Rashidi-Ranjbar Neda, Rajji Tarek K, Kumar Sanjeev, Herrmann Nathan, Mah Linda, Flint Alastair J, Fischer Corinne E, Butters Meryl A, Pollock Bruce G, Dickie Erin W, Anderson John A E, Mulsant Benoit H, Voineskos Aristotle N
Institute of Medical Science, University of Toronto, Toronto, ON, Canada.
Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, ON, Canada.
Neuropsychopharmacology. 2020 Aug;45(9):1567-1578. doi: 10.1038/s41386-020-0715-y. Epub 2020 May 18.
A history of depression is a risk factor for dementia. Despite strong epidemiologic evidence, the pathways linking depression and dementia remain unclear. We assessed structural brain alterations in white and gray matter of frontal-executive and corticolimbic circuitries in five groups of older adults putatively at-risk for developing dementia- remitted depression (MDD), non-amnestic MCI (naMCI), MDD+naMCI, amnestic MCI (aMCI), and MDD+aMCI. We also examined two other groups: non-psychiatric ("healthy") controls (HC) and individuals with Alzheimer's dementia (AD). Magnetic resonance imaging (MRI) data were acquired on the same 3T scanner. Following quality control in these seven groups, from diffusion-weighted imaging (n = 300), we compared white matter fractional anisotropy (FA), mean diffusivity (MD), and from T1-weighted imaging (n = 333), subcortical volumes and cortical thickness in frontal-executive and corticolimbic regions of interest (ROIs). We also used exploratory graph theory analysis to compare topological properties of structural covariance networks and hub regions. We found main effects for diagnostic group in FA, MD, subcortical volume, and cortical thickness. These differences were largely due to greater deficits in the AD group and to a lesser extent aMCI compared with other groups. Graph theory analysis revealed differences in several global measures among several groups. Older individuals with remitted MDD and naMCI did not have the same white or gray matter changes in the frontal-executive and corticolimbic circuitries as those with aMCI or AD, suggesting distinct neural mechanisms in these disorders. Structural covariance global metrics suggested a potential difference in brain reserve among groups.
抑郁症病史是痴呆症的一个风险因素。尽管有强有力的流行病学证据，但抑郁症与痴呆症之间的联系途径仍不清楚。我们评估了五组可能有患痴呆症风险的老年人额叶-执行和皮质-边缘回路的白质和灰质结构改变，这些老年人包括缓解期抑郁症（MDD）、非遗忘型轻度认知障碍（naMCI）、MDD+naMCI、遗忘型轻度认知障碍（aMCI）以及MDD+aMCI。我们还检查了另外两组：非精神科（“健康”）对照（HC）和患有阿尔茨海默病痴呆症（AD）患者。在同一台3T扫描仪上采集磁共振成像（MRI）数据。在对这七组数据进行质量控制后，我们从扩散加权成像（n = 300）中比较了白质分数各向异性（FA）、平均扩散率（MD），并从T1加权成像（n = 333）中比较了额叶-执行和皮质-边缘感兴趣区域（ROI）的皮质下体积和皮质厚度。我们还使用探索性图论分析来比较结构协方差网络和枢纽区域的拓扑特性。我们发现诊断组在FA、MD、皮质下体积和皮质厚度方面存在主要影响。这些差异主要是由于AD组的缺陷更大，与其他组相比，aMCI组的缺陷程度较小。图论分析揭示了几组之间在几个全局测量指标上的差异。缓解期MDD和naMCI的老年人在额叶-执行和皮质-边缘回路中的白质或灰质变化与aMCI或AD患者不同，这表明这些疾病存在不同的神经机制。结构协方差全局指标表明各组之间脑储备可能存在差异。
