Small molecular decoys in Alzheimer's disease
Sho Oasa1
Valentina L.Kouznetsova2
Igor F.Tsigelny3
Lars Terenius4
1.Department of Clinical Neuroscience,Center for Molecular Medicine,Karolinska Institutet,Stockholm,Sweden2.San Diego Supercomputer Center,University of California San Diego,La Jolla,CA,USA3.San Diego Supercomputer Center,University of California San Diego,La Jolla,CA,USA;Department of Neurosciences,University of California San Diego,La Jolla,CA,USA4.Department of Clinical Neuroscience,Center for Molecular Medicine,Karolinska Institutet,Stockholm,Sweden;Department of Clinical Neuroscience,Karolinska University Hospital,Karolinska Institutet,Stockholm,Sweden
摘要：Recent progress in the treatment of Alzheimer's disease(AD)using antibodies against amyloid sustains amyloid generation as a key process in AD.Amyloid formation starts with two amyloid-beta(Aβ)molecules interacting(dimer formation)followed by an accelerating build-up of so-called protofibrils,which turn into fibrils,which accumulate in the characteristic plaques.To interfere with the process at the root we used molecular modeling to define the surfaces of interaction in dimer formation.In a series of small molecules,we identified candidates that changed the course of interactions and generated aggregates with other macrostructures and reduced toxicity.We have introduced the term"decoys"to identify these molecules.
机标关键词：alzheimermolecularsmalldecoysdisease
论文发表日期：2024-08-28
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：2( 1658-1659 )