The Extinction of Homo Sapiens and Symbiotic Neanderthalisation: Relation to Archaeal Mediated RNA Viroidsand Amyloidosis

Ravikumar A. Kurup, Parameswara Achutha Kurup


Introduction: Prion proteins have been implicated in systemic disorders like neurodegenerations, cancer and metabolic syndrome. The beta amyloid in Alzheimer’s disease, alpha synuclein in parkinson’s disease, the TAR protein in frontotemporal dementia and copper zinc dismutase in motor neuron disease behaves like prion proteins. Prion proteins like behavior is also seen in the tumour suppressor P53 protein in cancer and the islet cell associated amyloid in diabetes mellitus. Prion diseases are conformational diseases. The abnormal prion protein seeded into the system converts the normal proteins with prion like domains to abnormal configuration. This abnormal protein resists digestion by lysosomal enzymes after its half-life is over and results in deposition of amyloid plaques. This produces organ dysfunction. Prion phenomena were initially described for Creutzfeldt Jakob’s disease, but now it is found to be wide spread in chronic disease pathogenesis. Ribonucleoproteins are well known to behave like prion proteins and form amyloid. We have demonstrated actinidic archaea which secretes RNA viroids in metabolic syndrome, neurodegenerations, cancer, autoimmune disease, schizophrenia, autism and CJD. The RNA viroids can bind with normal proteins with prion like domains eg., superoxide dismutase and produce a ribonucleoprotein resulting in prion phenomena and amyloidogenesis.
Materials and Methods: The following groups were included in the study:- alzheimer’s disease, multiple sclerosis, non-hodgkin’s lymphoma, metabolic syndrome x with cerebrovascular thrombosis and coronary artery disease, schizophrenia, autism, seizure disorder, creutzfeldt jakob disease and acquired immunodeficiency syndrome. There were 10 patients in each group and each patient had an age and sex matched healthy control selected randomly from the general population. The blood samples were drawn in the fasting state before treatment was initiated. Plasma from fasting heparinised blood was used and the experimental protocol was as follows (I) Plasma+phosphate buffered saline, (II) same as I+cholesterol substrate, (III) same as II+cerium 0.1 mg/ml, (IV) same as II+ciprofloxacine and doxycycline each in a concentration of 1 mg/ml. Cholesterol substrate was prepared as described by Richmond. Aliquots were withdrawn at zero time immediately after mixing and after incubation at 37oC for 1 hour. The following estimations were carried out:- Cytochrome F420, free RNA, Cytochrome F420 was estimated flourimetrically (excitation wavelength 420 nm and emission wavelength 520 nm).
Results: Plasma of control subjects showed increased levels of the above mentioned parameters with after incubation for 1 hour and addition of cholesterol substrate resulted in still further significant increase in these parameters. The plasma of patients showed similar results but the extent of increase was more. The addition of antibiotics to the control plasma caused a decrease in all the parameters while addition of cerium increased their levels. The addition of antibiotics to the patient’s plasma caused a decrease in all the parameters while addition of cerium increased their levels but the extent of change was more in patient’s sera as compared to controls.
Discussion: The actinidic archaeal growth results in increased digoxin synthesis and phenotypic conversion of homo sapiens to homo Neanderthals as reported earlier. The increased actinidic archaeal growth is due to global warming and these results in neanderthalisation.Homo neanderthalis tend to have more of civilisational diseases like metabolic syndrome, neurodegenerations, cancer, autoimmune disease, schizophrenia, autism and CJD. Actinidic archaeal secreted RNA viroids may play a crucial role in amyloid formation and pathogenesis of these disorders. The evolution and origin of homo sapiens and homo neanderthalis is on the basis of actinidic archaeal symbiosis and digoxin synthesis. Extreme climate change related increased actinidic archaeal symbiosis and digoxin synthesis results in homo neanderthalis. The homo sapien species results from inhibition of actinidic archaeal symbiosis and endogenous digoxin synthesis by normal global climate. Thus there are evolutionary swings between the two human species depending on extremes of climate and archaeal symbiosis. Endogenous digoxin can be considered as a Neanderthal hormone. The results show that there was increase in cytochrome F420 in CJD and other disease groups indicating increased archaeal growth. There was also an increase in free RNA indicating self-replicating RNA viroids in CJD and other disease groups. The RNA viroid generation was catalysed by actinides. The RNA viroids can bind with proteins having prion like domains forming ribonucleoproteins. These ribonucleoproteins can give an abnormal conformation to the protein resulting in generation of abnormal prions. The abnormal prions can act as a template to convert normal proteins with normal configuration to abnormal conformation. This can result in amyloidogenesis. The abnormal configured proteins will resist lysosomal digestion and accumulate as amyloid producing disease states and extinction.


Actinidic archaea, Prions, Amyloid, Systemic disease, Infectivity

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