加州大学圣克鲁兹分校研究人员发现，一种长期被认为无害的蛋白片段P3肽可能是阿尔茨海默病的隐藏贡献者1。该团队在《ChemBioChem》期刊发表评论指出，P3肽形成蛋白聚集体的速度至少与常见的致病物质淀粉样β蛋白相同，甚至可能更快1，这一发现挑战了科学界数十年来的研究重心。
长期以来，全球超过400项临床试验主要集中于靶向淀粉样β蛋白治疗阿尔茨海默病，但大多数试验均以失败或效果有限告终1。该研究团队发现，至少四篇同行评审期刊论文曾错误地引用他们的早期研究作为P3无害的证据1。Raskatov教授建议将P3肽更名为"淀粉样α"（Aα）以更好地区分其与淀粉样β1。英国独立研究小组已验证并扩展了该团队的发现1。全球约3500万人患有阿尔茨海默病，该疾病每年造成的成本超过8000亿美元1。
Researchers at the University of California, Santa Cruz have identified a peptide long considered harmless as a potential hidden contributor to Alzheimer's disease, challenging decades of research focus on a different protein target.1 The P3 peptide forms microscopic clumps and fibrous structures at a rate equal to or faster than amyloid-beta protein, another key suspect in the disease, and may trigger brain cell damage.1 This discovery, published as a commentary in the journal ChemBioChem, suggests that the scientific community's concentrated efforts on amyloid-beta may have inadvertently overlooked a significant pathological mechanism.
The findings emerge against a backdrop of limited success in Alzheimer's therapeutics.1 Over 400 clinical trials investigating Alzheimer's drugs have predominantly targeted amyloid-beta, yet most have failed or produced limited results.1 Approximately 35 million people worldwide suffer from Alzheimer's disease, with annual costs exceeding $800 billion.1
Professor Jevgenij Raskatov and his team discovered that other researchers had incorrectly cited their own work as evidence of P3's harmlessness in at least four peer-reviewed journal papers, a misrepresentation that may have influenced the field's assumptions.1 To clarify the distinction between the two peptides, Raskatov proposed renaming P3 as "amyloid-alpha" (Aα).1 An independent research group in the United Kingdom has already confirmed and expanded upon the team's findings.1
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