title: Elimination of Amyloid beta Neurotoxicity.
abstract: Aggregation of the Alzheimer amyloid beta peptide (Abeta) Abeta1-42 forms neurotoxic fibrils. In contact with human neurons the fibrils cause rapid influx of external calcium through AMPA/kainate-channels. If this molecular mechanism reflects in vivo events, it could explain the pathogenesis of Alzheimer's disease; activation of AMPA/kainate channels is therefore a likely target for therapeutic intervention. Here we show that short antagonistic "decoy peptides", made of D-amino acids, eliminate this "calcium effect" of Ab1-42. Since chronically elevated calcium levels in the disease trigger activation of pathways that lead to neuron dysfunction and cell death, our decoy peptides are obvious candidates for drug development.
authors.forename: Barbara J.
authors.initials: BJ
authors.lastname: Blanchard
authors.forename: Anne E.
authors.initials: AE
authors.lastname: Hiniker
authors.forename: Connie C.
authors.initials: CC
authors.lastname: Lu
authors.forename: Yelena
authors.initials: Y
authors.lastname: Margolin
authors.forename: Amy S.
authors.initials: AS
authors.lastname: Yu
authors.forename: Vernon M.
authors.initials: VM
authors.lastname: Ingram