Scottsmyname, PD makes slow progress in comparison to MSA. With...

Scottsmyname, PD makes slow progress in comparison to MSA. With the present treatments, it will usually take around 15 years to become highly dependent. So in one year, the symptom scores do not get higher quickly. But it is different in MSA as has been demonstrated by Claassen.
Side effects of ATH434 are not yet very well known but with the open study and more exactly in the randomized study these will become clearer.

Here at home, I am trying to study how the paper from Stanford ( A mitochondrial inside-out iron-calcium signal reveals drug targets for Parkinson's disease, https://pubmed.ncbi.nlm.nih.gov/38060381/) and Prof. Kosman's poster about ATH434 and mitochondrion (https://alteritytherapeutics.com/wp-content/uploads/Society-for-Neuroscience-2023_poster.pdf) could be fitted together.

The previous study concludes: "In this work, we have established a mitochondrial inside-out pathway of Fe2+-Ca2+-Miro1 dysregulation in our PD models (Figure 7G). Chelating iron, reducing Ca2+ entry into the cell, or blocking Miro1’s binding to Ca2+ is each neuroprotective (Figures 4, 5, and 7). Hence, this ionic axis may be important for PD pathogenesis and can be leveraged for better detecting and treating the disease".
So the problem is in the mitochondrial membrane.

Kosman's poster says: " 434 and 434-met rescue menadione-induced loss of mitochondrial membrane potential". "This antioxidant
activity supports and protects the mitochondria ...."

My simplistic conclusion is that a mitochondrial membrane problem is related to free iron overload and calcium overload in PD. Gentle iron chelation helps in animal models as does the calcium channel blocker already used in human PD (Zonisamide). But until ATH434 we do not have a gentle iron chelator to eliminate iron. Deferiprone was too strong and made the patients worse.