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• W2001824740 abstract "The amyloid-β peptide (Aβ) is believed to be the major causative agent responsible for Alzheimer's disease (AD). Aβ contains a high affinity metal binding site which modulates peptide aggregation and toxicity. Therefore, identifying molecules targeting this site represents a valid therapeutic strategy. To test this hypothesis a range of L-PtCl2 (L= [1,10]-phenathroline derivatives) complexes were examined in a range of in vitro assays testing the ability of the compounds to alter the biophysical and biochemical properties of Aβ. We were able to show that the compounds bound to Aβ and altered the chemical properties of the peptide inhibiting amyloid formation and the generation of reactive oxygen species. Coordination of the complexes to Aβ also inhibited neurotoxicity and rescueed Aβ-induced synapto-toxicty in mouse hippocampal slices. In comparison, the classic anti-cancer drug cisplatin did not affect any of the biochemical and cellular effects of Aβ. The lack of activity by cisplatin implies that the planar aromatic 1,10-phenathroline ligands L confer some specificity for Aβ onto the platinum complexes. The potent effect of the L-PtCl2 complexes identifies this class of compounds as novel potential therapeutic agents for AD." @default.
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• W2001824740 date "2008-07-01" @default.
• W2001824740 modified "2023-10-06" @default.
• W2001824740 title "P2-293: Platinum-based inhibitors of amyloid-β as therapeutic agents for Alzheimer's disease" @default.
• W2001824740 doi "https://doi.org/10.1016/j.jalz.2008.05.1369" @default.
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