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Prions & Autism: a pathogenic link?

Using bio-resonance screening to uncover patterns in clients who present with similar symptom sets

One of the most useful aspects of bio-resonance screening is its ability to cast a wide net when testing for patient-specific trigger points or patterns.

I have found this function to be invaluable and fascinating in the years that I have specialised my practice in working with children on the spectrum. On the one hand there is the scope for precise individuation:

  • What is specifically affecting this child?

  • Where do we need to consider treatment focus?

  • What kind of toxic load may be presenting a blockage to cure?

  • What adjunct treatment do they require to support drainage pathways or safe elimination?

On the other hand, it allows for the emergence of patterns and similarities in sometimes little researched or acknowledged areas that may be highly specific to the condition. This is particularly exciting in a field such as the treatment and support of neurodevelopmental challenges, because whilst there have been huge strides made in terms of understanding and research, there is still so much to uncover in terms of contributing factors and how this opens up new and innovative avenues for successful treatment strategies.

Prions and Autism - is there a link?

One area that consistently resurfaces in my work with children on the spectrum is the subject of prions.

What are prions?

Prions are a stand-alone infectious agent, they don't fit into the pathogenic model of all other known infections such as parasites, bacteria, fungi or viruses in that they do not have any individual DNA or RNA. The word itself is a derivative of the phrase 'proteinaceous infectious particle' - but they cause dysfunction by inducing other proteins to follow their mis-shape.

They are a 'misfolded' protein that is transmissable to other life forms (such as via the consumption of meat in CJD - Creutz-feld Jakob Disease) and with their ability to cause the misfolding in other proteins, trigger cell death in the affected cellular regions of the host. All known prion diseases affect the structure of the brain and other neural tissue. When similarly disordered protein chains bind together, they form a unit which will build up to a structure called amyloids which cause tissue damage and are associated with diseases such as Parkinson's and Alzheimers. Several yeast proteins have been found to have prion like qualities.

Prions and Autism - a genetic pathway link

A research study published in 2020 ( found a link between genetic pathways found to be active in Prion disease and those found to be 'enriched' in the brain tissue of a test sample of candidates with Autism. There is a very well established and on-going exploration into the role of infections in the pathogenesis of autism, and whilst it is highly debated, it is a compelling area of investigation and in the sphere of homeopathic and complementary medicine, there is no doubt that the use of remedies that interact with and support as systemic response to specific infections has brought about substantial gains and improvements in huge numbers of patients on the spectrum.

It should be stressed that the conclusions of this research paper did not identify autism as a prion-related disease. However they did indicate that there was significant enrichment of the 'prion disease' pathways in the brain tissue examined. This may be due a similarity between inflammatory stimulus and consequent modulation of inflammatory pathways in both conditions, such as activation of the microglial pathways.

CONCULSIONS - how does this open up novel treatment avenues for children and adults on the spectrum?

Essentially, the conclusions of this study indicated that there may be a similar genetic terrain that is dysfunctional or 'activated' between prion disease and ASD, rather than pointing to an infectious causation between the two conditions.

Given the focus on immune dysfunction and pathogens as a treatment direction for symptoms for children on the spectrum, this is a very key insight. The authors take their conclusions a step further to postulate that infections may not be responsible for ASD development, but because genes involved with infectious processes can interact with other key genes in autism, they may be CO-FACTORS and possibly worsen clinical presentations.

This makes a lot of sense and is also coherent with the curative impact we see from using remedies that target infection based responses in homeopathic and naturopathic treatment approaches. Homeopathic treatment focuses on how things 'present' themselves in the individual and then chooses the remedy closest to the individual symptom picture to stimulate an appropriate healing response.

This means that a remedy that interacts with the same processes that get derailed in an infectious process may have curative effects on a condition where the same processes are being derailed and effected, even if the underlying trigger force comes from a different source.

Further thoughts

For the authors of this study, their conclusions and discussion on the usefulness of these results centre on what they represent as a step forwards in characterising the molecular pathways that underlie ASD, and that this marks another point of understanding the individual landscape of in each person as well as opening up novel treatment avenues.

When screening data points us strongly towards the relevance of key infections or processes in the body that strongly resemble what this infection might cause, we unearth an array of potentially novel treatment approaches that may give us yet another strategy for supporting out patients. Nosodes (remedies that target and seek to address the impact of infections on the body) are an essential tool in the pharmacopeia of treating autism, and this important piece of research may open up a new valuable set of tools to help our children.

Key gene pathways interacting with ASD brain belonging to the 'prion diseases' pathway

  • tyrosine kinase Fyn - described as being expressed (in mice) in the hippocampus, amygdala and cerebellum (all key areas in ASD) 'Mutations of Fyn in mice lead to alterations in the architecture of the hippocampus with consequent impairment in learning and in the amygdala's long-term plasticity. Fyn regulates the focal adhesion kinase which is required for normal neuronal development'...Fyn strongly correlated with ATXN1, a DNA-binding protein that forms a transcriptional repressor complex with a capicua. Deletions in the chromosome that harbours ATXN1 are associated with developmental delay and ASD, and 'alteration of the ATXN1-CIC complex determines a spectrum of neurobehavioral phenotypes, including intellectual disability, ADD/ADHD and ASD.

  • Mesencephalic Astrocyte Derived Neurotrophic Factor (MANF)

  • Mitogen-Activated Protein Kinase 1 (MAPK1)

  • Heat shock protein 90 Beta Family Member 1 (HSP90B1)

  • RAB1A (Member RAS oncogene family)

  • Phosphoglycerate Kinase 1 (PGK1)

  • tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide (YWHAZ)

  • ADP-ribosylation factor 4 (ARF4)

  • Homocysteine-inducible, endoplasmic reticulum stress-inducible, ubiquitin-like domain member 1 (HERPUD1)

  • V-akt murine thymoma viral oncogene homolog 3 (AKT3)

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