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Lewy Body Dementia: Putting the Puzzle Pieces Together When The Lewy Body Dementia: Putting the Puzzle Pieces Together When the world first heard that Robin Williams committed suicide, most people were shocked. After the release of his final medical autopsy report that showed he had advanced Lewy Body Dementia: his suicide became more understandable. His mind was very sick, and his prognosis was not good. When we look at all the facts and observations about Lewy Bodies, we are presented with a puzzle that just doesn’t make sense. How do Lewy Bodies form? Why are some Lewy bodies located inside brain-neurons? While other Lewy Bodies float in the extracellular spaces between brain cells? Why are they observably different? Why do Lewy Bodies predominate in Parkinson’s regions of the brain like the Substantia Nigra, but can also be seen in the hippocampus, the temporal lobes, the basal forebrain and the neo-cortex? Lewy Bodies contain two common brain proteins Ubiquitin and Alpha Synuclein, but modifying proteins inside the neuron and chaperone proteins alter these two completely normal brain proteins, and the two proteins recombine in a way that is toxic to neurons. Alpha-Synuclein forms structured fibrils. The protein went from an amorphous flexible unstructured state to an organized rigid structure that forms fibrils. Traditional Lewy Body research points out the observed facts, but no Lewy Body researcher has ever answered the question: Why do Lewy Bodies form? Until the last six months no one had any new theories, but I am going to suggest something radical based on new observations and data from the work done at the Dr. Paul H. Duray Pathology research facility. (Dr. Alan MacDonald’s research) While doing our research on Alzheimer’s Brains, we made an association between Borrelia biofilms and the formation of amyloid plaques. When we stained for beta-amyloid and we found easily observable plaques, but then when we also stained the same exact slide for Borrelia, we found a Borrelia biofilm embedded and “married” to the plaque. Could Borrelia have been the initiator of amyloid formation? Judith Miklossy’s work on Rat brain neurons in culture absolutely suggest that this is an observable event. A brain cell culture enriched with microglia cells immediately produced amyloid precursor protein (APP) when Borrelia from a Dementia Patient’s brain was added to the culture. In short time this APP cleaved and became beta-sheet Amyloid as seen in Alzheimer’s patients. This is a hugely important observation that has been ignored by the medical community for the past 15 years. Lewy Bodies themselves have some similarities to amyloid plaques and when we stained these spherical Lewy Bodies for Borrelia burgdorferi, they indeed lit up just like the Amyloid Plaques in Alzheimers. Our work and observations on Lewy Body Dementia brain tissue indicates that the actual Lewy Bodies are also associated with Borrelia biofilms just like Amyloid plaques are in Alzheimers. So how are Lewy Bodies formed? Lewy Body Dementia Researchers are very good at pointing out what they observe, but very shy about explaining Why? Or How? Lewy Bodies form. Our preliminary hypothesis suggests that Alpha-Synuclein deposition inside the neurons may be a consequence of the presence of Borrelia inside the same neuron. Alpha-synuclein production and transformation, maybe a protective reaction to intraneuronal Borrelia. Unfortunately it appears to be a toxic reaction that can cause the neuron to die. As the two brain-proteins come together; alpha-synuclein changes its structure. The resulting Lewy Body grows in size and cellular changes occur with protein production and transport. Ubiquitin and alpha-synuclein deposition increases inside the neuron, and normal metabolism and protein transport are disrupted. Our observations indicate that Borrelia bacteria (biofilms) are tightly “married” to the alpha-synuclein-ubiquitin deposits, and remains tightly bound even when the neuron dies. As the neuron curls up and floats among the other living brain cells, it is now recognized as an extracellular Lewy Body. We know that intracellular Lewy Bodies inside neurons have a thin membrane and almost no spaces in its periphery. But an extracellular Lewy-Body has a variable membrane-like boundary with spaces and debris beneath the membrane. We do not see this in intraneuronal Lewy-Bodies that appear to not have a complex membrane structure. If we stain, these Extracellular Lewy Bodies for Borrelia species, they light up with excitations or Beacon- Signals for Borrelia. This indicates that the Lewy-Body contains Borrelia bacteria wrapped up inside the extracellular Lewy Body. (see attached photos and look for these observable differences) =========================================== This hypothesis helps make sense of certain observations that I have listed below. ===================================== What promotes the pathogenic transformation of Alpha-Synuclein protein? Possible Answer: The presence of Borrelia bacteria intracellular inside the infected neurons. The bacteria causes the neuron to fight back. The protein alterations may be a neuron defense mechanism that turns out to be a cellular toxic reaction that eventually kills the neuron. Why are their intracellular and extracellular Lewy bodies that have slightly different peripheral spaces including a membrane-like structure in extracellular Lewy-Bodies that is not seen in the intraneuronal Lewy Bodies? Possible Answer: The extracellular Lewy Bodies are actually rolled up dead neurons that still contain the neuron’s cytoplasmic components and a membrane. Why are certain regions of the brain more affected than others? Possible Answer: The neurons themselves in the substantia nigra region, may be more susceptible to Borrelia penetration and intracellular location, and the neurons in these areas might depend more on unbiquitin and alpha-synuclein proteins for metabolic functions especially for functions involving the mitochondria. So the more frequent inclusion of Borrelia bacteria inside these regional neurons would mean more Lewy Body formation in those specific regions of the brain that are more susceptible to Borrelia penetration. To prove this hypothesis would require some special in-vitro work with human brain neurons. But from what we have observed already in human Lewy Body Dementia cases, our observations supports this hypothesis. Tom Grier Notable people who suffered from Lewy body dementia include: • Actor Robin Williams • Actress Estelle Getty • Music industry icon Casey Kasem • Athlete: Artist Don Featherstone, creator of the lawn flamingo. .
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