Disruption of zinc and copper interactions with Aβ(1-40) by a non-toxic, isoniazid-derived, hydrazone: a novel biometal homeostasis restoring agent in Alzheimer's disease therapy?

Disruptions of biometal-Aβ(1-40) interactions by an isoniazid-derived hydrazone, INHHQ, were demonstrated via in vitro NMR titrations. The compound has adequate theoretical BBB absorption properties, assessed by in silico studies. In vivo acute toxicity assays indicate that INHHQ is innocuous up to...

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Veröffentlicht in:	Metallomics 2015-05, Vol.7 (5), p.743-747
Hauptverfasser:	Hauser-Davis, R A, de Freitas, L V, Cukierman, D S, Cruz, W S, Miotto, M C, Landeira-Fernandez, J, Valiente-Gabioud, A A, Fernández, C O, Rey, N A
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer Disease - drug therapy Amyloid beta-Peptides - metabolism Animals Blood-Brain Barrier - metabolism Copper - metabolism Homeostasis - drug effects Humans Hydrazones - chemistry Hydrazones - pharmacokinetics Hydrazones - pharmacology Isoniazid - analogs & derivatives Isoniazid - pharmacokinetics Isoniazid - pharmacology Male Peptide Fragments - metabolism Rats, Wistar Zinc - metabolism
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Zusammenfassung:	Disruptions of biometal-Aβ(1-40) interactions by an isoniazid-derived hydrazone, INHHQ, were demonstrated via in vitro NMR titrations. The compound has adequate theoretical BBB absorption properties, assessed by in silico studies. In vivo acute toxicity assays indicate that INHHQ is innocuous up to 300 mg kg(-1), showing potential as an anti-Alzheimer's drug.
ISSN:	1756-5901 1756-591X
DOI:	10.1039/c5mt00003c