Tourette Syndrome linked to Endotoxin
Abnormal behaviours including Tics are receiving more attention in the media, so I thought a quick delve would be in order.
Half of children with Tic disorders have contemplated Suicide, as reported by Australia’s taxpayer funded free-to-air News Service ABC.1
This tragedy has been shared on the commercial TV as well, for example Channel 7
Endotoxin Causal Link in Animals and Humans
Tourette Syndrome and related Tic disorders have a genetic inheritance risk and Males are affected about 3 times more often than Females. Onset usually occurs between 3 and 8 years of age2, but cases are known to be caused by Jabs in families that have not suffered in previous generations and compensation has been paid in the US.3
In 2013 German researchers studied circulating Endotoxin induced levels of Toll-Like Receptor (TLR) 4 on CD14 + monocytes and soluble CD14 (sCD14)in the serum of 33 Tourette patients and 31 healthy controls.4
Collected blood samples were stimulated with Endotoxin (Lipopolysaccharide, LPS) mimicking a bacterial infection.
The researchers concluded:
Higher levels of sCD14, lower levels of TLR4 expression after stimulation and a diminished up-regulation of TLR4 expression after LPS stimulation in patients might represent an impaired activation of the innate immune response in TS, especially in regard to bacterial infection. The impaired response to pathogens could eventually lead to a higher susceptibility for infections. Recurring infections and a chronic inflammation could trigger and maintain the symptoms of TS.
This is an example of Endotoxin Tolerance, which has a huge literature with 1,669 peer-reviewed papers easily found on PubMed.5
No doubt large numbers of papers have been published in languages other than English.
In 2017 Chinese researchers decided to have a deeper look.6
They used an established method of Tourette syndrome induction with the selective 5-HT2A/2C agonist 1-(2, 5-dimethoxy-4-iodophenyl) -2- aminopropane (DOI) and found Endotoxin treatment significantly increased stereotypic score and autonomic activity.
Endotoxin treatment, as expected, also significantly increased inflammatory cytokines such as interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in serum and striatum.
They also reported highly expressed TLR4, MyD88, P-NF-κBp65, P-IκBα in Tourette syndrome Rats.
They concluded recurrence of Tourette syndrome mechanism was related to the well known TLR/NF-κB pathway.
Robert F Kennedy Jr. should get CTD to Update
The US Comparative Toxicogenomics Database carries a misleading 1994 Definition:
A neuropsychological disorder related to alterations in DOPAMINE metabolism and neurotransmission involving frontal-subcortical neuronal circuits. Both multiple motor and one or more vocal tics need to be present with TICS occurring many times a day, nearly daily, over a period of more than one year. The onset is before age 18 and the disturbance is not due to direct physiological effects of a substance or another medical condition.
The disturbance causes marked distress or significant impairment in social, occupational, or other important areas of functioning.
Given the proven Science, I hope this is fixed soon.7
However, CTD is still a useful resource because it collects references despite sufficient Human Curation, associating Tourette Syndrme with 335 Chemicals.8
Histidine Decarboxylase (HDC)
CTD lists HDC as one of the genetic factors in Endotoxin Tourette Syndrome, but you can see the number of synonyms complicates research.
New paper from Korea uses Endotoxin
Thanks to one of my friends from Germany for sharing the announcement of a new paper from Korea that studied the influence of Endotoxin on Repetitive Behaviours in Mice.9
The paper is very detailed, and I found a figure in the Supplementary material is helpful. Subscribers might like to comment after reading it all.
Note the use of the known Neurotoxin and Carcinogen Tamoxifen10 to damage the brains.
Abbreviated Caption:
Figure S2.
Nlrp3D301N-cKI mice exhibit prolonged microglial activity and decreased density of excitatory and inhibitory post-synapses in the hippocampus after (Endotoxin) LPS administration (related to Fig. 1).
(A) Schematic illustration of the experimental procedure.
(B) Representative images of hippocampal CA1 regions of control and Nlrp3D301N-cKI mouse brains 6 days after LPS treatment.
Brain sections were immunostained for Iba-1 (red) and CD68 (green).
Scale bars: 50 μm (applies to all images).
(C and D) Quantification of the density (C) and the size (D) of Iba-1+ cells. Data are means ± SEMs. (control, n = 7; Nlrp3D301N-cKI, n = 7; ***p < 0.001).
(E) Quantification of the colocalization percentage of CD68+ area within Iba-1+ cells. Data are means ± SEMs (control, n = 7; Nlrp3D301N-cKI, n = 7; ***p < 0.001).
(F) Percentage of microglia displaying a ramified, bushy, or amoeboid morphology. Data are means ± SEM (control, n = 7; Nlrp3D301N-cKI, n = 7; ***p < 0.001 vs. Control group).
(G) Representative binary images of Iba-1 staining in hippocampal CA1 regions. Scale bars:
20 μm (applies to all images).
