Irene Volitakis

TL;DR: A 49% decrease in brain Abeta deposition is reported in a blinded study of APP2576 transgenic mice treated orally for 9 weeks with clioquinol, an antibiotic and bioavailable Cu/Zn chelator, support targeting the interactions of Cu and Zn with Abeta as a novel therapy for the prevention and treatment of AD.

TL;DR: This pilot phase 2 study supports further investigation of this novel treatment strategy using a metal-protein-attenuating compound, and the effect of treatment was significant in the more severely affected group.

TL;DR: The current data demonstrate that ionophore activity, inhibition of in vitro metal-mediated Abeta reactions, and blood-brain barrier permeability are indices that predict a potential disease-modifying drug for AD.

TL;DR: It is reported that tau-knockout mice develop age-dependent brain atrophy, iron accumulation and SN neuronal loss, with concomitant cognitive deficits and parkinsonism, which suggests the loss of soluble tau could contribute to toxic neuronal iron accumulation in Alzheimer's disease, Parkinson's disease and tauopathies, and that it can be rescued pharmacologically.

TL;DR: It is demonstrated that overexpression of the carboxyl-terminal fragment of APP, containing Aβ, results in significantly reduced copper and iron levels in transgenic mouse brain, while overexposure of the APP in Tg2576 transgenic mice results inificantly reduced copper, but not iron, levels prior to the appearance of amyloid neuropathology and throughout the lifespan of the mouse.