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定量临床前阿尔茨海默病中的疑似视网膜神经胶质增生。

Quantifying Putative Retinal Gliosis in Preclinical Alzheimer's Disease.

机构信息

School of Optometry, University of Alabama at Birmingham, Birmingham, Alabama, United States.

Department of Neurology, Alpert Medical School of Brown University, Providence, Rhode Island, United States.

出版信息

Invest Ophthalmol Vis Sci. 2024 May 1;65(5):5. doi: 10.1167/iovs.65.5.5.

Abstract

PURPOSE

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.

METHODS

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.

RESULTS

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.

CONCLUSIONS

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

目的

神经炎症在阿尔茨海默病(AD)的病理学中起着重要作用。AD 的小鼠模型和 AD 患者的死后活检显示,视网膜神经胶质的激活与中枢神经系统的免疫反应相当。我们假设,使用共焦光学相干断层扫描(OCT)成像在体内观察到的假定视网膜神经胶质增生的表面积在有临床前 AD 的患者中比对照组更大。

方法

使用 Spectralis II 仪器获取黄斑中心 20×20 和 30×25 度的光谱域 OCT 图像,共纳入 76 名参与者(132 只眼)。对 22 名有临床前 AD 的患者(40 只眼,平均年龄=69 岁,范围=60-80 岁)和 20 名对照参与者(32 只眼,平均年龄=66 岁,范围=58-82 岁,P=0.11)进行评估,比较假定视网膜神经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 9 个早期糖尿病视网膜病变研究(ETDRS)地图区域的假定视网膜神经胶质增生和 RNFL 厚度的表面积。

结果

临床前 AD 组的假定视网膜神经胶质增生表面积明显大于对照组(0.97±0.55mm2 比 0.68±0.40mm2;F(1,70)=4.41,P=0.039;Cohen's d=0.61)。9 个 ETDRS 区域的 RNFL 厚度在两组之间无显著差异,P>0.05。

结论

我们的分析表明,临床前 AD 患者的假定视网膜神经胶质增生比对照组更大。这表明假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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9817/11077916/fdeaf20eaf09/iovs-65-5-5-f001.jpg

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