Abstract：
BACKGROUND: Apathy, defined as a lack of motivation towards goal-directed behavior, is a common neuropsychiatric symptom in Alzheimer\'s (AD) and Parkinson\'s (PD) disease. However, the mechanism underlying apathy is still unclear. Studies have postulated that the degeneration of frontal cortical and subcortical structures may play a major role in the mechanism of apathy. This study investigates whether associations between degeneration in structural and functional connectivity between frontal and subcortical regions contributes to the development of apathetic behavior and whether these associations differ by diseases.
METHODS: Forty-four patients, 8 with AD, 14 amnestic mild cognitive impairment (aMCI), and 22 PD, received MRI brain scans, a decision-making behavioral task, cognitive and psychosocial assessments including the dimensional apathy scale (DAS). We quantified functional connectivity and white matter tract integrity for a set of frontal and subcortical regions of interest, and examined the associations among fronto-subcortical connectivity, behavioral measures, and the DAS. These associations were tested for patient group interactions.
RESULTS: Combining AD and aMCI into one patient group, the AD/aMCI group showed worse apathy than PD in terms of the total, the executive, and the behavioral/cognitive subscores (see Table 1), while the DAS emotional subscore was not different between the two groups. For the decision-making task, the proportion of trial acceptance was similar between the groups, but AD/aMCI had slower decision latency than PD. Group interaction with brain measures was observed in the association between DAS total score and the functional connectivity between the right pars triangularis in the inferior frontal gyrus and the caudate (See Figure 1; interaction effect: beta = -.367, p = .0422 FDR corrected). The white matter tract connecting the right pars triangularis to subcortical regions also showed a group interaction with DAS total score but at an uncorrected statistical level (Figure 2; beta = 3.61, p = .0454, uncorrected).
CONCLUSIONS: Our preliminary analyses exposed phenotypic differences in apathy profiles and decision-making behavior between AD and PD. Furthermore, the observed functional and structural neurodegenerative changes associated with higher apathy severity may also differ between the two diseases. Future analyses in a larger cohort will examine distinct neurodegeneration patterns between the two diseases.
METHODS: Forty-four patients, 8 with AD, 14 amnestic mild cognitive impairment (aMCI), and 22 PD, received MRI brain scans, a decision-making behavioral task, cognitive and psychosocial assessments including the dimensional apathy scale (DAS). We quantified functional connectivity and white matter tract integrity for a set of frontal and subcortical regions of interest, and examined the associations among fronto-subcortical connectivity, behavioral measures, and the DAS. These associations were tested for patient group interactions.
RESULTS: Combining AD and aMCI into one patient group, the AD/aMCI group showed worse apathy than PD in terms of the total, the executive, and the behavioral/cognitive subscores (see Table 1), while the DAS emotional subscore was not different between the two groups. For the decision-making task, the proportion of trial acceptance was similar between the groups, but AD/aMCI had slower decision latency than PD. Group interaction with brain measures was observed in the association between DAS total score and the functional connectivity between the right pars triangularis in the inferior frontal gyrus and the caudate (See Figure 1; interaction effect: beta = -.367, p = .0422 FDR corrected). The white matter tract connecting the right pars triangularis to subcortical regions also showed a group interaction with DAS total score but at an uncorrected statistical level (Figure 2; beta = 3.61, p = .0454, uncorrected).
CONCLUSIONS: Our preliminary analyses exposed phenotypic differences in apathy profiles and decision-making behavior between AD and PD. Furthermore, the observed functional and structural neurodegenerative changes associated with higher apathy severity may also differ between the two diseases. Future analyses in a larger cohort will examine distinct neurodegeneration patterns between the two diseases.
摘要：
背景：冷漠，定义为缺乏对目标导向行为的动机，是阿尔茨海默病（AD）和帕金森病（PD）的常见神经精神症状。然而,冷漠的潜在机制仍不清楚。研究表明，额叶皮质和皮质下结构的退化可能在冷漠机制中起主要作用。这项研究调查了额叶和皮质下区域之间结构和功能连接的变性之间的关联是否有助于冷漠行为的发展，以及这些关联是否因疾病而有所不同。
方法：44名患者，8、AD14遗忘型轻度认知障碍（aMCI），22PD,接受了核磁共振脑部扫描,决策行为任务，认知和心理社会评估，包括维度冷漠量表(DAS)。我们量化了一组感兴趣的额叶和皮质下区域的功能连通性和白质束完整性，并检查了额叶-皮质下连通性之间的关联，行为措施，和DAS。针对患者组的相互作用测试了这些关联。
结果：将AD和aMCI合并到一个患者组中，AD/aMCI组比PD组表现出更差的冷漠，行政人员,和行为/认知子得分(见表1)，而DAS情绪分评分在两组间无差异。对于决策任务，试验接受的比例在组间相似，但AD/aMCI的决策潜伏期比PD慢。在DAS总分与额下回右三角和尾状部之间的功能连接之间的关联中观察到与脑测量值的组相互作用(参见图1;相互作用效应:β=-.367,p=.0422FDR校正)。连接右侧三角条到皮质下区域的白质束也显示出与DAS总分的组相互作用，但处于未校正的统计水平（图2;β=3.61，p=.0454，未校正）。
结论：我们的初步分析揭示了AD和PD之间冷漠特征和决策行为的表型差异。此外，观察到的与较高的冷漠严重程度相关的功能和结构神经退行性变化在两种疾病之间也可能有所不同。在更大的队列中的未来分析将检查两种疾病之间不同的神经变性模式。
方法：44名患者，8、AD14遗忘型轻度认知障碍（aMCI），22PD,接受了核磁共振脑部扫描,决策行为任务，认知和心理社会评估，包括维度冷漠量表(DAS)。我们量化了一组感兴趣的额叶和皮质下区域的功能连通性和白质束完整性，并检查了额叶-皮质下连通性之间的关联，行为措施，和DAS。针对患者组的相互作用测试了这些关联。
结果：将AD和aMCI合并到一个患者组中，AD/aMCI组比PD组表现出更差的冷漠，行政人员,和行为/认知子得分(见表1)，而DAS情绪分评分在两组间无差异。对于决策任务，试验接受的比例在组间相似，但AD/aMCI的决策潜伏期比PD慢。在DAS总分与额下回右三角和尾状部之间的功能连接之间的关联中观察到与脑测量值的组相互作用(参见图1;相互作用效应:β=-.367,p=.0422FDR校正)。连接右侧三角条到皮质下区域的白质束也显示出与DAS总分的组相互作用，但处于未校正的统计水平（图2;β=3.61，p=.0454，未校正）。
结论：我们的初步分析揭示了AD和PD之间冷漠特征和决策行为的表型差异。此外，观察到的与较高的冷漠严重程度相关的功能和结构神经退行性变化在两种疾病之间也可能有所不同。在更大的队列中的未来分析将检查两种疾病之间不同的神经变性模式。
