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?

CLAUDIO O. FERNANDEZ

METALLOMICS

ROYAL SOC CHEMISTRY

Lugar: Cambridge; Año: 2015 vol. 7 p. 743 - 747

1756-5901

Disruptions of biometal?Ab(1?40) interactions by an isoniazid-derived neurodegenerative disorders. They compete with Abfor binding hydrazone,INHHQ,weredemonstratedviainvitroNMRtitrations.with redox-active metal ions and zinc, preventing Aboligomeriza- 5,8 ThecompoundhasadequatetheoreticalBBBabsorptionproperties,tion, as well as restoring metal homeostasis and decreasing assessedbyinsilicostudies.Invivoacutetoxicityassaysindicatethatoxidative stress. This strategy hasbeenproposedasawayofslowing 1INHHQisinnocuousupto300mgkg,showingpotentialasanor even reversing AD progression. Recently, our research group anti-Alzheimer?sdrug.reported a novel potential MPAC based on the anti-tuberculosis