Some very interesting points in an interview that Kad posted with Charley Rose and Stanley Pruisner (google it - the 2nd interview around 39 minutes) -
Stanley Pruisner cites three pathways - these are all pre-plaque deposit. Drugs that can cross the BBB and act prior to plaque deposit (as we know) are more likely to provide reversal or benefit (i.e, PBT2). Also, he says they may only need to act for a short time and then re-start as necessary but not necessarily work for a long time continuously. Kind of as we were thinking that if the HA is at first arrested and then the reduction attenuates it would still provide benefit. But clearly he thinks plaque removal is not the key.
I calculated the projected pathway of the treated group and the placebo cross overs and they don't cross after two years if the rate of HA reduction even attenuates in the second year and the placebo cross overs see the 35% reduction as seen in the first year of the IMAGINE treated group. So, if this happens after the first year of placebo cross the lines will become parallel (in theory) and never cross proving disease modification IMO.
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Some very interesting points in an interview that Kad posted...
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