Dybing Kaitlyn M, Vetter Cecelia J, Dempsey Desarae A, Chaudhuri Soumilee, Saykin Andrew J, Risacher Shannon L
Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Indiana Alzheimer's Disease Research Center, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
medRxiv. 2023 Dec 1:2023.11.30.23298528. doi: 10.1101/2023.11.30.23298528.
Traumatic brain injury (TBI) has been discussed as a risk factor for Alzheimer's disease (AD) due to its association with dementia 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 amyloid-β and/or tau to examine subjects with history of TBI who are at risk for AD due to advanced age. A comprehensive literature search was conducted on January 9, 2023, and 24 resulting citations met inclusion criteria. Common methodological concerns included small samples, limited clinical detail about subjects' TBI, recall bias due to reliance on self-reported TBI, and an inability to establish causation. For both amyloid and tau, results were widespread but inconsistent. The regions which showed the most compelling evidence for increased amyloid deposition were the cingulate gyrus, cuneus/precuneus, and parietal lobe. Evidence for increased tau was strongest in the medial temporal lobe, entorhinal cortex, precuneus, and frontal, temporal, parietal, and occipital lobes. However, conflicting findings across most regions of interest in both amyloid- 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 subjects at risk for AD.
创伤性脑损伤（TBI）已被视为阿尔茨海默病（AD）的一个风险因素，因为它与痴呆风险及更早出现认知症状有关。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。本综述涵盖了使用淀粉样蛋白-β和/或tau的正电子发射断层扫描（PET）来检查有TBI病史且因高龄而有患AD风险的受试者的文献。于2023年1月9日进行了全面的文献检索，共有24条检索结果符合纳入标准。常见的方法学问题包括样本量小、关于受试者TBI的临床细节有限、因依赖自我报告的TBI而存在回忆偏差以及无法确定因果关系。对于淀粉样蛋白和tau，结果广泛但不一致。显示淀粉样蛋白沉积增加最有力证据的区域是扣带回、楔叶/楔前叶和顶叶。tau增加的证据在内侧颞叶、内嗅皮质、楔前叶以及额叶、颞叶、顶叶和枕叶最为明显。然而，淀粉样蛋白PET和tau-PET研究中大多数感兴趣区域的结果相互矛盾，这表明未来迫切需要开展更大样本量且临床细节更丰富的研究，以更清晰地呈现TBI与有患AD风险的老年受试者蛋白质沉积之间的关系。
