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科学哲学方法对阿尔茨海默病淀粉样蛋白假说的研究。

A philosophy of science approach to the amyloid hypothesis of Alzheimer's disease.

机构信息

Bioethics Program, FLACSO Argentina, Buenos Aires, Argentina.

Science Norms Democracy UMR 8011, Sorbonne Université, Paris, France.

出版信息

Eur J Neurosci. 2024 Sep;60(5):4707-4722. doi: 10.1111/ejn.16500. Epub 2024 Aug 9.

DOI:10.1111/ejn.16500
PMID:39119857
Abstract

Disputes about the scientific validity of the amyloid-β hypothesis of Alzheimer's disease have been held since the early 1990s, with little constructive progress made between opposing sides despite recent therapeutic progress. Here, I argue that philosophy of science can improve the chance of constructive debate by giving researchers technical language to describe and assess scientific progress. To do so, I interpret the amyloid hypothesis using a modified version of the research programme concept from philosopher of science Imre Lakatos. I first outline the amyloid-β hypothesis and study critiques of its central place in Alzheimer's research. Then, I draw on the complexity of amyloid-β and Alzheimer's research to discuss the limits of using concepts from popular philosophers of science Karl Popper or Thomas Kuhn, before finally arguing that an adaptation of the research programme concept can foster constructive debates about the science of Alzheimer's and within it. I will argue that the amyloid-β hypothesis has contributed to significant progress in the Alzheimer's field based on what Lakatos called the "positive heuristic" (motivating the programme to test its predictions) and the "negative heuristic" (protecting the programme from refutation). I consider the amyloid research agenda to be progressive despite the fact that its claims about disease aetiology could be wrong.

摘要

自 20 世纪 90 年代初以来,人们就一直对阿尔茨海默病的淀粉样蛋白-β假说的科学有效性存在争议,尽管最近有了治疗进展,但双方仍几乎没有取得建设性的进展。在这里,我认为哲学可以通过为研究人员提供描述和评估科学进展的技术语言来提高建设性辩论的机会。为此,我使用科学哲学家伊姆雷·拉卡托斯(Imre Lakatos)的研究计划概念的一个修改版本来解释淀粉样蛋白假说。我首先概述了淀粉样蛋白-β假说,并研究了对其在阿尔茨海默病研究中核心地位的批评。然后,我利用淀粉样蛋白-β和阿尔茨海默病研究的复杂性来讨论使用流行的科学哲学家卡尔·波普尔(Karl Popper)或托马斯·库恩(Thomas Kuhn)的概念的局限性,最后我认为研究计划概念的适应可以促进关于阿尔茨海默病科学的建设性辩论,并在其中进行辩论。我将论证,根据 Lakatos 所谓的“积极启发法”(激励该计划检验其预测)和“消极启发法”(保护该计划免受反驳),淀粉样蛋白-β假说为阿尔茨海默氏病领域做出了重大贡献。尽管该假说关于疾病病因的说法可能是错误的,但我认为淀粉样蛋白研究议程是进步的。

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