慢性应激风险表型反映在人类视网膜作为一种神经退行性疾病。

IF 2.6 4区 心理学 Q2 BEHAVIORAL SCIENCES
Leoné Malan, Roelof van Wyk, Roland von Känel, Tjalf Ziemssen, Walthard Vilser, Peter M Nilsson, Martin Magnusson, Amra Jujic, Daniel W Mak, Faans Steyn, Nico T Malan
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引用次数: 0

摘要

大脑是协调应激反应的关键器官,应激反应转化为视网膜。视网膜是大脑的延伸,神经退行性疾病患者的视网膜症状证实眼睛是大脑的窗口。视网膜在这项研究中被用来确定慢性应激是否反映神经退行性疾病的神经退行性体征。一项为期三年的前瞻性队列研究(n = 333;采用Malan应激表型指数将年龄(46±9岁)的患者分为应激表型组(n = 212)和对照组(n = 121)。神经退行性危险标志物包括缺血(星形细胞S100钙结合蛋白B/S100B);24小时血压,蛋白质组学;炎症(肿瘤坏死因子-α/ TNF -α);神经元损伤(神经元特异性烯醇化酶);抗视网膜神经节细胞凋亡(β -神经生长因子),星形胶质细胞活性(胶质-纤维-酸性蛋白);红细胞压积(黏度)和视网膜随访数据[血管;stress-optic-neuropathy]。应力-视神经病变风险通过两个指标计算:与应力表型相关的新导出的舒张-眼灌注压切点≥68 mmHg;结合既定杯盘比临界值≥0.3。与对照组相比,应激型患者的应激-视神经病变(39%对17%)和高血压(73%对16%)患病率更高。舒张-眼灌注压升高,提示灌注不足,与应激表型中动脉狭窄和缺血增加趋势有关。基线、随访和三年变化时应激表型缺血与持续炎症(TNF-α和细胞因子-白细胞介素-17受体-a)、神经元特异性烯醇化酶升高、持续凋亡(几丁质酶-3样蛋白1、低β -神经生长因子)、胶质-纤维-酸性蛋白降低、黏度升高、静脉扩张(血视网膜屏障内皮功能障碍的危险标志)、静脉计数降低和应激-视神经病变升高有关。持续脑缺血、细胞凋亡和内皮功能障碍的应激表型和相关神经退行性体征损害了血视网膜屏障的通透性和视神经的完整性。事实上,压力表型可以识别神经退行性疾病高风险的人,以表明神经退行性疾病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The chronic stress risk phenotype mirrored in the human retina as a neurodegenerative condition.

The brain is the key organ that orchestrates the stress response which translates to the retina. The retina is an extension of the brain and retinal symptoms in subjects with neurodegenerative diseases substantiated the eye as a window to the brain. The retina is used in this study to determine whether chronic stress reflects neurodegenerative signs indicative of neurodegenerative conditions. A three-year prospective cohort (n = 333; aged 46 ± 9 years) was stratified into stress-phenotype cases (n = 212) and controls (n = 121) by applying the Malan stress-phenotype index. Neurodegenerative risk markers included ischemia (astrocytic S100 calcium-binding protein B/S100B); 24-h blood pressure, proteomics; inflammation (tumor-necrosis-factor-α/TNF-α); neuronal damage (neuron-specific-enolase); anti-apoptosis of retinal-ganglion-cells (beta-nerve-growth-factor), astrocytic activity (glial-fibrillary-acidic-protein); hematocrit (viscosity) and retinal follow-up data [vessels; stress-optic-neuropathy]. Stress-optic-neuropathy risk was calculated from two indices: a newly derived diastolic-ocular-perfusion-pressure cut-point ≥68 mmHg relating to the stress-phenotype; combined with an established cup-to-disk ratio cut-point ≥0.3. Higher stress-optic-neuropathy (39% vs. 17%) and hypertension (73% vs. 16%) prevalence was observed in the stress-phenotype cases vs. controls. Elevated diastolic-ocular-perfusion-pressure, indicating hypoperfusion, was related to arterial narrowing and trend for ischemia increases in the stress-phenotype. Ischemia in the stress-phenotype at baseline, follow-up and three-year changes was related to consistent inflammation (TNF-α and cytokine-interleukin-17-receptor-A), neuron-specific-enolase increases, consistent apoptosis (chitinase-3-like protein 1, low beta-nerve-growth-factor), glial-fibrillary-acidic-protein decreases, elevated viscosity, vein widening as risk marker of endothelial dysfunction in the blood-retinal barrier, lower vein count, and elevated stress-optic-neuropathy. The stress-phenotype and related neurodegenerative signs of ongoing brain ischemia, apoptosis and endothelial dysfunction compromised blood-retinal barrier permeability and optic nerve integrity. In fact, the stress-phenotype could identify persons at high risk of neurodegeneration to indicate a neurodegenerative condition.

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来源期刊
CiteScore
5.60
自引率
0.00%
发文量
25
审稿时长
6-12 weeks
期刊介绍: The journal Stress aims to provide scientists involved in stress research with the possibility of reading a more integrated view of the field. Peer reviewed papers, invited reviews and short communications will deal with interdisciplinary aspects of stress in terms of: the mechanisms of stressful stimulation, including within and between individuals; the physiological and behavioural responses to stress, and their regulation, in both the short and long term; adaptive mechanisms, coping strategies and the pathological consequences of stress. Stress will publish the latest developments in physiology, neurobiology, molecular biology, genetics research, immunology, and behavioural studies as they impact on the understanding of stress and its adverse consequences and their amelioration. Specific approaches may include transgenic/knockout animals, developmental/programming studies, electrophysiology, histochemistry, neurochemistry, neuropharmacology, neuroanatomy, neuroimaging, endocrinology, autonomic physiology, immunology, chronic pain, ethological and other behavioural studies and clinical measures.
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