Sir, Traumatic brain injury (TBI) as a risk factor for the development of late-life dementia, including Alzheimer’s disease (AD), is a matter of discussion [1–4], and only a few studies examined the potential relationship between residual TBI lesions and AD neuropathology [5–9]. Examining 4761 deceased participants from the National Alzheimer’s Coordination Center (NACC) of the years 2005 to 2017, Sugarman et al. [8] reported that among 453 cases with self-reported TBI with loss of consciousness (mean age: 77.76 12.3 years), 250 (73.1%) showed definite AD pathology (defined by the Consortium to Establish a Registry for Alzheimer’s Disease [CERAD] scores 2 or 3 and Braak scores 3), whereas among 4208 cases (mean age: 80.36 10.9 years; P, .01) without a history of remote TBI, 2572 (74.0%) were definite AD. These data indicated that self-reported TBI with loss of consciousness may not be an independent risk for clinical and pathological AD. They are in accordance with two clinicopathological studies showing that remote TBI may not increase the risk of AD [3,9]. Following previous studies on the incidence of AD pathology after blunt TBI and the frequency of TBI residuals in autopsy cases with and without definite AD [5], we examined 1677 autopsy cases from two large hospital centers in Vienna, Austria, between 1985 and 2009. The results were as follows: 1. Among 186 autopsy cases (mean age: 70.16 12.8 years) with residuals of blunt TBI (old concussion defects mainly in the frontobasal, frontopolar, polar, or temporopolar regions), 26 cases (13.9%; mean age: 77 6 10.7 years) revealed the pathological features of definite AD (CERAD score B or C, Braak score 4-5 to 6). APOE carriers were ε3/ε3 (n 5 20), ε3/ε4 (n 5 3), ε2/ε3 (n 5 3), and ε2/ε2 (n 5 1). The history of TBI dated between one and 30 years; the duration of AD ranged from3 to7years.Among1115 controls (CERAD score 0-A,Braak score, 4,mean age: 77.36 9.4 years), 159 cases or 14.1% (mean age: 68.9 6 10.7 years)

中文翻译：

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创伤性脑损伤和阿尔茨海默病神经病理学

先生，创伤性脑损伤 (TBI) 作为晚年痴呆症发展的危险因素，包括阿尔茨海默病 (AD)，是一个有待讨论的问题 [1-4]，并且只有少数研究检查了残余脑损伤之间的潜在关系。 TBI 病变和 AD 神经病理学 [5-9]。Sugarman 等人对 2005 年至 2017 年国家阿尔茨海默病协调中心 (NACC) 的 4761 名已故参与者进行了检查。[8] 报告称，在 453 例自我报告的 TBI 伴有意识丧失的病例中（平均年龄：77.76±12.3 岁），250 例（73.1%）显示出明确的 AD 病理学（由建立阿尔茨海默病注册联盟定义 [CERAD] 2 分或 3 分，Braak 评分 3 分），而在 4208 例（平均年龄：80.36±10.9 岁；P，0.01）没有远程 TBI 病史的患者中，2572 例（74.0%）是明确的 AD。这些数据表明，自我报告的意识丧失的 TBI 可能不是临床和病理性 AD 的独立风险。它们与两项临床病理学研究一致，表明远程 TBI 可能不会增加 AD 的风险 [3,9]。继之前对钝性 TBI 后 AD 病理发生率和有和没有明确 AD 的尸检病例中 TBI 残留频率的研究之后，我们检查了 1985 年至 2009 年间来自奥地利维也纳两个大型医院中心的 1677 例尸检病例。结果如下： 1. 186例尸检（平均年龄：70.16±12.8岁）有钝性TBI残留（旧脑震荡缺陷主要在额基底区、额极区、极区或颞极区）26例（13.9%；平均）年龄：77 6 10.7 岁）揭示了明确 AD 的病理特征（CERAD 评分 B 或 C，布拉克比分4-5比6）。APOE 载体是ε3/ε3 (n 5 20)、ε3/ε4 (n 5 3)、ε2/ε3 (n 5 3) 和ε2/ε2 (n 5 1)。TBI 的历史可以追溯到 1 到 30 年之间；AD病程3～7年。1115例对照组（CERAD评分0-A，Braak评分4，平均年龄：77.36±9.4岁）159例，占14.1%（平均年龄：68.9±10.7岁）