Altered Functional Connectivity and Amyloid Deposition in Posttraumatic Stress Disorder-Associated Cognitive Impairment.

Richard Dagher, Parisa Arjmand, Daniel A Stevens, Max Wintermark, Haris I Sair, Vivek Yedavalli, Licia P Luna
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Abstract

Background and purpose: Posttraumatic stress disorder (PTSD) has been linked to an increased risk of cognitive impairment and dementia, with neuroinflammation, metabolic dysfunction, and neuropathologic markers such as β-amyloid and τ implicated as potential mechanisms. However, the roles of altered functional connectivity and amyloid deposition as biomarkers in the progression of cognitive impairment among patients with PTSD remain unclear, with limited and often conflicting evidence from existing neuroimaging studies. This study examines these neuroimaging markers in patients with PTSD with and without cognitive impairment to better understand the neurobiologic pathways contributing to cognitive decline in PTSD.

Materials and methods: Data were obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) and Department of Defense (DOD) databases. A cohort of 178 age-matched male subjects was divided into 4 groups: posttraumatic stress disorder with cognitive impairment (PTSD-CI); posttraumatic stress disorder and cognitively normal (PTSD-CN); non-posttraumatic stress disorder with cognitive impairment (NPTSD-CI); and non-posttraumatic stress disorder and cognitively normal (NPTSD-CN). All subjects underwent resting-state functional MRI and amyloid PET imaging, with PTSD diagnosis and cognitive impairment (CI) confirmed through clinical assessments. Functional connectivity was analyzed by using the CONN Toolbox, and amyloid burden was quantified via standardized uptake value ratios. Analyses controlled for demographic and genetic factors, including age, education, apolipoprotein E4 status, and depression.

Results: Compared with the NPTSD-CN group, the PTSD-CI group showed significantly increased amyloid uptake in the temporal and parietal lobes, with corresponding functional connectivity increase between the bilateral temporal lobes and parietal operculum. In contrast, PTSD-CN patients exhibited no significant amyloid increase but showed increased connectivity between the salience network, postcentral gyri, and sensorimotor areas, and decreased connectivity between the sensorimotor network and anterior cingulate cortex. These distinct patterns suggest differing neurobiologic profiles between PTSD-CI and PTSD-CN patients.

Conclusions: The findings suggest that elevated amyloid and altered connectivity patterns are associated with cognitive impairment in PTSD, particularly in the temporal and parietal regions. In contrast, PTSD without cognitive decline was associated with functional connectivity changes in salience and sensorimotor networks but no increased amyloid deposition. This study underscores the importance of neuroimaging biomarkers in understanding PTSD-related cognitive decline and suggests avenues for further investigation into the mechanistic pathways involved.

ptsd相关认知障碍的功能连接改变和淀粉样蛋白沉积。
背景和目的:PTSD与认知障碍和痴呆的风险增加有关,神经炎症、代谢功能障碍和神经病理标志物如β -淀粉样蛋白和tau蛋白可能是其潜在机制。然而,功能连接改变和淀粉样蛋白沉积作为生物标志物在PTSD患者认知障碍进展中的作用尚不清楚,现有神经影像学研究的证据有限且经常相互矛盾。本研究在有认知障碍和无认知障碍的PTSD患者中检查这些神经影像学标志物,以更好地了解导致PTSD认知能力下降的神经生物学途径。材料和方法:数据来自阿尔茨海默病神经影像学倡议(ADNI)和国防部(DOD) ADNI数据库。178名年龄匹配的男性受试者被分为四组:PTSD合并认知障碍组(PTSD-CI);PTSD与认知正常(PTSD-CN);非创伤后应激障碍(NPTSD伴CI);NPTSD和CN (NPTSD-CN)。所有受试者均接受静息状态功能MRI和淀粉样蛋白PET成像,通过临床评估确认PTSD诊断和CI。使用CONN工具箱分析功能连通性,并通过标准化摄取值比量化淀粉样蛋白负担。分析控制了人口统计学和遗传因素,包括年龄、教育程度、APOE4状态和抑郁症。结果:与NPTSD-CN组相比,PTSD-CI组颞叶和顶叶淀粉样蛋白摄取明显增加,双侧颞叶和顶叶间相应的功能连通性增加。相比之下,PTSD-CN患者没有表现出明显的淀粉样蛋白增加,但突出网络、中枢后回和感觉运动区之间的连通性增加,感觉运动网络和前扣带皮层之间的连通性下降。这些不同的模式表明PTSD-CI和PTSD-CN患者之间存在不同的神经生物学特征。结论:研究结果表明,淀粉样蛋白升高和连接模式改变与创伤后应激障碍的CI有关,特别是在颞叶和顶叶区域。相比之下,没有认知能力下降的PTSD与显著性和感觉运动网络的功能连通性改变有关,但没有增加淀粉样蛋白沉积。这项研究强调了神经成像生物标志物在理解创伤后应激障碍相关认知能力下降中的重要性,并为进一步研究相关的机制途径提供了途径。缩写:ACC =扣带回前部;ad - cog =阿尔茨海默病评估量表-认知;临床医生管理PTSD量表;PTSD =创伤后应激障碍;CI =认知受损;CN =认知正常;日常认知;老年抑郁量表;蒙特利尔认知评估;NPTSD =非ptsd。
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