The published paper of PBT434 in several PD models ( Finkelstein et al, 2017) told us " PBT......prevented loss of substantia nigra pars compacta neurons (SNpc), lowered nigral α-synuclein accumulation, and rescued motor performance in mice exposed to the Parkinsonian toxins 6-OHDA and MPTP, and in a transgenic animal model (hA53T α-synuclein) of PD. These improvements were associated with reduced markers of oxidative damage, and increased levels of ferroportin (an iron exporter) and DJ-1."
Now today we got results in a MSA model " PBT434 prevents α-synuclein aggregation, preserves neurons, decreases the number of glial cell inclusions and slows motor dysfunction ". So the report today is very similar what we got over 1 y ago by Finkelstein, but not yet so detailed. I am sure that the poster will have much more detail info but perhaps is not yet allowed to be published. Need to wait until Sunday ?
However in this new report there is one promising point : " The data indicate that PBT434 targets the key pathology in MSA ". This kind of a strong statement is not very typical to Prana. This was not told us 3 months ago by Dr. Stamler when Prana informed about this HK congress and the "robust " effect of PBT434 in MSA. Neither there was so strong statement in the Finkelstein paper in several PD models. I think that the new poster will tell us something even more important when it can be published on Sunday at 1.45. But I may hope too much, unfortunately. In any case there will be much more info in the poster and I hope it is also presented to us.
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