The Origins of BSE - Page 3

Mn prions, circadian-vestibular disruption and TSE pathogenesis

The origins of TSE stem from a breakdown in the ability of the brain’s circadian and auditory -vestibular pathways to deal with unusually intense exposure to bouts of incoming visible/non visible EMR from the external environment (See Diagram 1). 

Diagram 1

In this respect, It is interesting that the retina contains both magneto and photo receptors for recieving and transducing several types of incoming visible/non visible EMR (26). Since this theory implicates an intensive inflow of these radiations into retinal and other EM receptors as one of the key causal prerequisites, it is interesting that the retina plays host to the initial pathological lesions in most types of TSE (16)(27)(28)(29), whilst the circadian, auditory and vestibular pathways exhibit the full spectrum of pathological damage in TSEs at the end of the day (1)(16).

The incoming flow of ultraviolet and low frequency acoustic radiation, etc, is largely transduced at receptors in the retina (26)(30) and at the hair cells in the cochlea respectively (31). Both visual and auditory pathways have analogous components. Each starts with sensory receptors that connect to early integration stages ( in the retina for vision and in the brainstem for hearing ), then to a thalmic relay. Both terminate via projections to the superior colliculus of the neocortex where the integration of auditory and visual information occurs (30). Whilst the role of light in mediating the circadian ryhthm is well recognised,  infrasound has also been shown to exert significant effects on the bio rhythms of the brain (32).

It is a disruption in the Cu mediated conduction of endogenous  electromagnetic energy (transduced from incoming light and sound) along the vestibular-circadian pathways that represents the primary disruption in TSE pathogenesis.

But what causes this Cu depletion and the resulting breakdown in electromagnetic homeostatis along the circadian-vestibular pathways; ultimately leading to the onset of TSE pathogenesis?

A three stage pathway of environmentally induced pathogenesis is proposed;  

1.  Foreign cation (eg Mn ) replacement of the vacant Cu domain at the octapeptide repeat region on PrP (4). This forms non pathogenic, protease resistant ‘sleeping’ Mn 2+ prions which begin to accumulate in the mammalian brain.

2.  Endogenous/exogenous sources of intensive oxidative stress (resulting from phagocytosis, intensive exposure to vaccinations, systemic insecticides, ultra violet radiation, ozone, etc), oxidize those Mn 2+ prions in retina, tonsils, astrocytes, lymphatic system, etc (the prion factory sites; See diagram 4 

Diagram 4

     into Mn3+ prions (5). Evidence in support of the suggestion of  the hyperoxidized status of the CNS in early stages of the TSE disease process has already been outlined (4)(5), and such an oxidative scenario can only be considerably facilitated by the deficit of Cu/Zn/Se activated antioxidant enzymes in the bio system (33). Analyses of traditional TSE cluster ecosystems consistently demonstrated low levels of the metal co factors (Cu, Se, Zn, Fe) which activate the various antioxidant enzyme groups (4).

3.  The Trivalent species of Mn is well known to absorb and resonate phonons (34) – the units of sound energy – and furthermore, an intense infrasonic shock is capable of metamorphosing the piezoelectric atomic structure of Mn 3+ component of the Mn3+ prion; whereupon the absorbed energy subsequently transforms the Mn3+ atom from paramagnetic to ferrimagnetic status. This occurs due to the dynamic lattice effects of the ‘Jahn-Teller’ type distortions of the oxygen octahedra around Mn3+ which enables a strong phonon-electron coupling to take place (34).  The freshly formed ‘ferrimagnetic’ strain of Mn3+prion is then readily susceptible to permanent polarization by any subsequent exposures to high levels of EMF from the external environment. Once the threshold of explosive ‘flash point’ is exceeded, self perpetuating chain reactions of free radical mediated neurodegeneration burst forth and full blown TSE ensues. In this respect, when the fully fledged, polarized prion is primed, it remains ‘infectious’ until heated to temperatures exceeding 500 + degrees, whereupon Mn’s  specific ‘curie point’ is surpassed and the Mn3+ atomic component of the prion is depolarised.