Targeting iron in AD by Bush ( a review ), page-3

And include HD as a likely candidate for iron chelation with a SAFE chelator. PBT434 was originally introduced as a possible treatment for movement disorders, of which Huntington's is one.

"The pathways regulating iron distribution and levels are complex, but energy-factories within cells — called mitochondria — need large amounts of iron to be able to function. A perfect example of the importance of iron to mitochondria is Friedreich’s ataxia, a disorder characterized by mitochondrial iron accumulation.In Huntington’s, there is a co-occurrence of iron deregulation and mitochondrial dysfunction, but the link between mitochondria and iron in disease progression remains unclear.Researchers showed that iron accumulation occurs within brain mitochondria in of a mouse model of Huntington’s disease. This finding was also confirmed through autopsy brain tissue samples of Huntington’s patients.The team found that iron accumulation inside mitochondria was mediated by a decrease in the expression of specific proteins that help manage iron levels, both in mice and humans. This means that in brains affected by Huntington’s disease, there is increased mitochondrial iron uptake but decreased utilization, which explains its accumulation.Chemically removing the excess iron with the help of an iron chelator rescued mitochondrial to work as intended.Treating a mouse model of Huntington’s disease for 10 days with an oral dose of Ferriprox (deferiprone), delivered as 150 mg/kg of body-weigh, twice-a-day – also rescued several features of mitochondrial health and improved mice motor endurance. Ferriprox is a U.S. Food and Drug Administration (FDA) approved therapy to remove transfusional iron overload due to thalassemia syndromes."

https://huntingtonsdiseasenews.com/2018/05/03/iron-buildup-in-brain-mitochondria-may-promote-huntingtons-disease-study-suggests/

There was a small sample of patients in Reach2HD for PBT2 and as I recall PBT2 did not reduce iron. Maybe Prana will also "discover" that PBT434 could boost treatment for HD.

"MAY 1, 2012Melbourne – 1 May 2012: Prana Biotechnology (NASDAQRAN; ASXBT) today commented on the publication of new data of relevance to the current clinical trial, testing Prana’s PBT2 as a treatment for Huntington disease.The authors of the publication are led by Professor Diana Rosas of the Center for Neuroimaging of Aging and Neurodegenerative disease at Massachusetts General Hospital (MGH) in Boston. The paper, entitled “Alterations in Brain Transition Metals in HD”, published in the Archives of Neurology* describes how the rise in levels of Iron in the brains of people carrying the mutant gene which causes Huntington disease, correlates with the severity of symptoms and also predicts the time of disease onset. The article concluded that “an important and early role of altered metal homeostasis is suggested in the pathogenesis of Huntington disease” and this points to “metals as potential therapeutic targets”. Selected patients in the current Reach2HD trial, testing PBT2, will be monitored using the imaging technology described in the publication"

So the iron level even predicts onset of the disease in HD. Looks like there could be markets for AD, PD and HD, just to name a few.

http://pranabio.com/news/prana-comments-on-archives-of-neurology-publication-which-highlights-critical-role-of-brain-metals-in-huntington-disease-progression-mgh-team-publishes-data-that-supports-the-use-of-pbt2-in-huntingto/#.XD8y_89KhE4