IMO, things are improving because there is evidence that the...

IMO, things are improving because there is evidence that the basic problem in PD (and related diseases) is in mitochondria (Gonzalez- Rodriquez P, Nov 2021 in Nature) and that iron deposition is related to the impairment of mitochondrion function in the PD (Prasuhn et al, Mar 2022). In animal studies, the movement function has been returned by our iron chelator ATH434.

It is easier to find a working drug when you know the problem. The hypothesis that ATH434 would help in PD or MSA was only a hypothesis but now IMO ATH is with its ph 2 study targeting the real cause (not 100%) of PD and related diseases, at least much closer to the real cause than when ph 1 study was done with ATH434. Not yet 100% sure but much closer than previously. In my mind at the moment safety is a bigger problem than efficacy.

Of course, everything can be spoiled by poor management. ATH has been slow but perhaps very careful (?). I do not think they will spoil the ph 2 study when they will get started.

So with ATH434 ATH seems to target just the right problem: iron overload. That was not the original case with PBT2 targeting AD but now the right target has been found: antibiotic-resistant bacteria.