As we have been told PBT434 works because it is a compound "designed to target a pool of pathological iron that is not held in high-affinity complexes in the tissue can maintain the survival of Substantia Nigra pars compacta neurons and could be disease-modifying in PD".
This perhaps a bit complex statement in the abstract of PBT434 paper by Finkelstein et al does not tell anything about why the nerves in substantia nigra die when a patient is developing Parkinson's disease, nothing about energy problem what is in general considered to be the reason why the nerves die.
Now this paper by Huang XT et al ( Oct 31, 2018, posted earlier ) tells that too much iron causes energy deficiency and mitochondrial fragmentation.
IMO PBT434 "prevented loss of substantia nigra pars compacta neurons (SNpc), lowered nigral α-synuclein accumulation, and rescued motor performance in mice exposed to the Parkinsonian toxins 6-OHDA and MPTP, and in a transgenic animal model (hA53T α-synuclein) of PD " because PBT434 improved the function of mitochondria and so energy supply of neurons.
"These improvements were associated with reduced markers of oxidative damage, and increased levels of ferroportin (an iron exporter) and DJ-1" and these can also be due to improved energy supply IMO.
So today we have a common understanding that PD and AD are mitochondrion diseases and iron accumulation is one cause and perhaps a very strong factor in this pathologic development. Huang et al found after overload of iron that " Gene Ontology enrichment analysis revealed that 58 mitochondria-associated proteins were found to be significantly altered, including three subunits of mitochondrial complex I and OPA1". So most likely there would be many other positive changes caused by PBT434 in the content of different molecules in various PD animal models what Finkelstein el al did not study but most likely they all can be explained by improved energy supply.
I think that it would be very important that Prana would now do experiments confirming the effect of PBT434 to be mitochondrion related and not only iron related. To have a safe mitochondrion drug is much more than to have an iron chelator IMO.
