坏死因子样凋亡弱诱导剂，和pentraxin-3(sTWEAK，PTX3)]关于发生在脑深部结构和皮质下白质中的LS。此外,我们调查了LS之间的联系，脑白质疏松症的存在（白质高信号，WMHs),和3个月时的功能结果。不良结局定义为3个月时改良的Rankin量表>2。
■深腔隙性梗死患者和近期小皮质下梗死患者的IL-6、PTX3和sTWEAK水平存在显著差异（20.8比15.6pg/mL，p<0.001；7221.3对4624.4pg/mL，p<0.0001；2528.5对1660.5pg/mL，p=0.001)。与具有良好结果的患者相比,在3个月时具有差结果的患者显示出显著更高浓度的这些生物标志物。相比之下,Aβ1-40和Aβ1-42在深部LS患者中显著降低(p<0.0001)。在预后较差的皮质下白质LS患者中，Aβ1-42水平明显较高。WMH严重程度仅与深度LS显著相关，与sTWEAK相关(p<0.0001)。
■脑深部结构腔隙性梗死的病理生理机制似乎与皮质下白质不同。因此,应探索具体的治疗和预防策略.
■研究将脑深部结构中的LS与皮质下白质中的LS区分开的分子谱。
■前瞻性病例对照研究，包括120例经影像学证实的LS患者和120例对照组。
■我们检查了阿尔茨海默病生物标志物[淀粉样β（Aβ1-40，Aβ1-42）]之间的关系，血清炎症标志物（白细胞介素-6，IL-6），和内皮功能障碍标志物[可溶性肿瘤坏死因子样凋亡弱诱导剂，和pentraxin-3(sTWEAK，PTX3)]关于发生在脑深部结构和皮质下白质中的LS。此外,我们调查了LS之间的联系，脑白质疏松症的存在（白质高信号，WMHs),和3个月时的功能结果。不良结局定义为3个月时改良的Rankin量表>2。
■深腔隙性梗死患者和近期小皮质下梗死患者的IL-6、PTX3和sTWEAK水平存在显著差异（20.8比15.6pg/mL，p<0.001；7221.3对4624.4pg/mL，p<0.0001；2528.5对1660.5pg/mL，p=0.001)。与具有良好结果的患者相比,在3个月时具有差结果的患者显示出显著更高浓度的这些生物标志物。相比之下,Aβ1-40和Aβ1-42在深部LS患者中显著降低(p<0.0001)。在预后较差的皮质下白质LS患者中，Aβ1-42水平明显较高。WMH严重程度仅与深度LS显著相关，与sTWEAK相关(p<0.0001)。
■脑深部结构腔隙性梗死的病理生理机制似乎与皮质下白质不同。因此,应探索具体的治疗和预防策略.
