de Souza-Talarico Juliana Nery, Alves Andrea Regiani, Brucki Sonia Maria Dozzi, Nitrini Ricardo, Lupien Sonia J, Suchecki Deborah
Department of Medical-Surgical Nursing, School of Nursing, Universidade de São Paulo, São Paulo, 05403 000, Brazil.
Department of Medical-Surgical Nursing, School of Nursing, Universidade de São Paulo, São Paulo, 05403 000, Brazil.
Psychoneuroendocrinology. 2020 May;115:104601. doi: 10.1016/j.psyneuen.2020.104601. Epub 2020 Feb 7.
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.
阿尔茨海默病（AD）患者表现出高皮质醇水平，这表明应激的生物介质可能在认知障碍的神经退行性过程中起作用。然而，关于皮质醇浓度是否代表认知障碍发展的危险因素，目前尚无定论。我们分析了129名50岁及以上、认知和功能能力保留的个体在基础和急性应激条件下认知障碍发生率与皮质醇浓度之间的潜在关联。所有参与者于2011年被招募，以评估认知表现和皮质醇水平。在连续两个典型日子的上午、下午和晚上，以及在暴露于急性心理社会应激源（特里尔社会应激测试 - TSST）期间采集的唾液样本中分析皮质醇。经过五年的随访，对其中69名志愿者进行了认知表现、功能评估、记忆主诉和抑郁的重新评估。非痴呆性认知障碍（CIND）的发生率为26.1%，且与TSST诱导的皮质醇释放增加（反应性）呈正相关[（95%可信区间 = 1.001 - 1.011；B = 0.006），p = 0.023]。此外，与未发生CIND的参与者相比，在诊断前五年，后来发生CIND的参与者对TSST的反应性更高（p = 0.019），皮质醇觉醒反应（CAR）更低（p = 0.018）。这些发现表明，较高的心理社会应激反应性特征可能代表认知障碍的临床前体征。
