Molecular Neurodegeneration ( IF 14.9 ) Pub Date : 2022-03-24 , DOI: 10.1186/s13024-022-00530-2 Hui Zheng 1 , David M Holtzman 2
John T. Trojanowski, MD, PhD
1946-2022
On February 8, 2022, the world lost a giant in the fields of neurodegenerative disease and brain aging. We lost a beloved colleague and friend in Dr. John Trojanowski. John had a distinguished career most of us could only envy. But he was so much more.
Dr. Trojanowski was a towering figure in the field of neuropathology of neurodegenerative diseases. Following his MD and PhD training at Tufts University and Pathology and Neuropathology Residencies at Massachusetts General Hospital and the Hospital of the University of Pennsylvania, Dr. Trojanowski joined the faculty of the University Pennsylvania in 1981 and stayed there until his passing. Through an academic career that spanned over four decades and together with his life and science partner Dr. Virginia Lee, he built a powerhouse neurodegenerative disease research program and made groundbreaking discoveries that are both wide-ranging and far-reaching. Remarkably, he identified the pathological hallmarks across multiple neurodegenerative diseases: tau and neurofibrillary tangles in Alzheimer’s disease and frontotemporal dementias, Lewy bodies composed of alpha-synuclein that mark Parkinson’s disease and Lewy body dementia, and the TDP43 proteinopathy characteristic of forms of frontotemporal degeneration and amyotrophic lateral sclerosis. Altogether, he co-authored close to 1400 papers and received an astonishing all-time h-index of 247 according to Google Scholar.
John Trojanowski was better known as part of “John and Virginia” than Dr. Trojanowski and his union with Virginia was truly one of a kind and legendary. John’s insights in neuropathology and Virginia’s expertise in biochemistry were a match made in the neurodegeneration research heaven and John’s dark sense of humor and Virginia’s in-your-face (by this we mean in John’s face) persona enlightened every room. People often fondly talk about their public discourse, but the reality is that they could finish each other’s sentences (or e-mails) and John was the ultimate gentleman. Standing at 6 ft 3 in., John was not to be unnoticed but he made sure the spotlight shined on Virginia. The two of them travelled the world together and we had the fortune to get to know them inside conference halls and through social engagements and dinner conversations. It was clear that, like a good bottle of wine that John always enjoyed, their admiration and love for each other only grew with age.
John was a scholar. And his encyclopedic knowledge on the complex pathological and clinical presentations across neurodegenerative diseases were both mesmerizing and intimidating. His penetrating insights brought mixed pathologies and age-related pathological changes to light and humbled our mouse modelers who tend to be fixated on one pathology, one pathway, and one molecule. While trying to understand the role of astrocytes in tau pathology and spreading in mice, one of us (HZ) asked John about the possible disease relevance. He gave me a lecture about the astroglial tau inclusions in various tauopathy conditions and introduced me to a phenomenon termed aging-related tau astrogliopathy (ARTAG). This was followed by e-mail attachments of a dozen of papers. (I have to confess that I did not read all of them.)
John was as energetic as he was knowledgeable. He often responded to e-mails within minutes, regardless of the time. In the beginning, I thought it was bounced back e-mails. Later on, this almost became expected. Indeed, it seemed that John was always working.
Above all, John was extremely generous and collaborative. He provided both of us large number of well-annotated, high-quality, human brain samples that made our work possible [1,2,3,4,5]. We asked for 1 g per sample and was delighted to learn that he has sent us more than 5 g each! When it comes to co-authorship, I quote an e-mail from John that speaks of his generosity and character: “We appreciate very much that you included us in this important study. We are eager for future collaborations with you and your team when the occasion arises … we just wanted to be sure it is appropriate in your mind for us to be listed as collaborators.” What a gentleman!
John was a pioneering neuropathologist, an inspiring leader, a skilled mentor, a devoted husband to Virginia, a beloved colleague and friend to so many, and a kind and generous human being. He will be sorely missed.
Martini-Stoica H, Cole AL, Swartzlander DB, Chen F, Wan Y-W, Bajaj L, et al. TFEB enhances astroglial uptake of extracellular tau species and reduces tau spreading. J Exp Med. 2018;215:2355–77.
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Ghosh A, Comerota ME, Wan D, Chen F, Propson NE, Hwang SH, et al. An epoxide hydrolase inhibitor reduces neuroinflammation in a mouse model of Alzheimer’s disease. Sci Transl Med. 2020;12:eabb1206 (With acknowledgement of Lee and Trojanowski).
