Small molecular decoys in Alzheimer's disease  

作　　者：Sho Oasa Valentina L.Kouznetsova Igor F.Tsigelny Lars Terenius 

机构地区：[1]Department of Clinical Neuroscience,Center for Molecular Medicine,Karolinska Institutet,Stockholm,Sweden [2]San Diego Supercomputer Center,University of California San Diego,La Jolla,CA,USA [3]Department of Neurosciences,University of California San Diego,La Jolla,CA,USA [4]Department of Clinical Neuroscience,Karolinska University Hospital,Karolinska Institutet,Stockholm,Sweden

出　　处：《Neural Regeneration Research》2024年第8期1658-1659,共2页中国神经再生研究（英文版）

基　　金：supported by several grant agencies as stated in the full paper(to LT)。

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 amyloidbeta(Aβ)molecules interacting(dimer formation)followed by an accelerating build-up of socalled protofibrils,which turn into fibrils,which accumulate in the characteristic plaques.

关 键 词：ALZHEIMER DECOY AΒ 

分 类 号：R749.16[医药卫生—神经病学与精神病学]