I take a bit simplified view of these results. The results...

I take a bit simplified view of these results. The results support that 434 reduces (most likely labile) iron based on the MRI results. I would think that the biggest effect on the cellular level happens when there is a lot of labile iron during the first 13 weeks. This is the period when the UMRS score improves most with 75mg. But when there is less labile iron after these 13 weeks (we have 6-month MRIs), it may be that even 434 at high dosage starts to cause more side-effects on the cell level, as the old iron chelators did. I do not think that all the time, more and more labile iron will come to the brain.

Unfortunately, the alpha-synuclein measurements were not successful ("Alpha-synuclein SAA requires continued refinement in MSA"). Because of that, Professor Claassen started his presentation with the info from the 434 ape study: "ATH434 reduces α-synuclein aggregation in vitro and
in vivo". It could be that if they can still measure these, we could perhaps find an answer as to why 75mg is worse than 50mg.

They do not report anything about neurofilament light; most likely, there were no differences. NFL is a measure of white matter degeneration, axons. However, we had brain atrophy in the MRI. My experience is that MSA also causes dementia, and perhaps the gray matter measure Tau, perhaps the p217Tau measure would go better with the atrophy seen in the MRI pictures.

Just my speculation.