title: Peptide inhibitors of beta-amyloid aggregation.
abstract: The aggregation of the beta-amyloid peptide (Abeta) into toxic oligomers is probably the key pathogenic event in the onset of Alzheimer's disease, and is therefore a target for the treatment of the disease. A plethora of organic molecules have been shown to inhibit Abeta aggregation and toxicity. Many inhibitors are peptides or peptidomimetics, typically based on the amino acids 16 to 20 of Abeta (KLVFF), which binds to Abeta in isolation. Peptides have been modified by adding bulky groups, charged sequences or polyethylene glycol to their termini, or by N-methylation, replacing a backbone amide by an ester, and by replacing a residue with proline.
authors.affiliation: Faculty of Life Sciences, Manchester Interdisciplinary Biocentre, University of Manchester, 131 Princess Street, Manchester, M1 7DN, UK. andrew.doig@manchester.ac.uk
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Doig
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy* / Q000378:metabolism; D016229:Amyloid beta-Peptides / Q000037:antagonists & inhibitors*; D000818:Animals; D015195:Drug Design; D006801:Humans; D010455:Peptides / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use; D011487:Protein Conformation