Hi pivalde. It is interesting how when tau came to the fore as a disease modifying target, evidence emerged that MPACs can reduce tau, and now with the focus on the mitocondria researchers have demonstrated MPAC utility correcting that problem. When you consider the efficacy evidence from the Euro and Reach2HD trial it is no surprise PBT2 is ticking all the boxes as research progresses. I am not sure if there are any other drugs with TMTB etc, CSF and atrophy marker improvements all together.
Now it is looking like MPACs will have utility over many diseases apart from neurodegeneration, as has been discussed here on several occasions.
That paper was a great find. Maybe the FDA has done us a favor forcing Prana to branch out in other directions. At the same time it is a sad time for HD patients IMO, because I don't believe there is much doubt PBT2 has already produced efficacy evidence from Reach2HD. Notice the results of the patient questionnaires heavily favored high dose PBT2 arm, regardless of TMTB results. Mitochondria?
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- PBT2 in experimental cardiac amyloidosis,
PBT2 in experimental cardiac amyloidosis,, page-14
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