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Cortisol reactivity to a psychosocial stressor significantly increases the risk of developing Cognitive Impairment no Dementia five years later
Psychoneuroendocrinology ( IF 3.7 ) Pub Date : 2020-05-01 , DOI: 10.1016/j.psyneuen.2020.104601
Juliana Nery de Souza-Talarico 1 , Andrea Regiani Alves 1 , Sonia Maria Dozzi Brucki 2 , Ricardo Nitrini 2 , Sonia J Lupien 3 , Deborah Suchecki 4
Affiliation  

Alzheimer's disease (AD) patients show high cortisol levels suggesting that biological mediators of stress may play a role in the neurodegenerative process of cognitive disorders. However, there is no consensus as to whether cortisol concentrations represent a risk factor for the development of cognitive impairment. We analyzed the potential association between the incidence of cognitive impairment and cortisol concentrations under basal and acute stress conditions in 129 individuals aged 50 years or older, with preserved cognitive and functional abilities. All participants were recruited in 2011 for assessment of cognitive performance and cortisol levels. Cortisol was analyzed in saliva samples collected during two typical and consecutive days, in the morning, afternoon, and night, and also during exposure to an acute psychosocial stressor (Trier Social Stress Test - TSST). After a five-year follow-up, 69 of these volunteers were reassessed for cognitive performance, functional evaluation, memory complaints, and depression. The incidence of cognitive impairment not dementia (CIND) was 26.1 %, and was positively associated with greater TSST-induced cortisol release (responsiveness) [(95 % CI = 1.001-1.011; B = 0.006), p = 0.023]. Moreover, five years before diagnosis, participants who later developed CIND had greater responsiveness to TSST (p = 0.019) and lower cortisol awakening response (CAR: p = 0.018), as compared to those who did not develop CIND. These findings suggest that higher psychosocial stress responsiveness profiles may represent a preclinical sign of cognitive impairment.

中文翻译:

皮质醇对社会心理压力的反应会显着增加五年后发生认知障碍的风险,而不是痴呆症

阿尔茨海默病 (AD) 患者表现出高皮质醇水平,这表明压力的生物介质可能在认知障碍的神经退行性过程中发挥作用。然而,对于皮质醇浓度是否代表认知障碍发展的危险因素,尚无共识。我们分析了 129 名 50 岁或 50 岁以上、认知和功能能力保留的个体在基础和急性压力条件下认知障碍的发生率与皮质醇浓度之间的潜在关联。所有参与者均于 2011 年招募,用于评估认知表现和皮质醇水平。在典型的连续两天(早上、下午和晚上)收集的唾液样本中分析皮质醇,以及在暴露于急性心理社会压力源期间(特里尔社会压力测试 - TSST)。经过五年的随访,其中 69 名志愿者接受了认知表现、功能评估、记忆力抱怨和抑郁症的重新评估。认知障碍而非痴呆 (CIND) 的发生率为 26.1%,与 TSST 诱导的皮质醇释放(反应性)呈正相关[(95% CI = 1.001-1.011;B = 0.006),p = 0.023]。此外,在诊断前五年,与未患 CIND 的参与者相比,后来患上 CIND 的参与者对 TSST 的反应更高(p = 0.019),皮质醇觉醒反应(CAR:p = 0.018)更低。这些发现表明,较高的社会心理压力反应谱可能代表认知障碍的临床前迹象。经过五年的随访,其中 69 名志愿者接受了认知表现、功能评估、记忆力抱怨和抑郁症的重新评估。认知障碍而非痴呆 (CIND) 的发生率为 26.1%,与 TSST 诱导的皮质醇释放(反应性)呈正相关[(95% CI = 1.001-1.011;B = 0.006),p = 0.023]。此外,在诊断前五年,与未患 CIND 的参与者相比,后来患上 CIND 的参与者对 TSST 的反应更高(p = 0.019),皮质醇觉醒反应(CAR:p = 0.018)更低。这些发现表明,较高的社会心理压力反应谱可能代表认知障碍的临床前迹象。经过五年的随访,其中 69 名志愿者接受了认知表现、功能评估、记忆力抱怨和抑郁症的重新评估。认知障碍而非痴呆 (CIND) 的发生率为 26.1%,与 TSST 诱导的皮质醇释放(反应性)呈正相关[(95% CI = 1.001-1.011;B = 0.006),p = 0.023]。此外,在诊断前五年,与未患 CIND 的参与者相比,后来患上 CIND 的参与者对 TSST 的反应更高(p = 0.019),皮质醇觉醒反应(CAR:p = 0.018)更低。这些发现表明,较高的社会心理压力反应谱可能代表认知障碍的临床前迹象。和抑郁症。认知障碍而非痴呆 (CIND) 的发生率为 26.1%,与 TSST 诱导的皮质醇释放(反应性)呈正相关[(95% CI = 1.001-1.011;B = 0.006),p = 0.023]。此外,在诊断前五年,与未患 CIND 的参与者相比,后来患上 CIND 的参与者对 TSST 的反应更高(p = 0.019),皮质醇觉醒反应(CAR:p = 0.018)更低。这些发现表明,较高的社会心理压力反应谱可能代表认知障碍的临床前迹象。和抑郁症。认知障碍而非痴呆 (CIND) 的发生率为 26.1%,与 TSST 诱导的皮质醇释放(反应性)呈正相关[(95% CI = 1.001-1.011;B = 0.006),p = 0.023]。此外,在诊断前五年,与未患 CIND 的参与者相比,后来患上 CIND 的参与者对 TSST 的反应更高(p = 0.019),皮质醇觉醒反应(CAR:p = 0.018)更低。这些发现表明,较高的社会心理压力反应谱可能代表认知障碍的临床前迹象。与没有发展为 CIND 的参与者相比,后来发展为 CIND 的参与者对 TSST 的反应更大(p = 0.019),皮质醇觉醒反应(CAR:p = 0.018)更低。这些发现表明,较高的社会心理压力反应谱可能代表认知障碍的临床前迹象。与没有发展为 CIND 的参与者相比,后来发展为 CIND 的参与者对 TSST 的反应更大(p = 0.019),皮质醇觉醒反应(CAR:p = 0.018)更低。这些发现表明,较高的社会心理压力反应谱可能代表认知障碍的临床前迹象。
更新日期:2020-05-01
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