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Racial and ethnic differences in the association between mild traumatic brain injury and work duty limitations in the US military.美国军队中轻度创伤性脑损伤与工作任务限制之间的种族和民族差异。
Brain Inj. 2024 Feb 23;38(3):210-216. doi: 10.1080/02699052.2024.2309276. Epub 2024 Jan 30.
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Tau filaments from amyotrophic lateral sclerosis/parkinsonism-dementia complex adopt the CTE fold.来自肌萎缩侧索硬化症/帕金森病痴呆复合征的 tau 丝采用 CTE 折叠。
Proc Natl Acad Sci U S A. 2023 Dec 19;120(51):e2306767120. doi: 10.1073/pnas.2306767120. Epub 2023 Dec 15.
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Reproducibility and Reliability of Computing Models in Segmentation and Volumetric Measurement of Brain.脑部分割与体积测量中计算模型的可重复性和可靠性
Ann Neurosci. 2023 Oct;30(4):224-229. doi: 10.1177/09727531231159959. Epub 2023 Apr 6.
4
Racial differences in concussion diagnosis and mechanism of injury among adults presenting to emergency departments across the United States.美国各地急诊室就诊成年人的脑震荡诊断和损伤机制中的种族差异。
Brain Inj. 2023 Dec 6;37(12-14):1326-1333. doi: 10.1080/02699052.2023.2248581. Epub 2023 Aug 21.
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Early Brain Amyloid Accumulation at PET in Military Instructors Exposed to Subconcussive Blast Injuries.脑内淀粉样蛋白在经历亚临床颅脑爆炸伤的军事教官中的 PET 早期聚集。
Radiology. 2023 Jun;307(5):e221608. doi: 10.1148/radiol.221608. Epub 2023 May 9.
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Posttraumatic stress symptom severity predicts cognitive decline beyond the effect of Alzheimer's disease biomarkers in Veterans.创伤后应激症状严重程度可预测退伍军人认知能力下降,超出阿尔茨海默病生物标志物的影响。
Transl Psychiatry. 2023 Mar 29;13(1):102. doi: 10.1038/s41398-023-02354-0.
7
2023 Alzheimer's disease facts and figures.2023 年阿尔茨海默病事实和数据。
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Tau, β-Amyloid, and Glucose Metabolism Following Service-Related Traumatic Brain Injury in Vietnam War Veterans: The Australian Imaging Biomarkers and Lifestyle Study of Aging-Veterans Study (AIBL-VETS).越南战争退伍军人中与服役相关的创伤性脑损伤后 Tau、β-淀粉样蛋白和葡萄糖代谢:澳大利亚成像生物标志物和老龄化退伍军人生活方式研究(AIBL-VETS)。
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创伤性脑损伤与阿尔茨海默病生物标志物:淀粉样蛋白和tau正电子发射断层扫描研究结果的系统评价

Traumatic Brain Injury and Alzheimer's Disease Biomarkers: A Systematic Review of Findings from Amyloid and Tau Positron Emission Tomography.

作者信息

Dybing Kaitlyn M, Vetter Cecelia J, Dempsey Desarae A, Chaudhuri Soumilee, Saykin Andrew J, Risacher Shannon L

机构信息

Ruth Lilly Medical Library, Indiana University School of Medicine, Indianapolis, USA.

Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, Indiana, USA.

出版信息

J Neurotrauma. 2025 Mar;42(5-6):333-348. doi: 10.1089/neu.2024.0055. Epub 2024 Dec 6.

DOI:10.1089/neu.2024.0055
PMID:39639808
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11971548/
Abstract

Traumatic brain injury (TBI) has been discussed as a risk factor for Alzheimer's disease (AD) due to its association with AD risk and earlier cognitive symptom onset. However, the mechanisms behind this relationship are unclear. Some studies have suggested TBI may increase pathological protein deposition in an AD-like pattern; others have failed to find such associations. This review covers literature that uses positron emission tomography (PET) of β-amyloid (Aβ) and/or tau to examine individuals with a history of TBI who are at increased risk for AD due to age. A comprehensive literature search was conducted on January 9, 2023, and 26 resulting citations met inclusion criteria. Common methodological concerns included small samples, limited clinical detail about participants' TBI, recall bias due to reliance on self-reported TBI, and an inability to establish causation. For both Aβ and tau, results were widespread but inconsistent. The regions that showed the most compelling evidence for increased Aβ deposition were the cingulate gyrus and cuneus/precuneus. Evidence for elevated tau was strongest in the medial temporal lobe, entorhinal cortex, precuneus, and frontal, temporal, parietal, and occipital lobes. However, conflicting findings across most regions in both Aβ- and tau-PET studies indicate the critical need for future work in expanded samples and with greater clinical detail to offer a clearer picture of the relationship between TBI and protein deposition in older individuals at risk for AD.

摘要

创伤性脑损伤(TBI)因其与阿尔茨海默病(AD)风险及更早出现认知症状相关,已被视为AD的一个风险因素。然而,这种关系背后的机制尚不清楚。一些研究表明,TBI可能会以类似AD的模式增加病理性蛋白质沉积;另一些研究则未发现此类关联。本综述涵盖了利用正电子发射断层扫描(PET)检测β-淀粉样蛋白(Aβ)和/或tau,以检查有TBI病史且因年龄因素患AD风险增加的个体的文献。于2023年1月9日进行了全面的文献检索,最终有26篇文献符合纳入标准。常见的方法学问题包括样本量小、关于参与者TBI的临床细节有限、因依赖自我报告的TBI存在回忆偏倚以及无法确定因果关系。对于Aβ和tau,结果广泛但不一致。显示Aβ沉积增加最有力证据的区域是扣带回和楔叶/楔前叶。tau升高的证据在内侧颞叶、内嗅皮质、楔前叶以及额叶、颞叶、顶叶和枕叶最为明显。然而,Aβ-PET和tau-PET研究中大多数区域的相互矛盾的结果表明,未来需要在扩大样本量并提供更多临床细节的情况下开展工作,以便更清楚地了解TBI与有AD风险的老年人蛋白质沉积之间的关系。