Lyme Crooks re-report on anti-brain antibodies in Post-LYMErix Syndrome
Mort Zuckerman
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Subject: Lyme Crooks re-report on anti-brain antibodies in Post-
LYMErix Syndrome
Date: Apr 5, 2010 4:27 PM
ARTICLE BELOW
Norman Latov showed that OspA-itself
caused anti-nerve antibodies. Not
that Klempner didn't know it too:
http://www.ncbi.nlm.nih.gov/pubmed/15363064
http://www.ncbi.nlm.nih.gov/pubmed/15652419
Hey, fellas, don't forget all your other
own Biomarkers of Disease that you refused
to turn over to the CT AG in his lawsuit
against you for SCIENTIFIC FRAUD AND
RACKETEERING:
http://www.actionlyme.org/BIOMARKERS2.htm
1) Glial Fibrillary Acidic protein in CSF
(destruction of brain cells, Yale's Robert Schoen)
2) Nitric Oxide in the CSF (Steere)
3) Matrix-metalloproteinases in the CSF (Klempner,
these are CNS-degrading enzymes)
4) Autoreactive T cells to OspA and C in the
CSF - caused by LYMERIX!!! (***Klempner***):
http://www.actionlyme.org/KFORSCHNER_DISCOVERS_LYME_TOXIN.htm
5) Anti-phospholipids (Steere, Yale, L2 Diagnostics:
"Lyme/LYMErix cause Lupus via activation of Epstein-Barr")
6) Anti-gangliosides (Benach)
7) QEEG (Lenny Munchmeister Sigal)
8) Circulating free immune complexes (Stroke, Reik,
Steere)
9) Mutant, immature, EBV-like B cells (IDSA):
http://www.actionlyme.org/IDSA_CLINIPATH_DURAY.htm
10) Immune complexes in the CSF (SUNY-Coyle, Schutzer)
11) Quinolinic Acid as an excitotoxin (ALS-Halperin)
12) Brain hypoperfusion (all, Steere)
13) MRI with gadolinium contrast (meningitis)
14) Dysregulated cytokines in the blood and CNS (Sigal)
15) Placental transfer (Yale, several autopsies of
dead new-babies and fetuses)
http://www.actionlyme.org/Schoen.htm
16) Anti-Heat-Shock proteins (MS, anti-flagellin,
anti-Bb-HSPs, Lenny Munchausen's)
Okay !! You're welcome, ANY TIME!!!
KMDickson
http://www.actionlyme.org
http://www.relapsingfever.org
=========================================
http://www.ncbi.nlm.nih.gov/pubmed/20227484
Brain Behav Immun. 2010 Mar 18. [Epub ahead of print]
Anti-neural antibody reactivity in patients with a history of Lyme
borreliosis and persistent symptoms.
Chandra A, Wormser GP, Klempner MS, Trevino RP, Crow MK, Latov N,
Alaedini A.
Department of Neurology and Neuroscience, Cornell University, New
York, NY, USA.
Some Lyme disease patients report debilitating chronic symptoms of
pain, fatigue, and cognitive deficits despite recommended courses of
antibiotic treatment. The mechanisms responsible for these symptoms,
collectively referred to as post-Lyme disease syndrome (PLS) or
chronic Lyme disease, remain unclear. We investigated the presence of
immune system abnormalities in PLS by assessing the levels of
antibodies to neural proteins in patients and controls. Serum samples
from PLS patients, post-Lyme disease healthy individuals, patients
with systemic lupus erythematosus, and normal healthy individuals were
analyzed for anti-neural antibodies by immunoblotting and
immunohistochemistry. Anti-neural antibody reactivity was found to be
significantly higher in the PLS group than in the post-Lyme healthy
(p<0.01) and normal healthy (p<0.01) groups. The observed heightened
antibody reactivity in PLS patients could not be attributed solely to
the presence of cross-reactive anti-borrelia antibodies, as the
borrelial seronegative patients also exhibited elevated anti-neural
antibody levels. Immunohistochemical analysis of PLS serum antibody
activity demonstrated binding to cells in the central and peripheral
nervous systems. The results provide evidence for the existence of a
differential immune system response in PLS, offering new clues about
the etiopathogenesis of the disease that may prove useful in devising
more effective treatment strategies. Copyright © 2010 Elsevier Inc.
All rights reserved.
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