title: Amyloid-β Receptors: The Good, the Bad, and the Prion Protein.
abstract: Several different receptor proteins have been identified that bind monomeric, oligomeric, or fibrillar forms of amyloid-β (Aβ). "Good" receptors internalize Aβ or promote its transcytosis out of the brain, whereas "bad" receptors bind oligomeric forms of Aβ that are largely responsible for the synapticloss, memory impairments, and neurotoxicity that underlie Alzheimer disease. The prion protein both removes Aβ from the brain and transduces the toxic actions of Aβ. The clustering of distinct receptors in cell surface signaling platforms likely underlies the actions of distinct oligomeric species of Aβ. These Aβ receptor-signaling platforms provide opportunities for therapeutic intervention in Alzheimer disease.
authors.affiliation: From the Institute of Brain, Behaviour and Mental Health, Faculty of Medical and Human Sciences, University of Manchester, Manchester M13 9PT and.
authors.forename: Heledd H
authors.initials: HH
authors.lastname: Jarosz-Griffiths
authors.affiliation: From the Institute of Brain, Behaviour and Mental Health, Faculty of Medical and Human Sciences, University of Manchester, Manchester M13 9PT and.
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Noble
authors.affiliation: the Faculty of Health and Life Sciences, De Montfort University, Leicester LE1 9BH, United Kingdom.
authors.forename: Jo V
authors.initials: JV
authors.lastname: Rushworth
authors.affiliation: From the Institute of Brain, Behaviour and Mental Health, Faculty of Medical and Human Sciences, University of Manchester, Manchester M13 9PT and nigel.hooper@manchester.ac.uk.
authors.forename: Nigel M
authors.identifier: http://orcid.org/0000-0002-5811-3484
authors.initials: NM
authors.lastname: Hooper
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology / Q000517:prevention & control; D016229:Amyloid beta-Peptides / Q000037:antagonists & inhibitors / Q000737:chemistry / Q000378:metabolism*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D006801:Humans; D008024:Ligands; D026503:Low Density Lipoprotein Receptor-Related Protein-1 / Q000819:agonists / Q000378:metabolism; D008954:Models, Biological; D058990:Molecular Targeted Therapy; D009419:Nerve Tissue Proteins / Q000037:antagonists & inhibitors / Q000737:chemistry / Q000378:metabolism*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D018697:Nootropic Agents / Q000494:pharmacology / Q000627:therapeutic use; D018621:PrPC Proteins / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism; D066329:Protein Aggregates / Q000187:drug effects; D066263:Protein Aggregation, Pathological / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D020033:Protein Isoforms / Q000037:antagonists & inhibitors / Q000737:chemistry / Q000378:metabolism; D011940:Receptor Aggregation / Q000187:drug effects; D000067759:Receptor for Advanced Glycation End Products / Q000819:agonists / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000819:agonists* / Q000037:antagonists & inhibitors / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D057900:Transcytosis / Q000187:drug effects
chemical_list: D016229:Amyloid beta-Peptides; D008024:Ligands; D026503:Low Density Lipoprotein Receptor-Related Protein-1; D009419:Nerve Tissue Proteins; D018697:Nootropic Agents; D018621:PrPC Proteins; D066329:Protein Aggregates; D020033:Protein Isoforms; D000067759:Receptor for Advanced Glycation End Products; D011956:Receptors, Cell Surface; D016194:Receptors, N-Methyl-D-Aspartate
keywords: Alzheimer disease; amyloid; oligomer; prion; receptor