目的:神经精神症状(NPS)增加患痴呆的风险,并与各种神经退行性疾病有关。包括轻度认知障碍(由阿尔茨海默病[AD]引起的MCI),脑血管疾病(CVD),和帕金森病(PD)。我们在各种神经退行性诊断中横向和纵向探索了NPS的结构神经相关性。
方法:该研究包括因AD而患有MCI的个体,(n=74),CVD(n=143),和PD(n=137)在基线,在2年的随访中(由于AD,MCI,n=37,CVDn=103,PDn=84)。我们使用神经精神调查问卷评估了NPS的严重程度。对于大脑结构,我们包括与皮质胶质和额叶执行回路相关的预定义感兴趣区域的皮质厚度和皮质下体积。
结果:横截面分析显示,在MCI和CVD组中,食欲与两个回路之间存在显着负相关,而在MCI和PD组中,冷漠与这些电路相关。纵向,MCI组冷漠评分的变化与额叶-执行回路的变化呈负相关.在CVD组中,躁动和夜间行为的变化与皮质边缘和额叶执行回路呈负相关,分别。在PD组,解除抑制和冷漠的变化与皮质边缘和额叶执行回路呈正相关,分别。
结论:观察到的相关性表明,大脑中潜在的病理变化可能导致与MBI相关的神经活动的改变。值得注意的是,横截面和纵向结果之间的差异表明,有必要进行纵向研究以获得可重复的发现并得出可靠的推论。
OBJECTIVE: Neuropsychiatric symptoms (NPS) increase risk of developing dementia and are linked to various neurodegenerative conditions, including mild cognitive impairment (MCI due to Alzheimer\'s disease [AD]), cerebrovascular disease (CVD), and Parkinson\'s disease (PD). We explored the structural neural correlates of NPS cross-sectionally and longitudinally across various neurodegenerative diagnoses.
METHODS: The study included individuals with MCI due to AD, (n = 74), CVD (n = 143), and PD (n = 137) at baseline, and at 2-years follow-up (MCI due to AD, n = 37, CVD n = 103, and PD n = 84). We assessed the severity of NPS using the Neuropsychiatric Inventory Questionnaire. For brain structure we included cortical thickness and subcortical volume of predefined regions of interest associated with corticolimbic and frontal-executive circuits.
RESULTS: Cross-sectional analysis revealed significant negative correlations between appetite with both circuits in the MCI and CVD groups, while apathy was associated with these circuits in both the MCI and PD groups. Longitudinally, changes in apathy scores in the MCI group were negatively linked to the changes of the frontal-executive circuit. In the CVD group, changes in agitation and nighttime behavior were negatively associated with the corticolimbic and frontal-executive circuits, respectively. In the PD group, changes in disinhibition and apathy were positively associated with the corticolimbic and frontal-executive circuits, respectively.
CONCLUSIONS: The observed correlations suggest that underlying pathological changes in the brain may contribute to alterations in neural activity associated with MBI. Notably, the difference between cross-sectional and longitudinal results indicates the necessity of conducting longitudinal studies for reproducible findings and drawing robust inferences.