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In recent years, a growing number of scientific studies have backed an alarming hypothesis: Alzheimer's disease isn't just a disease, it's an infection. 近年來，越來越多的科學研究都證明了一個驚人的假設：阿爾茨海默病并非僅僅是一種疾病，它還是一種感染。 While the exact mechanisms of this infection are something researchers are still trying to isolate, numerous studies suggest the deadly spread of Alzheimer's goes way beyond what we used to think. 盡管研究人員仍在嘗試分離造成感染的精確機制，但是眾多研究表明，阿爾茨海默病的致命傳播完全超出了我們的想象。 One such study, published in 2019, suggested what could be one of the most definitive leads yet for a bacterial culprit behind Alzheimer's, and it comes from a somewhat unexpected quarter: gum disease. 2019年發表的這樣一項研究表明，引起阿爾茨海默病的細菌可能是最明確的罪魁禍首之一，這個細菌的來源有點出人意料：牙周病。 In a paper led by senior author Jan Potempa, a microbiologist from the University of Louisville, researchers reported the discovery of Porphyromonas gingivalis – the pathogen behind chronic periodontitis (aka gum disease) – in the brains of deceased Alzheimer's patients. 在一篇以Jan Potempa，資深作者、路易斯維爾大學微生物學家領導的論文中，研究人員在去世的阿爾茨海默病患者的大腦中發現了牙齦卟啉單胞菌-一種導致慢性牙周病的病原體。 It wasn't the first time the two factors have been linked, but the researchers went further. 這已經不是第一次將這兩個因素聯系在一起了，但是研究人員在這個基礎上又進行了深入的研究。 In separate experiments with mice, oral infection with the pathogen led to brain colonization by the bacteria, together with increased production of amyloid beta (Aβ), the sticky proteins commonly associated with Alzheimer's. 在一項針對老鼠的單獨試驗中，口腔細菌感染會導致細菌在大腦中定殖并同時會產生更多的淀粉樣蛋白（Aβ）-一種通常與阿爾茨海默病相關的粘稠蛋白質。 The research team, coordinated by pharma startup Cortexyme, which was co-founded by first author Stephen Dominy, wasn't claiming to have discovered definitive evidence of Alzheimer's causation. 由第一作者Stephen Domity聯合創辦的醫藥初創公司Cortexyme所牽頭的研究團隊并未宣傳其已經發現了造成阿爾茨海默病的確切證據。 But it was clear they thought we had a strong line of investigation here. 但顯而易見的是，他們認為我們已經有了強有力的調查線索。 "Infectious agents have been implicated in the development and progression of Alzheimer's disease before, but the evidence of causation hasn't been convincing," Dominy said at the time. Dominy表示，“傳染性物質曾經被認為與阿爾茨海默病的發生和加重有關，但是關于成因卻一直缺乏令人信服的證據。” "Now, for the first time, we have solid evidence connecting the intracellular, Gram-negative pathogen, P. gingivalis, and Alzheimer's pathogenesis." “現在，我們首次有充分證據表明，細胞內革蘭氏陰性病原體-牙齦卟啉菌與阿爾茨海默病的發病機制有關。” Pathogenesis：發病機制 In addition, the team identified toxic enzymes called gingipains secreted by the bacteria in the brains of Alzheimer's patients, which correlated with two separate markers of the disease: the tau protein, and a protein tag called ubiquitin. 此外，團隊還發現了一種被稱為牙齦素的有毒的酶，這種酶是阿爾茨海默病患者大腦中的細菌所分泌的。這種酶與兩種不同的疾病標志物有關聯：tau蛋白和一種被稱為泛素的蛋白標記。 But even more compellingly, the team identified these toxic gingipains in the brains of deceased people who were never diagnosed with Alzheimer's. 但是，更加令人信服的是，團隊在從未被診斷為阿爾茨海默病的逝者的大腦中發現了這些有毒的牙齦素。 That's important, because while P. gingivalis and the disease have been linked before, it's never been known – to put it simply – whether gum disease causes Alzheimers, or whether dementia leads to poor oral care. 這一點很重要，因為盡管牙齦卟啉菌曾經與阿爾茨海默病聯系在一起，但是有一點卻始終無從知曉-簡單說來-就是到底是牙周炎引起了阿爾茨海默病，還是癡呆導致口腔護理不到位。 The fact that low levels of gingipains were evident even in people who were never diagnosed with Alzheimer's could be a smoking gun – suggesting they might have developed the condition if they had lived longer. 在從未被診斷為阿爾茨海默病的逝者的大腦中發現少量的牙齦素這一事實可能就是明確的證據-這一證據表明，如果這些逝者活得再久一些，他們就可能會患上阿爾茨海默病。 "Our identification of gingipain antigens in the brains of individuals with AD and also with AD pathology but no diagnosis of dementia argues that brain infection with P. gingivalis is not a result of poor dental care following the onset of dementia or a consequence of late-stage disease, but is an early event that can explain the pathology found in middle-aged individuals before cognitive decline," the authors explained in their paper. “我們在阿爾茨海默病逝者以及存在阿爾茨海默病病理但未被診斷為阿爾茨海默病逝者的大腦中發現的牙齦素抗原證明，大腦感染牙齦卟啉菌并非是由于出現癡呆之后口腔衛生護理不到位或者病程后期所導致的結果，而是早期的一個現象，這就可以解釋了在出現認知下降之前的中年人中所發現的病理學。” Further, a compound formulated by the company called COR388, showed in experiments with mice that it could reduce bacterial load of an established P. gingivalis brain infection, while also reducing amyloid-beta production and neuroinflammation. 此外，一種由公司研發的復合物-COR388在一項針對老鼠的實驗中表明，它可以減少已確定的牙齦卟啉菌大腦感染的細菌量，并同時減少淀粉樣蛋白-β的產生和神經炎癥。 We'll have to wait and see what future research will uncover about this link, but the research community is cautiously optimistic. 我們還需要繼續等待，看看未來的研究在這一關聯中還能獲得哪些發現，但是研究屆對此持謹慎樂觀的態度。 "Drugs targeting the bacteria's toxic proteins have so far only shown benefit in mice, yet with no new dementia treatments in over 15 years it's important that we test as many approaches as possible to tackle diseases like Alzheimer's," chief scientific officer David Reynolds from Alzheimer's Research commented in a statement. 阿爾茨海默病研究中心的首席科學官David Reynolds在聲明中評論說：“針對細菌中有毒蛋白質的藥物至今只在老鼠身上看到了效果，但是，在15年里都沒有治療癡呆癥的新療法的情況下，我們要盡可能多的嘗試各種方法來治療像阿爾茨海默病這樣的疾病。” 原文來源：ScienceAlert 編輯：譯銳翻譯 上海譯銳翻譯是一家專業的翻譯公司，我們致力于為客戶提供專業優質的翻譯服務。