(H) Quantification of the number of Iba-1+ cell process endpoints. Data are means ± SEMs (control, n = 7; Nlrp3D301N-cKI, n = 7; ***p < 0.001).
(I) Quantification of the total lengths of Iba-1+ cell processes. Data are means ± SEMs (control, n = 7; Nlrp3D301N-cKI, n = 7; ***p < 0.001).
(J) Representative images of hippocampal CA1 regions of control and Nlrp3D301N-cKI mouse brains 6 days after LPS treatment. Brain sections were immunostained for GFAP (red).
Scale bars: 50 μm (applies to all images).
(K) Quantification of the average intensity of GFAP+ signal in the layers of hippocampal CA1 regions. Data are means ± SEMs (control, n = 6; Nlrp3D301N-cKI, n = 5).
(L) Representative images of mPFC prelimbic regions of control and Nlrp3D301N-cKI mouse brains 6 days after LPS treatment. Brain sections were immunostained for GFAP (red) and S100β (green). Scale bars: 50 μm (applies to all images).
(M) Quantification of the average intensity of GFAP+ signal and the density of S100β+ cells.
Data are means ± SEMs (control, n = 4; Nlrp3D301N-cKI, n = 4; *p < 0.05).
Note also the use of CD68 staining that I have mentioned a number of times especially to look at Multiple Organ Failure in Autopsies of Jabbees.111213
CD68 is well understood by Dr Casey Means.14
Tourette linked to Parkinson’s and Alzheimer’s
Not surprisingly, there are common gene interactions with Endotoxin to explore in Human Brains for Parkinson’s Disease15 and Alzheimer’s Disease.16
Tourette Syndrome linked to Fluoride
Tourette Brain Damage has also been linked to Fluoride via neuronal nicotinic AcetylCholine Receptors (nAChRs), but that is a story for another day.
https://www.abc.net.au/news/2025-06-01/tourette-syndrome-bullying-plea-for-understanding/105359360
https://www.omim.org/entry/137580
https://x.com/catsscareme2021/status/1689225717387612160
Elif Weidinger, Daniela Krause, Agnes Wildenauer, Sebastian Meyer, Rudolf Gruber, Markus J Schwarz, Norbert Müller. 2014. Impaired activation of the innate immune response to bacterial challenge in Tourette syndrome. https://www.tandfonline.com/doi/10.3109/15622975.2014.907503
https://pubmed.ncbi.nlm.nih.gov/?term=Endotoxin+Tolerance
Long Hongyan, Si Zhenyang, Wang Chunyan, Pan Qingqing. 2017. Lipopolysaccharide aggravated DOI-induced Tourette syndrome: elaboration for recurrence of Tourette syndrome. https://link.springer.com/article/10.1007/s11011-017-0084-3
https://ctdbase.org/detail.go?type=disease&acc=MESH%3AD005879
https://ctdbase.org/detail.go?acc=MESH%3AD005879&view=chem&sort=chemNmSort&type=disease&dir=asc
Hyeji Jung, Byeongchan Kim, Gyubin Jang, Hyeonho Kim, Ae-Ree Lee, Sung-Hyun Yoon, Kyung-Seo Lee, Gaeun Hyun, Younghye Kim, Jaewon Ko, Je-Wook Yu, and Ji Won Um. 27 May 2025. The NLRP3 inflammasome in microglia regulates repetitive behavior by modulating NMDA glutamate receptor functions. Cell Reports 44:115656 https://www.cell.com/cell-reports/fulltext/S2211-1247(25)00427-9
https://en.wikipedia.org/wiki/Tamoxifen
CD68 Diseases caused by Endotoxin in Jabs
Myocarditis and Pericarditis are caused by upregulation of CD68 cells by Endotoxin in Covid19 jabs, as explained in an earlier article.
Lymphadenopathy Danger from Endotoxin in Pfizer Jabs
BioNTech/Pfizer and complicit marketers of their Covid19 jab, including government departments around the globe, lied to the public when the said that the Lipid NanoParticles and the mRNA floating inside or outside them, would simply enter muscle cells in the arm, take them over to force them to become factories for Synthetic Spike generation and result…
Pfizer Process 2 Endotoxin Myocarditis Death Toll - Dr Aseem Malhotra knows all about it
Jab pushers are outraged at the overwhelming success of the Australian lecture tour by British Cardiologist Dr Aseem Malhotra.
Casey Means Business
I saw John Leake of the Foster Coulson Big Pharma Fear Kit marketing profiteers “The Wellness Company” refer to Dr Casey Means MD as “Ms. Means”.
Parkinson's Disease after Pfizer jabs most likely due to Endotoxin in every vial
In a recent article I wrote about Endotoxin in Pfizer jabs being known to readily cross the Blood-Brain-Barrier and target Microglia, causing many of the common Adverse Events reported by hundreds of millions of Jabbees.
Alzheimer's Disease caused by Jab Endotoxin
Endotoxin in jabs, especially the small, most toxic, Lipid A, travels immediately after jabbing to the Brain as discussed previously.