title: Amyloid beta receptors responsible for neurotoxicity and cellular defects in Alzheimer's disease.
abstract: Alzheimer's disease (AD) is the most common neurodegenerative disease. Although a major cause of AD is the accumulation of amyloid-β (Aβ) peptide that induces neuronal loss and cognitive impairments, our understanding of its neurotoxic mechanisms is limited. Recent studies have identified putative Aβ-binding receptors that mediate Aβ neurotoxicity in cells and models of AD. Once Aβ interacts with a receptor, a toxic signal is transduced into neurons, resulting in cellular defects including endoplasmic reticulum stress and mitochondrial dysfunction. In addition, Aβ can also be internalized into neurons through unidentified Aβ receptors and induces malfunction of subcellular organelles, which explains some part of Aβ neurotoxicity. Understanding the neurotoxic signaling initiated by Aβ-receptor binding and cellular defects provide insight into new therapeutic windows for AD. In the present review, we summarize the findings on Aβ-binding receptors and the neurotoxicity of oligomeric Aβ.
authors.affiliation: Global Research Laboratory, School of Biological Sciences, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 151-747, Korea.
authors.forename: Tae-In
authors.initials: TI
authors.lastname: Kam
authors.forename: Youngdae
authors.initials: Y
authors.lastname: Gwon
authors.forename: Yong-Keun
authors.initials: YK
authors.lastname: Jung
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D006801:Humans; D008954:Models, Biological; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D020258:Neurotoxicity Syndromes / Q000378:metabolism*; D011485:Protein Binding; D011956:Receptors, Cell Surface / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D016229:Amyloid beta-Peptides; D011956:Receptors, Cell Surface