This was recently posted on YMB. More evidence Prana has nailed the problem with their metals theory in neurodegeneration. Here are a few passages from the full article. See the link.
[Oxidative Medicine and Cellular LongevityVolume 2013 (2013), Article ID 726954, 19 pageshttp://dx.doi.org/10.1155/2013/726954Review Article Metal Dyshomeostasis and Inflammation in Alzheimer’s and Parkinson’s Diseases: Possible Impact of Environmental Exposures Oddvar Myhre,1 Hans Utkilen,2 Nur Duale,1 Gunnar Brunborg,1 and Tim Hofer1 1Division of Environmental Medicine, Department of Chemicals and Radiation, The Norwegian Institute of Public Health, P.O. Box 4404, Nydalen, 0403 Oslo, Norway 2Division of Environmental Medicine, Department of Food, Water and Cosmetics, The Norwegian Institute of Public Health, P.O. Box 4404, Nydalen, 0403 Oslo, Norway
Received 14 December 2012; Revised 6 February 2013; Accepted 7 February 2013
Abstract A dysregulated metal homeostasis is associated with both Alzheimer’s (AD) and Parkinson’s (PD) diseases; AD patients have decreased cortex and elevated serum copper levels along with extracellular amyloid-beta plaques containing copper, iron, and zinc. For AD, a putative hepcidin-mediated lowering of cortex copper mechanism is suggested. An age-related mild chronic inflammation and/or elevated intracellular iron can trigger hepcidin production followed by its binding to ferroportin which is the only neuronal iron exporter, thereby subjecting it to lysosomal degradation. Subsequently raised neuronal iron levels can induce translation of the ferroportin assisting and copper binding amyloid precursor protein (APP); constitutive APP transmembrane passage lowers the copper pool which is important for many enzymes. Using in silico gene expression analyses, we here show significantly decreased expression of copper-dependent enzymes in AD brain and metallothioneins were upregulated in both diseases. Although few AD exposure risk factors are known, AD-related tauopathies can result from cyanobacterial microcystin and ß-methylamino-L-alanine (BMAA) intake. Several environmental exposures may represent risk factors for PD; for this disease neurodegeneration is likely to involve mitochondrial dysfunction, microglial activation, and neuroinflammation. Administration of metal chelators and anti-inflammatory agents could affect disease outcomes.]
[Notably, brain tissue is composed of several types of cells (astrocytes, neurons, microglia, and endothelial cells, etc.) where neuron supporting astrocytes numerically dominate, but the results show that crucial copper-dependent enzymes (COX, SOD1, and PAM) and ATOX1 (a copper-chaperone protein) are underexpressed in AD brains.]
[ Many issues confront the use of chelators including metal saturation. The compounds’ ability to reach the intended site is affected by metabolic instability, and toxicity is an important issue (administration of copper chelators to dissolve Aß-plaques could further lower neuronal copper levels, etc). Current clinical oral administration of lipophilic membrane permeable iron chelators includes deferiprone (produced by ApoPharma) and deferasirox (Novartis). These are today mainly used for treatment of thalassemia major and anaemia, respectively; only a few reports concern their uses in relevant neurodegenerative situations [98]. Molecular modifications may be needed for improved BBB passage and stability [99]. For efficient iron removal from the brain, it has been suggested that the lipophilic chelator-iron (III) complex should have a molecular mass less than 500?Da and be uncharged for cell membrane and BBB permeability [93]. The copper/zinc chelator clioquinol (CQ) [100] was suggested to inhibit Aß accumulation due to its ability to remove metals from the brain; however, CQ is now considered toxic. This led to the development of the analogue PBT2, a potential therapeutic compound for AD which reduced cerebrospinal fluid (CSF) Aß42 and improved cognition without serious adverse effects, according to a phase II clinical trial [101]; the compound is being further investigated. Other chelators tested in AD models having showed positive effects include the iron chelator M30 [92], the copper chelators JKL-169 [102] and IQM-622 [103], and the calcium/copper/zinc chelators DP-109 and DP-460 [104, 105]. On the contrary, a clinical trial of D-penicillamine, a copper chelator, was unable to produce any clinical improvement in AD patients and resulted in toxicities [106]. Nanoparticle-based chelators that can cross the blood-brain barrier are also being developed [107].]
They appear to be misrepresenting the PBT2 chaperone as a chelator, and issues mentioned with chelators can possibly be avoided by using a chaperone like PBT2 which just repositions available metals, and restors the brain's ability to self regulate brain iron levels. There is a LOT more on the link.
(20min delay)