Stress responses are essential for survival, but become detrimental to health and cognition with chronic activation. Chronic hypothalamic-pituitary-adrenal axis release of glucocorticoids induces hypothalamic-pituitary-adrenal axis dysfunction and neuronal loss, decreases learning and memory, and modifies glucocorticoid receptor/mineralocorticoid receptor expression. Elderly who report increased stress are nearly 3 times more likely to develop Alzheimer’s disease, have decreased global cognition and faster cognitive decline than those reporting no stress. Patients with mild cognitive impairment are more sensitive to stress compared to healthy elderly and those with Alzheimer’s disease. Stress may also transduce neurodegeneration via the gut microbiome. Coping styles determine hippocampal mineralocorticoid receptor expression in mice, indicating that coping modifies cortisol’s effect on the brain. Identifying neuroprotective coping strategies that lessen the burden of stress may prevent or slow cognitive decline. Treatments and education designed to reduce stress should be recognized as neuroprotective.

压力反应对于生存至关重要，但随着慢性激活，对健康和认知产生不利影响。糖皮质激素的慢性下丘脑-垂体-肾上腺轴释放诱导下丘脑-垂体-肾上腺轴功能障碍和神经元丢失，减少学习和记忆，并修饰糖皮质激素受体/盐皮质激素受体表达。与没有压力的人相比，那些压力增加的老年人患阿尔茨海默氏病，整体认知能力下降和认知能力下降的可能性要高出将近三倍。与健康的老年人和患有阿尔茨海默氏病的患者相比，轻度认知障碍的患者对压力更敏感。压力也可能通过肠道微生物组转导神经变性。应对方式决定了小鼠海马盐皮质激素受体的表达，表明应对改变了皮质醇对大脑的影响。确定减轻压力负担的神经保护应对策略可以预防或减缓认知能力下降。旨在减轻压力的治疗和教育应被认为具有神经保护作用。