Effects of Aβ-derived peptide fragments on fibrillogenesis of Aβ.
Ontology highlight
ABSTRACT: Amyloid β (Aβ) peptide aggregation plays a central role in Alzheimer's disease (AD) etiology. AD drug candidates have included small molecules or peptides directed towards inhibition of Aβ fibrillogenesis. Although some Aβ-derived peptide fragments suppress Aβ fibril growth, comprehensive analysis of inhibitory potencies of peptide fragments along the whole Aβ sequence has not been reported. The aim of this work is (a) to identify the region(s) of Aβ with highest propensities for aggregation and (b) to use those fragments to inhibit Aβ fibrillogenesis. Structural and aggregation properties of the parent Aβ1-42 peptide and seven overlapping peptide fragments have been studied, i.e. Aβ1-10 (P1), Aβ6-15 (P2), Aβ11-20 (P3), Aβ16-25 (P4), A
SUBMITTER: Abedin F
PROVIDER: S-EPMC8479085 | biostudies-literature | 2021 Sep
REPOSITORIES: biostudies-literature
ACCESS DATA