Stocky, one more thing I forgot. How they deal with toxic oligomers, the fibrils suspectd by some of doing the main damage in Alzheimers.
"Methods: Our goal is to assess whether PBT2 a novel metal chaperone can neutralize Abeta toxicity and restore synaptic function in AD. A wide variety of preclinical studies have been used to determine PBT2?s suitability as a disease modifying agent for AD and it is currently undergoing clinical evaluation in AD and Huntington's disease.
Results: Not only can PBT2 prevent Abeta/metal interactions which give rise to toxic oligomers but acting as a metal chaperone PBT2 induces neuroprotective signaling cascades. This signaling which includes inhibition of the phosphatase calcineurin leading to increased p-GSK3beta, with decreased levels of phospho-tau also protects against glutamate induced excitotoxicity. PBT2 increases dendritic spine density and levels of proteins associated with learning and memory such as NMDA receptor subunits 1A 2A, CamKII and BDNF, a property strictly dependent on its ability to deliver metals
Conclusions: These data suggest that PBT2 represents a more holistic approach to treating AD in that it can reverse Abeta pathology, inhibit the actions of other proteins implicated in the disease process and reverse synaptic dysfunction. Kevin Barnham, The Mental Health Reseach Isntitute Robert Cherny, Prana Biotechnology, and The Mental Health research Institute"
The preclinical results against Parkinsons were astounding and if you havnt seen them let me know and I will post them. It appeared to stop Parkinsons in the mouse model in its tracks.
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