Alzheimer’s Disease: Deadly Infectious Cause Known And Hidden – Prions

Alzheimer’s Disease: Deadly Infectious Cause Known and Hidden – Prions (Ed Ward, MD’s Blog, June 21, 2013):

Alzheimer’s Disease: Deadly Infectious Cause Known and Hidden – Prions

Government’s, Corporation’s and Search Engines Deadly Secret: “Alzheimer’s Disease is a Prion Disease.” Original brief article

Alzheimer’s Disease Is a Prion Disease. A TSE, Transmissable (Transmittable) Spongiform Encephalopathy: Variants, Sub Variants of TSE Prions – Mad Cow Disease – BSE, Bovine Spongiform Encephalopathy, CJD, Creutzfeldt-Jakobs Disease, Kuru, Sheep and Goat Scrapie, Cat – FSE, Elk and Deer – CWD, Chronic Wasting Disease.  There are also ‘inherited’ genes that may cause a small portion of CJD, GSS and FFI.  But, as will be discussed briefly later in the article, may or may not be correct.

One side is your brain. The other side is your brain on prions.

“Alzheimer’s disease is the sixth leading cause of death in the United States and is the fifth leading cause among people aged 65 years and over. People aged 85 years and over have a 5.4 times greater risk of dying from Alzheimer’s disease than people aged 75–84 years.

The age-adjusted death rate from Alzheimer’s disease increased by 39 percent from 2000 through 2010 in the United States.” There is a 400% increase expected by 2050.

The primary transmission of prion diseases is ingestion of prions from the Central Nervous System (Brain, Eyes, Spine and Spinal Fluid) of animals. These unwanted ‘left overs’ were used in animal ‘feed’ for ‘protein’ and ‘mystery meats’ (hotdogs, etc) as ‘filler’. These resilient, nearly indestructible by nature, or cooking, individual factories of plague were spread throughout the populations (animal and human) and around the planet awaiting their ‘activation’ by hydration.

Non-infectious form of prion protein could cause brain degeneration. (Note: This is the outdated 2009 original quote. We know it Does cause brain degeneration.  Non-infectious since we don’t eat their brains, there is absolutely no reason these prions are any different than any other prions. If eaten they will go to work) … with the amyloid-â peptides that are hallmarks of Alzheimer’s disease.

SCIENTISTS CONFIRM THAT ALZHEIMER’S IS A PRION DISEASE …. 25th Feb 2009 ALZHEIMER’S – PRION CAUSES AMYLOID PLAQUE BUILD UP (An excellent, informative article to come back to if one is a ‘novice’ to prions.) To download an English .doc and PP reader from microsoft

Prions? WHAT? Prions are about the smallest and simplest a pathogen can get.  A virus is like a major corporation, with genomes, multiple RNAs (prion doesn’t even have RNA, at least officially. But, it performs 2 major RNA functions – replication and survival even better than RNA does), and a lot more.  Prions could only dream of that.  There are a couple of things about this simple, single protein, an instant assembly line of itself, that make it so devastating.

Prion: Here’s what Nobel Prize winner on the subject of Prions had to say on ‘Prions’ A little dated and technical, but worth the trip. He believes prions are big link to many neurodegenrative diseases, and rightly so, IMO based on the referenced facts. . A prion is to all species as smallpox was to Native Americans. The only difference is onset of death.

It turns out that prions are molecules of a normal body protein that have changed their three-dimensional configuration.


The normal protein is called PrPC (for cellular) is a transmembrane glycoprotein normally found at the surface of certain cells (e.g., neural and hematopoietic stem cells); has its secondary structure dominated by alpha helices (probably 3 of them); is easily soluble; is easily digested by proteases; is encoded by a gene designated (in humans) PRNP located on our chromosome 20.


The abnormal, disease-producing protein is called PrPSc (for scrapie); has the same amino acid sequence as the normal protein; that is, their primary structures are identical but; its secondary structure is dominated by beta conformation; is insoluble in all but the strongest solvents; is highly resistant to digestion by proteases; When PrPSc comes in contact with PrPC, it converts the PrPC into more of itself (even in the test tube). These molecules bind to each other forming aggregates.

Association analyses confirm the dominance of PRNP as a risk factor relative to all other genes. Prion strains are known to determine key clinical features such as age of onset and …showed weak evidence of a modifying effect on age of onset of sCJD (as a quantitative trait) with the risk allele being associated with an earlier age of onset  Concerning common genetic variation, it is likely that the PRNP locus contains the only strong risk factors that act universally across human prion diseases.

