Robertson Ian H
Institute of Neuroscience and School of Psychology, Trinity College Dublin, Dublin, Ireland.
Neurobiol Aging. 2014 Jun;35(6):1375-85. doi: 10.1016/j.neurobiolaging.2013.11.028. Epub 2013 Dec 4.
High levels of education, occupational complexity, and/or premorbid intelligence are associated with lower levels of cognitive impairment than would be expected from a given brain pathology. This has been observed across a range of conditions including Alzheimer's disease (Roe et al., 2010), stroke (Ojala-Oksala et al., 2012), traumatic brain injury (Kesler et al., 2003), and penetrating brain injury (Grafman, 1986). This cluster of factors, which seemingly protect the brain from expressing symptoms of damage, has been termed "cognitive reserve" (Stern, 2012). The current review considers one possible neural network, which may contribute to cognitive reserve. Based on the evidence that the neurotransmitter, noradrenaline mediates cognitive reserve's protective effects (Robertson, 2013) this review identifies the neurocognitive correlates of noradrenergic (NA) activity. These involve a set of inter-related cognitive processes (arousal, sustained attention, response to novelty, and awareness) with a strongly right hemisphere, fronto-parietal localization, along with working memory, which is also strongly modulated by NA. It is proposed that this set of processes is one plausible candidate for partially mediating the protective effects of cognitive reserve. In addition to its biological effects on brain structure and function, NA function may also facilitate networks for arousal, novelty, attention, awareness, and working memory, which collectively provide for a set of additional, cognitive, mechanisms that help the brain adapt to age-related changes and disease. It is hypothesized that to the extent that the lateral surface of the right prefrontal lobe and/or the right inferior parietal lobe maintain structural (white and gray matter) and functional integrity and connectivity, cognitive reserve should benefit and behavioral expression of pathologic damage should thus be mitigated.
与特定脑病理学所预期的情况相比，高水平的教育、职业复杂性和/或病前智力与较低水平的认知障碍相关。这一现象在一系列病症中都有观察到，包括阿尔茨海默病（Roe等人，2010年）、中风（Ojala - Oksala等人，2012年）、创伤性脑损伤（Kesler等人，2003年）和穿透性脑损伤（Grafman，1986年）。这一组似乎能保护大脑不表现出损伤症状的因素被称为“认知储备”（Stern，2012年）。本综述考虑了一个可能有助于认知储备的神经网络。基于神经递质去甲肾上腺素介导认知储备保护作用的证据（Robertson，2013年），本综述确定了去甲肾上腺素能（NA）活动的神经认知相关性。这些涉及一组相互关联的认知过程（唤醒、持续注意力、对新奇事物的反应和意识），其在右半球、额顶叶有强烈的定位，同时工作记忆也受到NA的强烈调节。有人提出，这一组过程是部分介导认知储备保护作用的一个合理候选因素。除了对脑结构和功能的生物学影响外，NA功能还可能促进唤醒、新奇性、注意力、意识和工作记忆的网络，这些共同提供了一组额外的认知机制，帮助大脑适应与年龄相关的变化和疾病。据推测，只要右前额叶外侧表面和/或右下顶叶保持结构（白质和灰质）和功能完整性及连通性，认知储备就会受益，病理损伤的行为表现也会因此减轻。
