Does an infrasonic acoustic shock wave resonance of the manganese 3+ loaded/copper depleted prion protein initiate the pathogenesis of TSE?

• Published in: Medical hypotheses 2003-06, Vol.60 (6), p.797-820
• Main Author: Purdey, Mark
• Format: Article
• Language: English
• Subjects: Animals; Cattle; Copper - chemistry; Copper - deficiency; Disasters; Electromagnetic Fields - adverse effects; Environmental Exposure - adverse effects; Humans; Manganese - chemistry; Manganese - metabolism; Prion Diseases - epidemiology; Prion Diseases - etiology; Prion Diseases - metabolism; Prions - chemistry; Prions - metabolism; Prions - radiation effects; Ultrasonics - adverse effects; Ultraviolet Rays - adverse effects; United Kingdom - epidemiology; United States - epidemiology
• ISSN: 0306-9877; 1532-2777
• DOI: 10.1016/S0306-9877(03)00007-0

Intensive exposures to natural and artificial sources of infrasonic acoustic shock (tectonic disturbances, supersonic aeroplanes, etc.) have been observed in ecosystems supporting mammalian populations that are blighted by clusters of traditional and new variant strains of transmissible spongiform encephalopathy (TSE). But TSEs will only emerge in those ‘infrasound-rich’ environments which are simultaneously influenced by eco-factors that induce a high manganese (Mn)/low copper (Cu)–zinc (Zn) ratio in brains of local mammalian populations. Since cellular prion protein (PrPc) is a cupro-protein expressed throughout the circadian mediated pathways of the body, it is proposed that PrP’s Cu component performs a role in the conduction and distribution of endogenous electromagnetic energy; energy that has been transduced from incoming ultraviolet, acoustic, geomagnetic radiations. TSE pathogenesis is initiated once Mn substitutes at the vacant Cu domain on PrPc and forms a nonpathogenic, protease resistant, ‘sleeping’ prion. A second stage of pathogenesis comes into play once a low frequency wave of infrasonic shock metamorphoses the piezoelectric atomic structure of the Mn 3+ component of the prion, thereby ‘priming’ the sleeping prion into its fully fledged, pathogenic TSE isoform – where the paramagnetic status of the Mn 3+ atom is transformed into a stable ferrimagnetic lattice work, due to the strong electron–phonon coupling resulting from the dynamic ‘Jahn-Teller’ type distortions of the oxygen octahedra specific to the trivalent Mn species. The so called ‘infectivity’ of the prion is a misnomer and should be correctly defined as the contagious field inducing capacity of the ferrimagnetic Mn 3+ component of the prion; which remains pathogenic at all temperatures below the ‘curie point’. A progressive domino-like ‘metal to ligand to metal’ ferrimagnetic corruption of the conduits of electromagnetic superexchange is initiated. The TSE diseased brain can be likened to a solar charged battery on continuous charge; where the Mn contaminated/Cu depleted circadian-auditory pathways absorb and pile up, rather than conduct the vital life force energies of incoming ultra violet, acoustic and geomagnetic radiation. Instead of harnessing these energies for the body’s own bio-rhythmic requirements, an infrasonic shock induced metamorphosis of the Mn atom intervenes; initiating an explosive pathogenesis that perverts the healthy pathways of darkness and light; Cu prions