Seven Provocative Findings -p7

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Fifth Provocative Discovery: 

 

Alan then decided to take another look at his Alzheimer’s brain samples. Had he missed nematode worms in the brain?

 

When Alan looked at both Alzheimer’s brains and Lewy-Body brains he did indeed find nematodes, and inside the nematodes were Borrelia bacteria!.

borrelia-in-worm-alzheimers

 

 

This changes everything, we ever thought about dementia!  Since this is the single most provocative discovery in all of Alan’s work, he decided to confirm his findings. He used a red “pan Cytokeratin” stain to recheck the samples.

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Cytokeratin should never be in the human brain. If it is in the brain it came from somewhere else. In this case Alan found clearly defined spirochetes and something that chilled me to the bone: worm eggs!  Hundreds and hundreds of nematode eggs. This explains why dementia is progressive. It explains why dementia accelerates with time.

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Since nematodes have both a mouth and an anus it dictates that if the nematodes are eating that they are also pooping. Alan found nematodes in all life cycles including eggs, and found their excrement throughout the brains of Alzheimer’s patients.

 

Once again everything we knew about the treatment of dementia had changed. These patients need both an antiparasitic drug, and antibiotics. And yes the nematodes contain Borrelia bacteria; so killing them probably releases more Borrelia into the brain.

 

In the case of Lewy Body dementia, no one had ever found an adequate hypothesis to explain what caused the formation of Lewy-Bodies, and no one knew why Lewy-Bodies that were outside neurons were bigger and contained “granules and spaces” surrounding the alpha-synuclein spherical bodies.

 

The fact that Borrelia bacteria can penetrate neurons and the fact that neurons produce the alpha-synuclein that forms the Lewy-Bodies once again seemed like a coincidence that had to be explored.

 

It turns out that there may be several possible explanations in the formation of toxic alpha synuclein which have not been considered up till now.  (See Alan MacDonald’s paper on Nematodes and Lewy-Bodies at the F1000 website)

 

One possibility is that Borrelia or more likely Nematode worms causes the brain-neuron to produce the Lewy-Body inside the nerve cell by inducing alpha-synuclein production in the nucleus.  Then with time the Borrelia and Nematode secretions and alpha-synuclein kill the neuron. The neuron wraps itself around the alpha-synuclein sphere and becomes an extracellular Lewy-Body (outside of the nerve cell).

 

The nematodes too could theoretically be responsible for the Lewy Body formation. The worms produce a type of protein called LEA. When Alan stained the worms using an antibody-based stain to detect human alpha-synuclein. they lit up.  But no nematodes have ever been known to produce alpha-synuclein. It may well be that the LEA proteins which are similar in shape to the alpha-synuclein, were cross-reacting. And this might mean that nematode worm proteins are mimicking human alpha synuclein in the brains of people with dementia.

 

The neurons would be duped into taking up the foreign protein. It would then destroy them, with the dead neurons coiling up into Lewy Bodies.

 

Staining these extracellular Lewy-Bodies for neuron proteins reveals the truth. Extracellular Lewy-Bodies were once healthy neurons. What killed the neurons? Was it Nematodes? Was it Borrelia?  Much is to be learned but both nematodes and Borrelia seem to be playing a major role in Lewy-Body Dementia.

 

What does this mean to Alzheimer’s and other dementia patients? 

 

 It means antibiotics isn’t enough. Many doctors have tried antibiotics in Alzheimer’s disease with limited success and mostly disappointment. Treatment should begin with a systemic antiparasite medication for nematodes and treatment must be prolonged to kill all life stages of the parasites. Since the nematodes carry live Borrelia in their gut, therapy must include several rounds of antibiotics. Since the tests for parasites and Borrelia are poor for a central nervous system infection, diagnosis and therapy are made on the basis of clinical symptoms and response to treatment.

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