■联系压力和血管疾病的心理生物学过程仍然知之甚少。视网膜和大脑具有共同的胚胎间脑起源和血液屏障生理学,例如持续缺血促进S100B释放,并具有星形细胞活性和神经胶质纤维酸性蛋白表达(GFAP)。然而,GFAP降低揭示了抑郁症/自杀病例的前额叶皮质中的星形胶质细胞病理学;并且可能是应激-疾病途径中的关键机制。
■一种与年龄无关的慢性情绪压力表型,种族或性别被用来将当前的前瞻性队列(N=359;年龄46±9岁)分为应激组(N=236)和无应激组(N=123)。获得神经胶质缺血风险标志物的前瞻性数据,包括24小时BP,空腹S100B,GFAP,HbA1C和肿瘤坏死因子-α(TNF-α)。在3年的随访中:测量舒张压(指示低灌注风险),并从散瞳眼中的数字图像中量化视网膜血管口径。
■高血压(75%vs.16%),糖尿病(13%vs.0%)和视网膜病变(57%vs.与无压力个体相比,在压力中观察到45%)的患病率。压力很大的人一直在提高S100B,TNF-α,HbA1C和高舒张眼压,但GFAP和GFAP:S100B下降。此外,中风风险标志物,动脉狭窄和静脉扩张与S100B持续升高相关,GFAP:S100B(p=0.060),TNF-α和较高的眼压舒张压[Adj.R20.39-0.41,p≤0.05]。在无压力组中没有明显的视网膜-胶质细胞关联。
■视网膜神经胶质缺血和炎症是由慢性应激引起的。持续较高的炎症和具有GFAP的S100B降低进一步反映了人视网膜中应力诱导的星形胶质细胞病理学。建议提高对慢性应激和脑缺血易感性的认识。
UNASSIGNED: Psychobiological processes linking stress and vascular diseases remain poorly understood. The retina and the brain share a common embryonic-diencephalon origin and blood-barrier physiology e.g. ongoing ischemia facilitates S100B release with astrocytic activity and glial-fibrillary-acidic-protein expression (GFAP). However, GFAP decreases revealed astrocyte pathology in the prefrontal cortex of depression/suicide cases; and might be a key mechanism in stress - disease pathways.
UNASSIGNED: A chronic emotional stress phenotype independent of age, ethnicity or sex was used to stratify the current prospective cohort (N = 359; aged 46 ± 9 years) into Stress (N = 236) and no-Stress groups (N = 123). Prospective data for
glia ischemia risk markers were obtained, including 24 h BP, fasting S100B, GFAP, HbA1C and tumor-necrosis-factor-α (TNF-α). At 3-yr follow-up: diastolic-ocular-perfusion-pressure (indicating hypo-perfusion risk) was measured and retinal vessel calibers were quantified from digital images in the mydriatic eye.
UNASSIGNED: Higher hypertension (75% vs. 16%), diabetes (13% vs. 0%) and retinopathy (57% vs. 45%) prevalence was observed in Stress compared to no-Stress individuals. Stressed individuals had consistently raised S100B, TNF-α, HbA1C and higher diastolic-ocular-perfusion-pressure, but decreases in GFAP and GFAP:S100B. Furthermore stroke risk markers, arterial narrowing and venous widening were associated with consistently raised S100B, GFAP:S100B (p = 0.060), TNF-α and higher diastolic-ocular-perfusion-pressure [Adj. R2 0.39-0.41, p ≤ 0.05]. No retinal-
glia associations were evident in the no-Stress group.
UNASSIGNED: Retinal-
glia ischemia and inflammation was induced by chronic stress. Persistent higher inflammation and S100B with GFAP decreases further reflected stress-induced astrocyte pathology in the human retina. It is recommended to increase awareness on chronic stress and susceptibility for brain ischemia.