I found the abstract I was referring to that begins with a discussion about PBT2 MOA, and has a later alternative approach they experimented with...I believe that's what this is all about...
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3087126/
As both CuII(gtsm) and CuII(atsm) are capable of crossing the blood brain barrier (Fodero-Tavoletti et al., 2010) the therapeutic potential of intracellular copper delivery was evaluated in the APP/PS1 transgenic AD model mice (Crouch et al., 2009). CuII(gtsm) which delivers bioavailable copper significantly inhibited GSK3ß in the brains of APP/PS1 transgenic AD model mice. CuII(gtsm) also decreased the abundance of Aß trimers and phosphorylated tau, and restored performance of AD mice in the Y-maze test to levels expected for cognitively normal animals. Improvement in the Y-maze correlated directly with decreased Aß trimer levels. CuII(atsm) does not deliver bioavailable copper and had no effects on cognition or disease relevant biomarkers. This study demonstrates that increasing intracellular copper bioavailability can restore cognitive function by inhibiting the accumulation of neurotoxic Aß trimers and phosphorylated tau (Crouch et al., 2009).
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