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):
http://www.actionlyme.org/RICOCHRON.htm
http://www.actionlyme.org/BRAIN_PERMANENT.htm (<<
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."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3745032/
.
.
.
Shrunken Energy-producing cells (microglia)
in the well-known-to-be-incurable Syphilis, and guess what ma,
no biofilms ;)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1048417/pdf/brjvendis00098-0012.pdf
.
.
.
=================================
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."
http://www.actionlyme.org/BRAIN_PERMANENT.htm
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:
http://www.actionlyme.org/BIOMARKERS.htm
.
.
http://www.ohioactionlyme.org/wp-content/uploads/2015/02/Biomarkers1.pdf
.
.
Interaction of the Lyme Disease Spirochete Borrelia
burgdorferi with Brain Parenchyma Elicits Inflammatory
Mediators from Glial Cells as Well as Glial and Neuronal
Apoptosis
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2570132/
.
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
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2570132/
.
.
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.
http://www.ncbi.nlm.nih.gov/pubmed/8740104
Means destruction of glial cells occurs.
.
.
Microglia in infectious
diseases of the central nervous system.
http://www.ncbi.nlm.nih.gov/pubmed/19728102
.
.
Lyme Neuroborreliosis and Dementia.
http://www.ncbi.nlm.nih.gov/pubmed/24762944
.
.
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:
http://www.ncbi.nlm.nih.gov/pubmed/16783164
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.
http://www.ncbi.nlm.nih.gov/pubmed/14722303
.
.
http://www.ncbi.nlm.nih.gov/pubmed/16940505