Blowing the Whistle at the FDA, Jan 2001, exposing Dearborn and how OspA causes immunosuppression rather than, "was a vaccine."

01 Oct 2017


File List, RICO

1988 Steere says Lyme is like a B cell leukemia

Assoc Blogs-n-Webs:




Fungal Exosomes Inhibit Apoptosis

IDSA: "Vaccines serve the mfgs, not their victims"


BlumenthalAntiTrust Lawsuit

Exosomes, Blebs


CDC Admits Fraud, 2016
Dattwyler, 1988
Golightly, 1988
Dressler, 1994
BarbourFish, 1993
Dearborn, 1994

Pathogenic Fungi

Bush's warcrimes, Oct 2000






How it was always known spirochetes cause dementia, which is malpractically called Crazy by the crooks and the SSA (the whole govt).


Why would they do that?


I think to assure we do not acquire guns, LOL.

DISCLAIMER: I hate guns; but you should know: when talking to a hunter re bears and always carrying a bear gun, ie., as they do in the Alaska TV shows, he said use pepper spray - it's better at repelling bears. So that may be something to consider to have on you in case of psycho cops


White people are known to be more susceptible to dementia from borrelia or syphilis - and this was the reason for the Tuskegee and Guatemala syphilis crimes)

Toll-like Receptor Polymorphisms Are Associated with Increased Neurosyphilis Risk

"Clinicians in the early 20th century posited that race influenced susceptibility to neurosyphilis, citing a decreased risk in African Americans compared to Caucasians (7). Subsequent work suggested a genetic basis for such differences, with an increased risk of syphilitic dementia, but not other forms of neurosyphilis, in patients with certain HLA types (8) that differed in African Americans compared to Caucasians (9). While more recent reports suggest that there may be genetic contributions to syphilis susceptibility (10-13), to the best of our knowledge there have been no recent investigations of genetic susceptibility to neurosyphilis."

I wonder if they found white people were more susceptible to the immunosuppression from exposure to the likes of OspA and OspA-covered blebs or exosomes, and having EBV reactivated (the Cold Spring Harbour DNA bioweapons lab), resulting in the New Great Imitator, chronic, neurologic Lyme outcomes... ??



There are dozens of reports here in these 2 pages which I did not think were necessary to make into charge sheets since I always thought it was "well-known" that spirochetes were permanent brain infections.  The first one is the older historical data, and the second is where the crooks report that Lyme is an incurable brain infection.  One report is by a group of dentists who showed oral treponemes were fairly heavily associated with Alzheimer's (#22):  (<<  Alzheimer's and oral treponemes, #22 here)



MECHANISMS and Signs of "SPIROCHETAL DEMENTIA," which I guess is the real term for it. Make your own file for this data on your harddrive. Please. The reason YOU need this is bc the crooks and SSD wants to say you are crazy rather than have Organic brain disease, which is malpractice.


"The fact that very few chemokines and related genes changed in response to stimulation with B. burgdorferi was unexpected. However, these data make sense in the context of a spirochetal pathogen. These organisms have a reputation for ‘stealth’ and persistence even in immunocompetent hosts. While possessing a number of pathogen associated molecular patterns and inflammatory stimulants like lipoproteins, B. burgdorferi lacks LPS (lipopolysaccharide) in its outer membranes. Therefore B. burgdorferi’s effects on glia and other supporting cells such as HBMEC, may be more subtle than that observed in acute, severe infections of the CNS.


"Together these data and that presented herein show that B. burgdorferi can stimulate up-regulation of chemokines from brain microvascular endothelia and astrocytes, which potentiate entry of neurotoxic neutrophils into the brain. Such an event can lead to neuronal loss and may contribute to the cognitive impairments and other neurological deficits associated with neuroborreliosis. This is the first study to investigate comprehensively the chemokine-centered responses of primary human astrocytes and HBMEC to B. burgdorferi. Understanding the contributions of individual glia cell types to the damage induced by B. burgdorferi will ultimately allow for the development of targeted, cell type-specific interventions and therapies."



