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Alzheimer's disease (AD) is a progressive neurodegenerative disease and associated with the extracellular deposits of amyloid-  β   peptide in hippocampus region. Metal ions like Cu, Fe and Zn are known to associate with the amyloid beta (A  β  ) at high concentration and interaction of these ions with soluble and aggregated forms of A  β   peptide help in development of AD. Here we showed Cu mediated neurotoxicity in the eye tissues of transgenic  Drosophila  expressing human amyloid   β   and its rescue through a novel Cu chelator. In this context, we have synthesised and characterized the compound L 2,6-Pyridinedicarboxylic acid, 2,6-bis[2-[(4-carboxyphenyl) methylene] hydrazide] by Mass spectra (MS) and Elemental analysis (EA). The Cu chelation potential of the compound L is tested  in vivo  in  Drosophila . Oral administration of Copper to the transgenic larvae resulted in severe degeneration in eye tissues, which was rescued by the supplementation of compound L. The levels of anti-oxidant markers like SOD and MDA were measured in compound L treated flies and found a significant rescue ( P  < 0.001). Further rescue of the eye degeneration phenotypes as revealed by SEM affirm the role of copper in A  β   toxicity. Hence, use of compound L, an amidoamine derivative, could be a possible therapeutic measure for A  β   induced neurotoxicity.

international journal of alzheimer's disease

Neuroprotective Role of a Novel Copper Chelator against<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mtext>A</mml:mtext><mml:msub><mml:mrow><mml:mi mathvariant="bold-italic">β</mml:mi></mml:mrow><mml:mrow><mml:mtext>42</mml:mtext></mml:mrow></mml:msub></mml:math>Induced Neurotoxicity

Neuroprotective Role of a Novel Copper Chelator againstAβ42Induced Neurotoxicity