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淀粉样蛋白病理特征可区分创伤后应激障碍和创伤性脑损伤。

Amyloid pathology fingerprint differentiates post-traumatic stress disorder and traumatic brain injury.

机构信息

Queensland Brain Institute, The University of Queensland, Brisbane, QLD 4072, Australia.

School of Psychology and Counselling and IHBI, Queensland University of Technology, Brisbane, QLD 4059, Australia; QIMR-Berghofer Institute, Brisbane, QLD 4006, Australia.

出版信息

Neuroimage Clin. 2018 Jun 5;19:716-726. doi: 10.1016/j.nicl.2018.05.016. eCollection 2018.

DOI:10.1016/j.nicl.2018.05.016
PMID:30009128
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6041560/
Abstract

INTRODUCTION

Traumatic brain injury (TBI) and post-traumatic stress disorder (PTSD) are risk factors for early onset of Alzheimer's disease (AD) and may accelerate the progression rate of AD pathology. As amyloid-beta (Aβ) plaques are a hallmark of AD pathology, we hypothesized that TBI and PTSD might increase Aβ accumulation in the brain.

METHODS

We examined PET and neuropsychological data from Vietnam War veterans compiled by the US Department of Defense Alzheimer's Disease Neuroimaging Initiative, to examine the spatial distribution of Aβ in male veterans' who had experienced a TBI and/or developed PTSD. Subjects were classified into controls, TBI only, PTSD only, and TBI with PTSD (TBI_PTSD) groups and data were analyzed using both voxel-based and ROI-based approaches.

RESULTS

Compared to controls, all three clinical groups showed a pattern of mainly increased referenced standard uptake values (SUVR) for the amyloid tracer [F]-AV45 PET, with rank order PTSD > TBI_PTSD > TBI > Control, and same rank order was seen in the deficits of cognitive functions. SUVR increase was observed in widespread cortical regions of the PTSD group; in white matter of the TBI_PTSD group; and cerebellum and precuneus area of the TBI group, in contrast with controls. The [F]-AV45 SUVR correlated negatively with cerebrospinal fluid (CSF) amyloid levels and positively with the CSF tau concentrations.

CONCLUSION

These results suggest that both TBI and PTSD are substantial risk factors for cognition decline and increased Aβ deposition resembling that in AD. In addition, both PTSD and TBI_PTSD have a different pathways of Aβ accumulation.

摘要

简介

颅脑创伤(TBI)和创伤后应激障碍(PTSD)是阿尔茨海默病(AD)早期发病的危险因素,并可能加速 AD 病理的进展速度。由于淀粉样蛋白-β(Aβ)斑块是 AD 病理的一个标志,我们假设 TBI 和 PTSD 可能会增加大脑中的 Aβ 积累。

方法

我们检查了美国国防部阿尔茨海默病神经影像学倡议汇编的越南战争退伍军人的 PET 和神经心理学数据,以检查经历过 TBI 和/或 PTSD 的男性退伍军人大脑中 Aβ 的空间分布。将受试者分为对照组、TBI 组、PTSD 组和 TBI_PTSD 组,并使用基于体素和基于 ROI 的方法进行数据分析。

结果

与对照组相比,所有三个临床组的 [F]-AV45 PET 示踪剂的参考标准摄取值(SUVR)均表现出主要增加的模式,其等级顺序为 PTSD>TBI_PTSD>TBI>Control,且认知功能障碍的等级顺序相同。PTSD 组观察到广泛的皮质区域 SUVR 增加;在 TBI_PTSD 组的白质中;以及 TBI 组的小脑和楔前叶区域,与对照组相比。[F]-AV45 SUVR 与脑脊液(CSF)中的淀粉样蛋白水平呈负相关,与 CSF 中的 tau 浓度呈正相关。

结论

这些结果表明,TBI 和 PTSD 都是认知能力下降和 Aβ 沉积增加的重要危险因素,类似于 AD。此外,PTSD 和 TBI_PTSD 具有不同的 Aβ 积累途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/6041560/ad8289d9392a/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/6041560/61380c530a88/gr1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/6041560/81560314ed16/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/6041560/f7e34a2128c2/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/6041560/c901173ba1e8/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/6041560/3ba7662e333f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/6041560/ad8289d9392a/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/6041560/61380c530a88/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/6041560/ac1fa2272141/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/6041560/81560314ed16/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/6041560/f7e34a2128c2/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/6041560/c901173ba1e8/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/6041560/3ba7662e333f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a1d/6041560/ad8289d9392a/gr7.jpg

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