WTF !!!, page-42

I think I recall Stamler said they were going to insert the brain mass endpoint as a primary endpoint. That would be a big call. I went looking for that in the trials site, but didn't see the change yet. I was happy they added brain mass, because they also saw that effect from their old chelator/chaperone pbt2 trials. Still the FDA has to sign off on the change. As long as the trial is still blinded, who knows,

The 202 trial for me has already identified that stat sig sub group. Early stage patients. Happily the phase 3 trial already running is in early stage patients. Stamler seems to really know what he is doing.

As much as I hate to use any mouse model results, the Verdiperstat results clearly illustrate what is going on IMO. Treating mice with Verdiperstat reduced microglial activation, a-syn aggregation and improved motor function. Delaying treatment till mice had developed full blown pathology still reduced microglial activation and a-syn aggregation, but did not improve neuron loss or motor impairments. Looks like once the synapses obstructed, its over. all IMHO
alzforum.org/therapeutics/verdiperstat