Bahadi, RandaFarrelly, PeterKenna, BronwynCurtain, CyrilMasters, ColinCappai, RobertoBarnham, KevinKourie, Joseph2015-12-132015-12-130363-6143http://hdl.handle.net/1885/86075We found that the amyloid β peptide Aβ(1-42) is capable of interacting with membrane and forming heterogeneous ion channels in the absence of any added Cu2+ or biological redox agents that have been reported to mediate Aβ(1-42) toxicity. The Aβ(1-42)-Keywords: amyloid beta protein; chelating agent; clioquinol; copper ion; prion protein; zinc ion; amyloid beta protein (1 42); amyloid beta-protein (1-42); chelating agent; clioquinol; copper; ion channel; peptide fragment; Alzheimer disease; article; binding site; Calcium homeostasis; Ion channel pathologies; Membrane injuries; Neurodegenerative diseases; Transitional metals20032015-12-12