Alzheimer's Disease caused by Jab Endotoxin

Endotoxin is present in all brands of Covid19 jabs and is known to upregulate microRNA miR-155-5p that enhances extracellular Aβ Aggregation

Endotoxin in jabs, especially the small, most toxic, Lipid A, travels immediately after jabbing to the Brain as discussed previously.¹ ²

There it initiates a number of destructive pathways³ and upregulates expression of numerous microRNAs, including miR-155 that I have shown causes Myocarditis⁴ and other diseases.

A 2023 review⁵ provides many useful references. Here is Figure 1 from Liu and coworkers.

I have slightly modified their Figure caption to explain some abbreviations.

miR-155 regulates the deposition of Aβ (extracellular amyloid-β) by inducing SKP2 (S-phase kinase-associated protein) or SNX27(Sorting Nexin). miR-155 might be involved in NFT (intracellular NeuroFibrillary Tangles) by regulating GSK3β (Glycogen Synthase Kinase-3), AMPK (Adenosine-Monophosphate activated Protein Kinase), PKI-α (Protein Kinase A Inhibitor), mTOR (Mammalian Target of Rapamycin), MAPK (Mitogen-Activated Protein Kinase), or Wnt (Wingless-related integration site) pathways, which evolves from assembled hyperphosphorylated tau protein and induces synaptic dysfunction. miR-155 was also involved in synaptic dysfunction by regulating c/EBPβ (Enhancer Binding Protein)/SNX27 signaling pathway. miR-155 can activate microglia via targeting SOCS-1(Suppressor Of Cytokine Signaling) or SHIP1(SH2 domain containing Inositol-5-Phosphatase). The activated microglia can phagocytize aggregated Aβ but also can release pro-inflammatory cytokine, which accelerates Aβ aggregation and leads to neuroinflammation. NLRP4 (Nucleotide-binding and Leucine-rich repeat Receptor Pyrin Domain Containing). IL (Interleukin). TNF (Tumor Necrosis Factor). IFN (Interferon)

Wang and coworkers demonstrated the importance of miR-155-5p by investigating the Nuclear Factor Kappa B (NF-κB) pathway and inhibitor of NF-κB kinase β (IKKβ) that are involved in Alzheimer disease (AD) pathogenesis.⁶

Can Endotoxin Induced Alzheimer’s be reversed?

A paper from 2018 discusses the role of Lipopolysaccharide Binding Protein countering Endotoxin.⁷

The authors concluded:

We therefore suggest that LBP might eventually be used as treatment to prevent the damaging effect of LPS on fibrin(ogen) and hypercoagulation, and even to prevent (at least in part) the deposition of amyloid-β (Aβ) plaques in the brain and the loss of cognitive function that accompanies this neurodegenerative disease. However, we note that a control protein, such as human IgG should, in future, be used to present the specific effect of LBP on amyloid formation, to further elucidate the physiological processes discussed in this paper. In future, our hypothesis could also be tested in a transgenic murine model of AD (TgAD) or the 5xFAD (amyloid over-producing) model or equivalent.

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5. Liu JJ, et al. 2023. Pathogenesis of miR-155 on nonmodifiable and modifiable risk factors in Alzheimer’s disease. https://alzres.biomedcentral.com/articles/10.1186/s13195-023-01264-z

6. Wang W, et al. 2021. MicroRNA-155-5p Targets SKP2, Activates IKKβ, Increases Aβ Aggregation, and Aggravates a Mouse Alzheimer Disease Model. https://academic.oup.com/jnen/article/81/1/16/6448595

7. Etheresia Pretorius, Janette Bester, Martin J. Page and Douglas B. Kell. 2018. The Potential of LPS-Binding Protein to Reverse Amyloid Formation in Plasma Fibrin of Individuals With Alzheimer-Type Dementia. https://www.frontiersin.org/articles/10.3389/fnagi.2018.00257/full