PDF(Pubmed)
Abstract：
UNASSIGNED: Neuroinflammation plays a significant role in the pathology of Alzheimer\'s disease (AD). Mouse models of AD and postmortem biopsy of patients with AD reveal retinal glial activation comparable to central nervous system immunoreactivity. We hypothesized that the surface area of putative retinal gliosis observed in vivo using en face optical coherence tomography (OCT) imaging will be larger in patients with preclinical AD versus controls.
UNASSIGNED: The Spectralis II instrument was used to acquire macular centered 20 × 20 and 30 × 25-degrees spectral domain OCT images of 76 participants (132 eyes). A cohort of 22 patients with preclinical AD (40 eyes, mean age = 69 years, range = 60-80 years) and 20 control participants (32 eyes, mean age = 66 years, range = 58-82 years, P = 0.11) were included for the assessment of difference in surface area of putative retinal gliosis and retinal nerve fiber layer (RNFL) thickness. The surface area of putative retinal gliosis and RNFL thickness for the nine sectors of the Early Treatment Diabetic Retinopathy Study (ETDRS) map were compared between groups using generalized linear mixed models.
UNASSIGNED: The surface area of putative retinal gliosis was significantly greater in the preclinical AD group (0.97 ± 0.55 mm2) compared to controls (0.68 ± 0.40 mm2); F(1,70) = 4.41, P = 0.039; Cohen\'s d = 0.61. There was no significant difference between groups for RNFL thickness in the 9 ETDRS sectors, P > 0.05.
UNASSIGNED: Our analysis shows greater putative retinal gliosis in preclinical AD compared to controls. This demonstrates putative retinal gliosis as a potential biomarker for AD-related neuroinflammation.
UNASSIGNED: The Spectralis II instrument was used to acquire macular centered 20 × 20 and 30 × 25-degrees spectral domain OCT images of 76 participants (132 eyes). A cohort of 22 patients with preclinical AD (40 eyes, mean age = 69 years, range = 60-80 years) and 20 control participants (32 eyes, mean age = 66 years, range = 58-82 years, P = 0.11) were included for the assessment of difference in surface area of putative retinal gliosis and retinal nerve fiber layer (RNFL) thickness. The surface area of putative retinal gliosis and RNFL thickness for the nine sectors of the Early Treatment Diabetic Retinopathy Study (ETDRS) map were compared between groups using generalized linear mixed models.
UNASSIGNED: The surface area of putative retinal gliosis was significantly greater in the preclinical AD group (0.97 ± 0.55 mm2) compared to controls (0.68 ± 0.40 mm2); F(1,70) = 4.41, P = 0.039; Cohen\'s d = 0.61. There was no significant difference between groups for RNFL thickness in the 9 ETDRS sectors, P > 0.05.
UNASSIGNED: Our analysis shows greater putative retinal gliosis in preclinical AD compared to controls. This demonstrates putative retinal gliosis as a potential biomarker for AD-related neuroinflammation.
摘要：
■神经炎症在阿尔茨海默病（AD）的病理学中起着重要作用。AD小鼠模型和AD患者的死后活检显示视网膜神经胶质激活与中枢神经系统免疫反应性相当。我们假设，在临床前AD患者中，使用表面光学相干断层扫描（OCT）成像在体内观察到的推定视网膜胶质增生的表面积将比对照组更大。
■使用SpectralisII仪器获取76名参与者（132只眼）的黄斑中心20×20和30×25度谱域OCT图像。22例临床前AD患者（40眼，平均年龄=69岁，范围=60-80岁)和20名对照参与者(32只眼睛，平均年龄=66岁，范围=58-82年，P=0.11）用于评估推定的视网膜胶质增生和视网膜神经纤维层（RNFL）厚度的表面积差异。使用广义线性混合模型比较了早期治疗糖尿病视网膜病变研究（ETDRS）图9个部分的假定视网膜胶质增生的表面积和RNFL厚度。
■与对照组（0.68±0.40mm2）相比，临床前AD组推定的视网膜胶质增生的表面积（0.97±0.55mm2）明显更大；F（1,70）=4.41，P=0.039；Cohen\sd=0.61。在9个ETDRS扇区中，RNFL厚度组间无显著差异，P>0.05。
■我们的分析显示，与对照组相比，临床前AD中推定的视网膜胶质增生更大。这证明了推定的视网膜神经胶质增生是AD相关神经炎症的潜在生物标志物。
■使用SpectralisII仪器获取76名参与者（132只眼）的黄斑中心20×20和30×25度谱域OCT图像。22例临床前AD患者（40眼，平均年龄=69岁，范围=60-80岁)和20名对照参与者(32只眼睛，平均年龄=66岁，范围=58-82年，P=0.11）用于评估推定的视网膜胶质增生和视网膜神经纤维层（RNFL）厚度的表面积差异。使用广义线性混合模型比较了早期治疗糖尿病视网膜病变研究（ETDRS）图9个部分的假定视网膜胶质增生的表面积和RNFL厚度。
■与对照组（0.68±0.40mm2）相比，临床前AD组推定的视网膜胶质增生的表面积（0.97±0.55mm2）明显更大；F（1,70）=4.41，P=0.039；Cohen\sd=0.61。在9个ETDRS扇区中，RNFL厚度组间无显著差异，P>0.05。
■我们的分析显示，与对照组相比，临床前AD中推定的视网膜胶质增生更大。这证明了推定的视网膜神经胶质增生是AD相关神经炎症的潜在生物标志物。
