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It is
proposed that the origins of TSEs do not stem from the exposure of PrP
susceptible individuals to infectious, exogenous prions, but are caused
by simultaneous exposure of the PrP susceptible individual to a specific
combination of environmental prerequisites; high Mn, low Cu, and high
intensities of visible/non visible electromagnetic radiation (EMR)
– a package of factors that is “common” to pockets around the
world where TSE clusters have traditionally emerged, whilst remaining
absent in adjoining TSE-free regions (4)(5).
Combined
exposure of PrP susceptible genotypes to these environmental
prerequisites invokes a ‘Jekyll and Hyde’ de novo
transformation of the normal native Cu PrPc into its rogue, protease
resistant, pathogenic Mn3+ PrPtse isoform (5).
See Diagram 3
Diagram
3
Therefore,
this theory does not consider that the BSE-vCJD epidemics were caused by
a modified scrapie prion jumping from sheep to cattle to humans via
prion contaminated meat products, but considers that it was caused by
exposure of the various different species to the same set of
environmental prerequisites with resulting de novo formation of prion
‘tombstones’ in the CNS of susceptible individuals.
Healthy
Cu prion proteins, electromagnetic conduction and circadian homeostatis.
Evidence
gleaned from PrP ‘knock out’ experiments in mice demonstrates a
possible functional role of PrPc in the circadian rhythm (14)(15).
Likewise the clinical and neuropathological profiles of TSE
indicate a wide ranging disruption of the vestibular - circadian –
serotonergic – sympathetic pathways (1)(16)(17)(18)(19).
Research
has established that the prion protein is a metalloprotein which
preferentially bonds onto copper or zinc at its octapeptide repeat
region (20)(21). It seems that some hitherto unidentified facet of
PrP’s association with copper/zinc may eventually resolve the riddle
surrounding the function of this elusive protein. In this respect, It is
proposed that the Cu component of normal PrP (20)(21) may perform some
role in maintaining the electromagnetic homeostatis of the
circadian pathways; where Cu conducts electromagnetic energy along the
circadian regulated melatonin - serotonergic sympathetic pathways;
conducting that energy in order to activate a wide array of
physiological functions; sleep/wake rhythms, sexual cycles, mood/behaviour, immune response, gastrointestinal rhythms, growth and repair
of cells; including the growth of tumour cells, etc (See
Diagram 1)
Diagram
1
Interestingly,
the healthy prion protein is intensively expressed/localised in
those neural/extra neural tissues which are directly under circadian
mediated electromagnetic influence – the retina, pineal, hypothalamus,
visual cortex, pituitary, medulla, glial cells, sympathetic neurones,
spleen, lymphatic, tonsils, appendix, gastrointestinal membranes, nerve
growth factor mediated cells involved in growth and repair, etc
(1)(16)(22)(23)(24) (25).
In
this respect, the proposal of an electro-conduction function of
the copper prion protein may turn out to offer further scientific
insight into mechanisms involved in the electromagnetic meridians/nodes
recognised by Chinese medicine; where the healthy Cu PrP performs some
regulatory role in maintaining electro homeostatis at the nodal points
and along the meridians, whilst abnormal Mn PrP serves to absorb,
thereby blocking that conduction.
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