Aβ43-producing PS1 FAD mutants cause altered substrate interactions and respond to γ-secretase modulation.

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作者： Johannes,Trambauer ^[1] ; Rosa María,Rodríguez Sarmiento ^[2] ; Akio,Fukumori ^[3] ; Regina,Feederle ^[4] ; Karlheinz,Baumann ^[5] ; Harald,Steiner ^[6]

作者单位： Biomedical Center (BMC), Metabolic Biochemistry, Ludwig-Maximilians-University, Munich, Germany. ^[1] Roche Pharma Research and Early Development, Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd., Basel, Switzerland. ^[2] Department of Aging Neurobiology, National Center for Geriatrics and Gerontology, Obu, Japan. ^[3] Department of Mental Health Promotion, Osaka University Graduate School of Medicine, Toyonaka, Japan. ^[4] Institute for Diabetes and Obesity, Monoclonal Antibody Core Facility, Helmholtz Center Munich, German Research Center for Environmental Health, Neuherberg, Germany. ^[5] German Center for Neurodegenerative Diseases (DZNE), Munich, Germany. ^[6]

关键词 Aβ 43 amyloid β-peptide familial Alzheimer's disease presenilin γ-secretase modulator

主题词人类(Humans);阿尔茨海默病(Alzheimer Disease);淀粉样β肽类(Amyloid beta-Peptides);淀粉样β蛋白前体(Amyloid beta-Protein Precursor);淀粉样前体蛋白分泌酶类(Amyloid Precursor Protein Secretases);突变(Mutation);早老素1(Presenilin-1)

DOI 10.15252/embr.201947996

PMID 31762188

发布时间 2024-03-27

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