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2022-8-04更新
我所提的“证伪”是逻辑学上的命题的否定,而非神学、哲学和科学边界划分的“可证伪性”。
即淀粉样变性假说原命题:Aβ的生成和清除失衡是导致神经元变性和痴呆发生的起始事件。
若Aβ沉积,则神经元变性
此命题的否定为:若Aβ沉积,神经元没有损伤。
命题的否定与原命题真假互逆。
Lesné博士证明了原命题的否定为假,即证明了Aβ假说为真。
如后文所提,Lesné博士造假的部分,不能证明Aβ假说原命题的真伪,此即我所提到的,不能被证伪。这里并不能被理解成Aβ假说没有可证伪性,并因此推断整个假说甚至神经科学都是伪科学。
(我本人关闭私信和回复的通知,很多争议是看不到的。知乎毕竟不是写论文的地方,表述不会那么严谨,如果我的表述对你造成了误解,请见谅。)
——————原答案编辑于2022-7-24——————
结论加黑:
淀粉样蛋白的假说仍然不能被证伪,被实锤的是淀粉样蛋白的一种亚型”Aβ*56“,它的中文翻译应该是”淀粉样蛋白 β 星 56“
咱们前因后果细细聊
1.支持淀粉样变性假说的依据
a. 尸检显示,阿尔茨海默病患者的脑中淀粉样蛋白水平高于认知健全的个体。
Amyloid oligomers had been linked to impaired communication between neurons in vitro and in animals, and autopsies have shown higher levels of the oligomers in people with Alzheimer’s than in cognitively sound individuals. b. 以淀粉样变性为理论基础的转基因动物模型也表现出阿尔兹海默症的症状。
In the mid-1990s, she created a transgenic mouse that churns out human Aβ, which forms plaques in the animal’s brain. The mouse also shows dementia-like symptoms. It became a favored Alzheimer’s model. 2.否定淀粉样变性假说的依据
a.针对缓解淀粉样变性的的治疗策略和研发的药物全部失效,一个机构16亿美金16年时间全部打水漂
Stopping amyloid deposits became the most plausible therapeutic strategy.
Yet Aβ still dominates research and drug development. NIH spent about $1.6 billion on projects that mention amyloids in this fiscal year, about half its overall Alzheimer’s funding. b.淀粉样变性命题的否定,不能被证明为假(致命缺陷),即当时无法证明Aβ蛋白可以直接导致认知减退
But no one had proved that any one of the many known oligomers directly caused cognitive decline. 2006年,在阿尔兹海默症发现100周年的时间点,各位科研大佬争利用自己的假说取科研经费获取学术资源的时间点,一位被研究所雇来的博士生,年轻的科学家,Lesné,带着Aβ*56来了。
The 2006 paper’s first author, sometimes credited as the discoverer of Aβ*56, was Lesné, a young scientist Ashe had hired straight out of a Ph.D. program at the University of Caen Normandy in France. 他成功证明了,Aβ*56可以使健康小鼠表现出阿尔兹海默症的症状。
The group isolated Aβ*56 and injected it into young rats. The rats’ capacity to recall simple, previously learned information—such as the location of a hidden platform in a maze—plummeted. 即他成功证伪淀粉样变性的命题的否定,也就证明了淀粉样变性的真实性,为他和他代表的假说赢取巨额的科研经费。
Since then, annual NIH support for studies labeled “amyloid, oligomer, and Alzheimer’s” has risen from near zero to $287 million in 2021. Lesné and Ashe helped spark that explosion, experts say. 那么他哪里造假了呢
造假的地方在于Aβ*56在小鼠和人类体内分离不出来,即虽然Aβ*56可以导致动物阿尔兹海默症的症状,但是他并不是人体自然病程的产物。
“In science, once you publish your data, if it’s not readily replicated, then there is real concern that it’s not correct or true. There’s precious little clearcut evidence that Aβ*56 exists, or if it exists, correlates in a reproducible fashion with features of Alzheimer’s—even in animal models.” 目前,争议的主人Lesné博士及其研究受益者仍认为,分离不出来是Aβ*56结构不稳定,无关学术行为不端。
Such oligomers are notoriously unstable, converting to other oligomer types spontaneously.
这次造假,使阿尔兹海默症研究领域退回到16年前,学术上再次分为神经免疫假说、炎症假说和淀粉样蛋白变性假说。
没有可以证伪的学说,意味着整个领域还处于盲人摸象的状态。 |
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