Chronic traumatic encephalopathy (CTE), a degenerative brain disease, is the result of a slow spreading of tau proteins in a pattern that is unique to CTE, as a result of repetitive hits to the head. Over time, CTE patients experience progressive memory issues, severe mood changes, and erratic, often suicidal and/or violent, behavior.(2) In 2017, a JAMA paper by McKee and co-workers(2) described a very high incidence (110 out of 111 subjects, or 99%) of CTE in National Football League (NFL) players. This report garnered a great deal of attention in the lay press and raised concerns about the safety of the sport for younger children. However, CTE is not restricted to NFL players. As detailed in an highly read editorial on the subject (just under 10,000 article views),(3) CTE was first described as “punch drunk” in boxers in the 1920s, but has now been found, postmortem, in military veterans, soccer payers, hockey players, and victims of repeated domestic abuse. A key issue is that the disease can only be definitively diagnosed postmortem by brain tissue analysis.(1−3) Genetics also play a significant role in disposing one to CTE, as many NFL players, and other at risk groups, never show signs of CTE. As a result, ACS Chemical Neuroscience has actively solicited and published a number of papers detailing new assays to detect various forms of tau, to better understand aggregation of tau as it related to phosphorylation states, to profile new therapeutic strategies to potential treat tauopathies (such as CTE and AD), and, importantly, to showcase preclinical and human data with new tau PET imaging agents, and other imaging modalities, to detect and quantify tau protein and aggregates in living subjects (rats, monkeys, and humans). The latter is a major step, as not having to wait for postmortem analysis will enable detection, risk assessment, and disease progression of CTE. Here, we have compiled in a single, virtual issue all of the key papers that describe fundamentally new strategies to assess, detect, monitor, and potentially treat CTE and other tauopathies. As progress here will impact not only CTE but also AD, PD, and other neurodegenerative diseases, there are few areas of research of greater importance in the neuroscience field. I hope you find this exciting virtual issue informative, and I encourage you all to continue submitting your research on all aspects of tau, CTE, and other prion disease to ACS Chemical Neuroscience. Views expressed in this editorial are those of the author and not necessarily the views of the ACS. This article references 3 other publications.

中文翻译：

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慢性创伤性脑病（CTE）：一个虚拟问题，致力于理解，诊断和潜在治疗Tauopathies的进展。

慢性外伤性脑病（CTE）是一种变性性脑疾病，是tau蛋白以重复击中头部的方式缓慢扩散的结果，这种tau蛋白以CTE独有的方式传播。随着时间的流逝，CTE患者会经历渐进性记忆问题，严重的情绪变化以及不稳定的，经常自杀和/或暴力的行为。（2）2017年，《美国医学会杂志》（JAMA）McKee及其同事的论文（2）描述了在国家橄榄球联盟（NFL）运动员中CTE的发生率很高（111名受试者中有110名，占99％）。这份报告引起了非新闻界的广泛关注，并引起了对年幼儿童运动安全性的关注。但是，CTE不仅限于NFL球员。正如对此主题的高度评价的社论（不到10,000篇文章观点）中所详述的那样，（3）CTE在1920年代被拳击手首次描述为“拳头醉酒”，但在事后，军事退伍军人，足球付款人中被发现，曲棍球运动员和屡次家庭虐待的受害者。一个关键问题是，只有通过脑组织分析才能明确诊断出该病。（1-3）遗传学在将一个人分配给CTE，许多NFL参与者以及其他处于危险中的人群中也起着重要作用，从不显示CTE迹象。结果是，ACS化学神经科学积极征求并发表了许多论文，详细介绍了检测各种形式tau的新方法，以更好地了解tau与磷酸化状态相关的聚集，概述了可能治疗tauopathies（例如CTE和AD）的新治疗策略，以及重要的是，使用新型tau PET成像剂和其他成像方式展示临床前和人类数据，以检测和量化活体受试者（大鼠，猴子和人类）中的tau蛋白和聚集体。后者是重要的一步，因为不必等待验尸分析即可进行CTE的检测，风险评估和疾病进展。在这里，我们将所有关键论文汇编成一个虚拟的虚拟论文，这些论文从根本上描述了评估，检测，监测和潜在治疗CTE和其他手段的新策略。由于这里的进展不仅会影响CTE，而且会影响AD，PD和其他神经退行性疾病，因此在神经科学领域，很少有研究领域具有更重要的意义。我希望您能从这个激动人心的虚拟问题中受益匪浅，并鼓励大家继续将有关tau，CTE和其他病毒疾病的各个方面的研究提交给ACS化学神经科学。本社论中表达的观点只是作者的观点，不一定是ACS的观点。本文引用了其他3个出版物。