Shrunken Energy-producing cells (microglia) in the well-known-to-be-incurable Syphilis, and guess what ma, no biofilms ;)



I think it was Charles Ray Jones who said people lose between 30-60 IQ points with Lyme dementia. Hence, the difficulty we have fighting the crooks. This is in addition to the Chronic Fatigue and other signs. *Now* we know the Tuskegee and Guatemala syphilis crimes were exactly about white people getting dementia whereas that occurs less frequently in African American (don't know about native Americans, who are Guatemalans). Now they want to say we're crazy - whole new campaign launched by LIfespan and Johns Hopkins - to set up "Coping Clinics" because of the FEAR of Lyme disease.
Why would they go that route? We know stress actives EBV but so does OspA (lipoproteins) via activating cortisol (yes, no need for stress, OspA itself activates the cortisol, as well as causes the immunosuppression that results in the activation of EBV). The last few reports I sent up here on Syphilis and other Treponemes (they were all called Treponemes at one time even Borrelia) *confirms* that spirochetes are un-eradicable especially in the brain and that this is "well-known."

We do not have a lot of data on how the other infections set off by Lyme and LYMErix cause dementia, since we have not looked for it much. But because this is the way the crooks are going, with the "crazy" approach, we should look there too.
I conclude that this move by the crooks to call us crazy **again** has to do with OspA causing the same disease/dementia. It is a way of saying Dearborn was real, once again. It is a way of maintaining the PRETENSE that Dearborn was not research fraud and not even a consensus.


BIOMARKERS of CNS disease by the crooks:






Interaction of the Lyme Disease Spirochete Borrelia burgdorferi with Brain Parenchyma Elicits Inflammatory Mediators from Glial Cells as Well as Glial and Neuronal Apoptosis
Neuroborreliosis may manifest early, within the first few weeks to months of the appearance of erythema migrans, as a meningitis, often as part of the Garin-Bujadoux-Bannwarth syndrome, or, more seriously, as encephalomyelitis. The latter is less common than the meningitis but shares with it the presence of lymphocytic pleocytosis in the cerebrospinal fluid (CSF) and intrathecal anti-B. burgdorferi antibody production. This disorder’s importance is derived from the fact that it can lead to irreversible CNS damage,4 of the type that may be attributed to neuronal loss. Later in the course of disease, several months after infection, encephalopathies may appear. Patients with this late symptom complain of specific memory and/or intellectual impairment, often associated with incapacitating fatigue.4 Brain lesions from Lyme neuroborreliosis patients show vasculitis and subarachnoid hemorrhage5,6,7,8 as well as multifocal encephalitis with large areas of demyelination in perivascular white matter, at times associated with the presence of B. burgdorferi DNA.9,10,11,12 Neurological disturbance limited to the spinal cord can manifest clinically as acute transverse myelitis and leptomeningitis.9,12
Cited by the crooks (Schoen) when trying to sell their non-vaccine:

Increased cerebrospinal fluid levels of glial fibrillary acidic protein (GFAp) in Lyme neuroborreliosis.

Means destruction of glial cells occurs.



Microglia in infectious diseases of the central nervous system.




Lyme Neuroborreliosis and Dementia.



NIH's Martin and Marques from the Lyme-MS group discovering that it is OspA that causes the reverse inflammation; inflammation in the brain and no humoral antibodies:


Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression.



Most Neuroborreliosis patients have reactivated EBV and CMV (if not more) due to the immunosuppression revealed above my Martin and Marques as a result of being exposed to Lyme and LYMErix (OspA shed):

Systemic immune deficiency necessary for cytomegalovirus invasion of the mature brain.





Human cytomegalovirus inhibits neuronal differentiation and induces apoptosis in human neural precursor cells.