Kiss of the Prion: Pucker Up for Parkinson’s, Alzheimer’s and more? Because: The last mode of transmission is of particular interest because it indicates that the consumption of meat and other products derived from animals experiencing prion disorders may pose a real risk to humans. Recent reports suggest that, in addition to meat, bodily fluids such as blood, saliva, feces, and milk may well be risk factors for possible transmission of TSEs to humans. Successful oral transmission among different animal species (interspecies) has been demonstrated. Association analyses confirm the dominance of PRNP as a risk factor relative to all other genes.

As can be clearly seen, once a prion gets inside the body, its small, simple size allows it access to the entire body including the meat itself. Not noted in the quote are the concentrations (quantity X volume) vary between the different organs.

The CNS, Central Nervous System – Brain, Spine, Motor and Sensory Nerves and all their Fluids contain the highest concentrations of the protein. Although recent studies have shown that the intestine is also a ‘reservoir’ of prions and would account for the high concentration of prions in feces. The ‘meat’ concentrations should have the least amount of contamination, minus any nerves in the meat as those are high concentrations of prions.

Killing it by cooking? Not going to happen unless you get above: New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication.

” When it comes to infectious agents, it doesn’t get much worse than prions. These misfolded proteins are highly resistant to a wide variety of extreme disinfectant procedures. They have been identified as the culprits behind mad cow disease and chronic wasting disease in animals and humans, and are also implicated in Creutzfeldt-Jakob disease and other prion-related disorders.

But an interdisciplinary University of Alberta research team has come a step closer to finding a way of inactivating these highly infectious proteins. Ozone. How many corporate butchers are using ozone as a disinfectant?  Zero that I know.  How many are even concerned about cross contamination of meat with major concentrations of prions in the spine?  Once any portion of the spine or its major nerves releases all CNS fluids into and on the meat.

A known genetic factor for susceptibility to prion disease is the common single nucleotide polymorphism (SNP) at codon 129 in PRNP, the gene that encodes PrP in human beings.

“Many of the neurodegenerative diseases share fundamental mechanisms involving protein misfolding and prio-like spreading of pathology associated with abnormally aggregated proteins in brain tissue.”

All prions eventually make beta amyloid.  Beta Amyloid is specifically Alpha-Synuclein (AS). Beta Amyloid Plaques are also called a Lewy Body.  Lewy body diseases are characterized by the presence of Lewy bodies, alpha-synuclein(AS)-positive inclusions in the brain. Lewy body diseases (LBD) share alpha-synuclein (AS) aggregation and Lewy body (LB) formation as their key pathogenic events. A list of the different Synuclein Proteins, Cross Species Adaption of alpha synuclein. The third protein discovered to be homologous to alpha synuclein is gamma synuclein (also termed persyn or breast specific cancer gene-1; BSCG-1)

Hello.  With the introduction of cancer into the spectrum of prions another group of disease is seen. This is a significant variance from the semi-limited view of just CNS disease, to a cellular cancer link for prions. If there are two pathologic processes for prions in that vast a spectrum, there should be more. How many more paths of disease can prions activate?

Prions certainly appear to be a causative agent in at least two widely varied pathologic methodology.  As stated prior, Prions are very similar to RNA in the way they work.  Essentially the ‘workhorse’ of RNA strands? Are Prions one or the basic building blocks of many ‘unknown’ cause diseases?  Prions and Synuclein Proteins certainly seem a promising route of investigation for many diseases.

Partial List of Human Diseases with Lewy Bodies: Frontotemporal Dementias, Pick Disease, Corticobasal Degeneration (CBD), Multiple System Atrophy (MSA), has features that overlap striatonigral degeneration, olivopontocerebellar atrophy, and Shy-Drager syndrome; Progressive Supranuclear Palsy (PSP), Multi-infarct Dementia (MID), Huntingon’s Disease, Parkinson’s Disease, Amyotropic Lateral Sclerosis (ALS), Creutzfeldt-Jakob Disease (CJD). Kuru, Spinocerebellar Degeneration, and Gaucher’s Disease are a few more. All these diseases leave their footprint in beta amyloid production – Synucleids.

Prions are the only thing we know that leave these amyloid plaque Lewy body remnants.  Whether the origin be internal genome mutation or outside invasion, if given enough time and the right circumstances, they will leave their ‘evidence’ behind.    In the chart below, where they know of no particular pathogen, they somehow decided to show the path of alpha synucleid, which as far as we know are only caused by prions:

“There is a growing list of mutations linked to Parkinson’s disease. They account for 2–3% of the late-onset cases and ~50% of early-onset forms. Typical, late-onset Parkinson’s disease with Lewy body pathology is linked to mutations in three genes: SNCA (encoding α-synuclein), LRRK2 (encoding leucine-rich repeat kinase 2) and EIF4G1 (elongation initiation factor 4G1; M.F., unpublished data). Missense mutations in SNCA were first linked to familial parkinsonism with late onset, and subsequent SNCA duplications were found in kindreds in which age of onset, progression and associated comorbidities relate to gene dosage.”

