Laboratory for Neurodegenerative Research, Center for Neurologic Diseases, Brigham & Women's Hospital, Harvard Institutes of Medicine, Boston, Massachusetts, USA.
Prog Mol Biol Transl Sci. 2012;107:101-24. doi: 10.1016/B978-0-12-385883-2.00012-6.
Alzheimer's disease is a devastating disorder that is estimated to affect more than 25 million people worldwide and for which there are no preventive, disease-modifying, or curative therapies. Substantial evidence indicates that the amyloid β-protein (Aβ) is a seminal factor in disease causation and may be a tractable therapeutic target. The ability of Aβ to self-associate to form oligomeric assemblies appears to underlie the early toxic events that lead to memory impairment and subsequent neurodegeneration. We review here research on Aβ folding, self-assembly, and toxicity, highlighting areas critical for the development of efficacious Aβ-directed therapeutics.
阿尔茨海默病是一种破坏性疾病，据估计，全球有超过 2500 万人受其影响，目前尚无预防、改善或治愈该病的疗法。大量证据表明，β 淀粉样蛋白（Aβ）是疾病发病的主要因素，可能是一个有治疗前途的靶点。Aβ 能够自我聚集形成寡聚体，这似乎是导致记忆障碍和随后神经退行性变的早期毒性事件的基础。在这里，我们回顾了 Aβ 折叠、自组装和毒性的研究，强调了开发有效 Aβ 靶向治疗的关键领域。