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Affiliations
Huffington Center on Aging, Baylor College of Medicine, Houston, TX, 77030, USA
Hui Zheng
Department of Neurology, Washington University School of Medicine, St. Louis, MO, 63110, USA
David M. Holtzman
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Zheng, H., Holtzman, D.M. In Memoriam of John T. Trojanowski, MD, PhD 1946-2022. Mol Neurodegeneration 17, 24 (2022). https://doi.org/10.1186/s13024-022-00530-2
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中文翻译：
纪念 John T. Trojanowski, MD, PhD 1946-2022
John T. Trojanowski，医学博士，博士
1946-2022
2022年2月8日，世界失去了神经退行性疾病和大脑衰老领域的巨人。我们失去了一位心爱的同事和朋友 John Trojanowski 博士。约翰有着我们大多数人只能羡慕的杰出职业。但他远不止这些。
Trojanowski 博士是神经退行性疾病的神经病理学领域的杰出人物。在塔夫茨大学接受医学博士和博士培训后，在马萨诸塞州总医院和宾夕法尼亚大学医院接受病理学和神经病理学住院医师培训后，Trojanowski 博士于 1981 年加入宾夕法尼亚大学，并一直留在那里直到去世。通过跨越四个十年的学术生涯，他与他的生命和科学合作伙伴弗吉尼亚李博士一起建立了一个强大的神经退行性疾病研究计划，并取得了广泛而深远的开创性发现。值得注意的是，他确定了多种神经退行性疾病的病理特征：阿尔茨海默病和额颞叶痴呆中的 tau 蛋白和神经原纤维缠结，路易体由标记帕金森病和路易体痴呆的 α-突触核蛋白组成，以及额颞叶变性和肌萎缩性侧索硬化形式的 TDP43 蛋白病特征。根据 Google Scholar 的数据，他总共发表了近 1400 篇论文，并获得了惊人的 247 的历史 h 指数。
约翰·特洛亚诺夫斯基作为“约翰和弗吉尼亚”的一部分而比特洛亚诺夫斯基博士更为人所知，他与弗吉尼亚的结合确实是一种传奇。约翰在神经病理学方面的见解和弗吉尼亚在生物化学方面的专业知识在神经退行性变研究的天堂和约翰的黑暗幽默感和弗吉尼亚在你的脸上（我们指的是约翰的脸）的角色启发了每个房间。人们经常喜欢谈论他们的公开演讲，但现实是他们可以完成彼此的句子（或电子邮件），而约翰是终极绅士。约翰身高 6 英尺 3 英寸，不容忽视，但他确保聚光灯照在弗吉尼亚身上。他们两人一起环游世界，我们有幸在会议厅内、社交活动和晚餐谈话中认识了他们。
约翰是个学者。他对神经退行性疾病的复杂病理和临床表现的广博知识既令人着迷又令人生畏。他敏锐的洞察力带来了混合的病理和与年龄相关的病理变化，并使我们的小鼠建模者谦卑，他们往往专注于一种病理、一种途径和一种分子。在试图了解星形胶质细胞在 tau 病理学和在小鼠中传播的作用时，我们中的一个人 (HZ) 向 John 询问了可能的疾病相关性。他给我做了一场关于各种 tau 病变条件下星形胶质 tau 夹杂物的讲座，并向我介绍了一种称为衰老相关 tau 星形胶质病 (ARTAG) 的现象。随后是十几篇论文的电子邮件附件。（我不得不承认我没有读完所有这些。）
约翰知识渊博，精力充沛。他经常在几分钟内回复电子邮件，不管时间长短。一开始，我以为是退回的电子邮件。后来，这几乎成为了预期。事实上，约翰似乎一直在工作。
最重要的是，约翰非常慷慨和合作。他为我们俩提供了大量注释良好、高质量的人脑样本，使我们的工作成为可能 [1,2,3,4,5]。我们要求每个样品 1 克，很高兴得知他给我们寄来的每个样品超过 5 克！谈到共同作者，我引用了约翰的一封电子邮件，其中谈到了他的慷慨和性格：“我们非常感谢您将我们纳入这项重要的研究。当机会出现时，我们渴望与您和您的团队进行未来的合作……我们只是想确保您认为我们被列为合作者是合适的。” 多么绅士啊！
约翰是一位开创性的神经病理学家，一位鼓舞人心的领导者，一位技术娴熟的导师，一位忠诚于弗吉尼亚的丈夫，一位深受许多人喜爱的同事和朋友，一位善良而慷慨的人。他会非常想念。
Martini-Stoica H、Cole AL、Swartzlander DB、Chen F、Wan YW、Bajaj L 等。TFEB 增强星形胶质细胞对细胞外 tau 物质的摄取并减少 tau 扩散。J Exp Med。2018；215：2355–77。
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Litvinchuk A、Wan YW、Swartzlander D、Chen F、Propson NE、Cole AL 等。补体 C3aR 失活减弱 tau 病理并逆转 tau 病模型和阿尔茨海默病中失调的免疫网络。神经元。2018;100:1337-53（感谢 Lee 和 Trojanowski）。
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Leyns CEG、Gratuze M、Narasimhan S、Jain N、Koscal LJ、Jiang H 等。TREM2 功能阻碍神经炎斑块中的 tau 播种。纳特神经科学。2019；22：1217-22。
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Roy ER、Wang B、Wan YW、Chiu G、Cole AL、Yin Z 等。I 型干扰素反应驱动阿尔茨海默病中的神经炎症和突触丢失。J临床投资。2020；130：1912-30。
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Ghosh A、Comerota ME、Wan D、Chen F、Propson NE、Hwang SH 等。一种环氧化物水解酶抑制剂可减少阿尔茨海默病小鼠模型中的神经炎症。科学翻译医学。2020;12:eabb1206（感谢 Lee 和 Trojanowski）。
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华盛顿大学医学院神经内科，圣路易斯，密苏里州，63110，美国
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Zheng, H., Holtzman, DM 纪念 John T. Trojanowski, MD, PhD 1946-2022。摩尔神经变性 17, 24 (2022)。https://doi.org/10.1186/s13024-022-00530-2
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