| Literature DB >> 17786851 |
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.Entities:
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Year: 2007 PMID: 17786851
Source DB: PubMed Journal: Curr Opin Drug Discov Devel ISSN: 1367-6733