Memory and Aging Center, Department of Neurology, Sandler Neurosciences Center, University of California, San Francisco, CA 94158, USA.
Proc Natl Acad Sci U S A. 2013 Jun 11;110(24):9944-9. doi: 10.1073/pnas.1301119110. Epub 2013 May 28.
Emotional changes are common in mild cognitive impairment (MCI) and Alzheimer's disease (AD). Intrinsic connectivity imaging studies suggest that default mode network degradation in AD is accompanied by the release of an emotion-relevant salience network. We investigated whether emotional contagion, an evolutionarily conserved affect-sharing mechanism, is higher in MCI and AD secondary to biological alterations in neural networks that support emotion. We measured emotional contagion in 237 participants (111 healthy controls, 62 patients with MCI, and 64 patients with AD) with the Interpersonal Reactivity Index Personal Distress subscale. Depressive symptoms were evaluated with the Geriatric Depression Scale. Participants underwent structural MRI, and voxel-based morphometry was used to relate whole-brain maps to emotional contagion. Analyses of covariance found significantly higher emotional contagion at each stage of disease progression [controls < MCI (P < 0.01) and MCI < AD (P < 0.001)]. Depressive symptoms were also higher in patients compared with controls [controls < MCI (P < 0.01) and controls < AD (P < 0.0001)]. Higher emotional contagion (but not depressive symptoms) was associated with smaller volume in right inferior, middle, and superior temporal gyri (PFWE < 0.05); right temporal pole, anterior hippocampus, parahippocampal gyrus; and left middle temporal gyrus (all P < 0.001, uncorrected). These findings suggest that in MCI and AD, neurodegeneration of temporal lobe structures important for affective signal detection and emotion inhibition are associated with up-regulation of emotion-generating mechanisms. Emotional contagion, a quantifiable index of empathic reactivity that is present in other species, may be a useful tool with which to study emotional alterations in animal models of AD.
情绪变化在轻度认知障碍 (MCI) 和阿尔茨海默病 (AD) 中很常见。内源性连接成像研究表明，AD 中默认模式网络的退化伴随着与情绪相关的显着性网络的释放。我们研究了情绪传染是否更高，这是一种进化保守的情感共享机制，是否由于支持情绪的神经网络的生物学改变而在 MCI 和 AD 中更高。我们使用人际反应指数个人困扰子量表测量了 237 名参与者（111 名健康对照组、62 名 MCI 患者和 64 名 AD 患者）的情绪传染。使用老年抑郁量表评估抑郁症状。参与者接受了结构 MRI 检查，并使用基于体素的形态测量法将全脑图谱与情绪传染相关联。协方差分析发现，在疾病进展的每个阶段，情绪传染都显著更高[对照组< MCI（P<0.01）和 MCI<AD（P<0.001）]。与对照组相比，患者的抑郁症状也更高[对照组< MCI（P<0.01）和对照组<AD（P<0.0001）]。较高的情绪传染（但不是抑郁症状）与右侧下、中、上颞叶（PFWE<0.05）；右侧颞极、前海马、海马旁回；和左中颞叶体积减小相关（所有 P<0.001，未校正）。这些发现表明，在 MCI 和 AD 中，颞叶结构的神经退行性变对于情感信号检测和情绪抑制很重要，与情绪产生机制的上调有关。情绪传染是一种可量化的同理心反应指标，在其他物种中也存在，它可能是研究 AD 动物模型中情绪改变的有用工具。