“Mutations in and overexpression of α-synuclein seem to be especially toxic to dopaminergic neurons, as dopamine-synuclein adducts may inhibit chaperone-mediated autophagy. Even with the limited mechanistic insight currently available, reduction of α-synuclein expression may represent a potential therapeutic approach.”

“Recently, heterozygous mutations in GBA (encoding glucocerebroside and famously linked to Gaucher disease) have been associated with a typical phenotype of Parkinson’s disease and Lewy body pathology. It is now clear that this heterozygous loss-of-function mutation also leads to a >5-fold–increased risk of Parkinson’s disease in all populations as well as to earlier disease onset (typically in the early 50s).”

And now a little about familial inherited and genomes.  Chromosomal DNA genomes definitely play a place in the ‘expression’ of the prion diseases. Their role ranges from abnormal production of the normal protein to the making of an abnormal protein – ‘prion’, all the way to how long an invasive or auto-produced ‘prion’ incubates before killing its host. So are familial inherited caused by the genome, or merely more quickly ‘expressed’ by less resistance by the genome.

This protein goes everywhere.  Saliva, breast milk, feces, etc, a blood brain barrier, placental barrier, cellular barrier (membrane) are like 4 lane private interstates to prions. Once a prion enters a familial blood line how does one remove it. The diseased prion reproduces even if you don’t, and is surely carried by any prodigy. It’s a chicken and egg thing, IMO.

Radioactive fish is looking better and better… I’m done with any ‘mystery meat’.  And I definitely will not be having any Brains and Eggs, thank you very much.  But, for meat eaters ‘corporate butchery’ needs major health changes regarding the handling of ‘meat’ and handling of CNS ‘left over protein’.

History of Prions: Worth the trip. Prions aren’t new. They’ve been around since the 1700′s.

*Try Startpage (Google results) search for the title of my June 2012 article: “Alzheimer’s Disease is a Prion Disease.”  Note how search engines are hiding information from the public. Deadly corporate government agents that need trials for crimes against humanity, IMO. I’m sure I have written and posted about prions, CWD, CJD, kuru, and Parkinson’s long before this hidden 2012.  I can’t seem to find them on the net, not surprised, but they are not where I usually post significant information.  So, the only thing I can figure is that it was in one or two of my ‘Daily DrEd’ information postings. Similar to this one day example in 2006 during its 3 month history. Th  Then try a search for – Alzheimer’s disease causes – to see the government’s and ‘Corporate Medicine’s list of useless, scam, deadly BS while avoiding prions.

And last, search for – Alzheimer’s Disease Prions.  Viola!

A small aside from the disease itself.  Note how censorship and disinformation works.  Once you know what you are looking for, it’s easy to find.  But, if you don’t know the answer and are looking for it, it’s almost impossible to find.

Photos: ;

Ed Ward, MD – ; ;

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Dr. Ed Ward MD, AS, BS, MD – Reporting and investigating Constitutional abuses of the US government for almost 2 decades. AS, BS in Medical Technology – Minor in Organic Chemistry and Physics, volunteer during the Viet Nam war 6 years stateside active duty ‘med tech’ ‘US Air Farce’ – a decade experience in Medical Technology. MD degree from LSU, New Orleans – 2 decades in the field of General Practice. (My) Articles are also referenced by valid experts in their field. Dr Ed

1 thought on “Alzheimer’s Disease: Deadly Infectious Cause Known And Hidden – Prions

  1. Extremely useful information. My husband of 40 yrs died of Lewy body dementia in March 2015. Age 68. He was symptomatic for a decade. His father died with a strange dementia, never correctly diagnosed, and his brother is in nursing home with dementia, sister w dementia. Very difficult to get a DX. Seen by multiple highly trained physicians. Frustrating. 2 brain MRI missed DX. Required a PET Scan to see proteins. Stumbled upon Lewy body site, completed symptom checklist. Gave to his psychiatrist who had to press long and hard for PET. Died 8 weeks later. No one can do anything about this prion problem if it is not acknowledged. No known treatment without killing host it sounds like. Hopeless. We have 4 children. You are saying there is both a genetic component and transmission spread. Hopeless?

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