J Neurosci:老年人记忆力减退与压力荷尔蒙分泌有关
科技日报 · 2014/06/25
据凤凰科技报道,一项发表在期刊《神经科学》上的研究称,较高的皮质醇水平——一种体内存在的自然荷尔蒙,在我们感到有压力时会增加——会在我们逐渐衰老的过程中导致记忆的丢失。


近日美国爱荷华大学进行的一项最新研究报告称老年人的短期记忆丧失与压力荷尔蒙有关。据凤凰科技报道,这项发表在期刊《神经科学》上的研究揭示了较高的皮质醇水平——一种体内存在的自然荷尔蒙,在我们感到有压力时会增加——会在我们逐渐衰老的过程中导致记忆的丢失。

皮质醇水平的短期增加至关重要,它将帮助我们变得更警惕且反应更加迅速,从而让我们更好的应对生活中的挑战。然而,异常高的皮质醇水平或者皮质醇水平峰值时间持续过长——正如我们应对长期压力时所发生的情形一样——可能会导致负面的效果,大量有关人体的研究显示这会引发消化问题、焦虑、体重增加和较高的血压。

在这项研究里,美国爱荷华大学的研究学者将升高的皮质醇水平与前额皮质突触的逐渐流失相联系,后者是负责短期记忆的大脑区域。突触是帮助我们处理、储存和回忆信息的关联点。当我们逐渐衰老时,反复和长期暴露在皮质醇下可能会导致后者的锐减和消失。

虽然这项研究仍处于初步阶段,但它的发现提供了一种可能性,也即通过利用某些降低敏感个体皮质醇水平的疗法,逐渐衰老的成年人的短期记忆衰退过程或可以减慢甚至预防,莱德利这样说道。这意味着或可以治疗那些具有与生俱来较高皮质醇水平的人们——例如那些长期面临压力的人,或者那些因痛苦的创伤,例如爱人的死亡,而面临反复长期的压力的人们。
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  • Adrenocortical Status Predicts the Degree of Age-Related Deficits in Prefrontal Structural Plasticity and Working Memory

    Cognitive decline in aging is marked by considerable variability, with some individuals experiencing significant impairments and others retaining intact functioning. Whereas previous studies have linked elevated hypothalamo-pituitary-adrenal (HPA) axis activity with impaired hippocampal function during aging, the idea has languished regarding whether such differences may underlie the deterioration of other cognitive functions. Here we investigate whether endogenous differences in HPA activity are predictive of age-related impairments in prefrontal structural and behavioral plasticity. Young and aged rats (4 and 21 months, respectively) were partitioned into low or high HPA activity, based upon averaged values of corticosterone release from each animal obtained from repeated sampling across a 24 h period. Pyramidal neurons in the prelimbic area of medial prefrontal cortex were selected for intracellular dye filling, followed by 3D imaging and analysis of dendritic spine morphometry. Aged animals displayed dendritic spine loss and altered geometric characteristics; however, these decrements were largely accounted for by the subgroup bearing elevated corticosterone. Moreover, high adrenocortical activity in aging was associated with downward shifts in frequency distributions for spine head diameter and length, whereas aged animals with low corticosterone showed an upward shift in these indices. Follow-up behavioral experiments revealed that age-related spatial working memory deficits were exacerbated by increased HPA activity. By contrast, variations in HPA activity in young animals failed to impact structural or behavioral plasticity. These data implicate the cumulative exposure to glucocorticoids as a central underlying process in age-related prefrontal impairment and define synaptic features accounting for different trajectories in age-related cognitive function.

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