title: Amyloid β-interacting partners in Alzheimer's disease: From accomplices to possible therapeutic targets.
abstract: Alzheimer's disease (AD) is one of the most devastating neurodegenerative diseases in modern society because of insurmountable difficulties in early diagnosis and lack of therapeutic treatments. AD pathogenesis is tightly linked to the abnormal accumulation and aggregation of amyloid β (Aβ), seemingly the main causative factor of AD; however, intensive research on Aβ has not yet explained the complexity of AD pathogenesis. Consequently, the role of other supportive partners of Aβ have been elucidated and evaluated in the etiology of AD, and their potential molecular mechanisms have emerged as possible therapeutic targets. In this review, we compile information regarding Aβ-interacting partners in normal conditions and AD pathology, and analyze their etiological roles in diverse areas. Furthermore, we integrate this information into suggestions for probable clinical applications for AD diagnosis and therapeutics. We include Aβ-interacting partners localized to the cell surface and intracellular and extracellular compartments of different cell types ranging from the central nervous system to peripheral regions. Additionally, we expand the range of Aβ-interacting partners by including not only proteins, but also inorganic substances like metals, expecting that one of these partners may yield a critical breakthrough in the field of AD diagnostics and therapeutic drug development.
authors.affiliation: Department of Biochemistry and Biomedical Sciences, Seoul National University, College of Medicine, 28 Yungun-dong, Jongro-gu, Seoul 110-799, South Korea.
authors.forename: Sun-Ho
authors.initials: SH
authors.lastname: Han
authors.affiliation: Department of Biochemistry and Biomedical Sciences, Seoul National University, College of Medicine, 28 Yungun-dong, Jongro-gu, Seoul 110-799, South Korea.
authors.forename: Jong-Chan
authors.initials: JC
authors.lastname: Park
authors.affiliation: Department of Biochemistry and Biomedical Sciences, Seoul National University, College of Medicine, 28 Yungun-dong, Jongro-gu, Seoul 110-799, South Korea. Electronic address: inhee@snu.ac.kr.
authors.forename: Inhee
authors.initials: I
authors.lastname: Mook-Jung
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D053327:Apolipoprotein E4 / Q000378:metabolism / Q000627:therapeutic use; D001798:Blood Proteins / Q000378:metabolism / Q000627:therapeutic use; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D006801:Humans; D026502:LDL-Receptor Related Proteins / Q000378:metabolism; D008670:Metals / Q000378:metabolism / Q000627:therapeutic use; D011328:Prions / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D053327:Apolipoprotein E4; D001798:Blood Proteins; D026502:LDL-Receptor Related Proteins; D008670:Metals; D011328:Prions; D011956:Receptors, Cell Surface
keywords: Alzheimer's disease; Amyloid β; Amyloid β-interacting protein; Blood–brain barrier; Cerebrospinal fluid