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Another relatively easy article on prions...

Discussion in 'The Cave' started by Penny, May 14, 2021.

  1. Penny

    Penny New Member

    Interesting - if you look at the interview with Del Bigtree and Dr. Flemming - Flemming has a picture of the spike protein and 1/3 of it is a prion... so maybe that is how it "infects" other cells... this stuff is so complicated... :)

    "Prion diseases are more specifically called transmissible spongiform encephalopathies (TSEs), and infection can spread through exposure to misfolded proteins as “infective” agents, without requiring a live pathogen [20]. PrP is the name given to the specific prion protein associated with these TSEs. Misfolded PrP proteins act as a seed or catalyst that then recruits other molecules of PrP to misfold in the same way and glom together into pathogenic fibrils...
  2. Dan2

    Dan2 Pedantic schlub

    Yeah there are lots of things that have been found to block the ACE2 attachment. That's just one of the problems though; it also binds to porphyrin:



    "Perhaps the most important paper yet published (referenced) about COVID-19 was published last summer to little fanfare. In it, the authors note that the SPIKE PROTEIN has a MUCH HIGHER AFFINITY for PORPHYRIN MOLECULES than ACE2. At the same time the virus increases free heme and free iron (Fe), but more importantly, decreases functional hemoprotein. COVID-19 produces dysfunctional hemoproteins and dysfunctional porphyrin that are no longer capable of making heme. This leads to more hemoprotein available for COVID-19 to bind to, which leads to the release of more free iron, and as a result, increased inflammation [6]. In addition, the iron released by dying cells has additive toxic effects. This has devastating consequences on the mitochondria. The ROS formed by COVID-19′s iron-induced “cytokine storm” create inflammation that is destructive to the mitochondria in the electron transport chain (ETC). If insufficient mitochondria in cells is evident, such as in white adipose cells, these cells are unable to accommodate the severe ROS formed leading to overwhelming inflammation. Brown adipose cells are better at handling ROS due to higher concentrations of mitochondria. ... And if you survive? The unprecedented outpouring of toxic iron into the body is most likely the cause of Long COVID and the incoming cancers and neurodegenerative diseases. Excess iron is tightly associated with tumorigenesis in multiple human cancer types through a variety of mechanisms including catalyzing the formation of mutagenic hydroxyl radicals, regulating DNA replication, repair and cell cycle progression, affecting signal transduction in cancer cells, and acting as an essential nutrient for proliferating tumor cells.

    Please understand the major finding. All of this is due to the SPIKE PROTEIN's interactions. COVID-19 produces a severe systemic inflammatory reaction, likely the result of increased free heme levels and decreased levels of HO-1 activity and functional hemoprotein. The spike protein of COVID-19 binds ACE-2 receptors and porphyrin molecules with weak and strong affinity, respectively. Porphyrins are the building blocks of heme and allow COVID-19 access to invade cells along with ACE-2 receptors and bind functional hemoprotein within the cell. ..."
    - Walter M Chestnut


    But for the ACE2 binding, HCQ blocks the spike protein binding to it.

    A tree bark was used for quinine before the synthetic quinines were invented in the mid 20th century. It's called cinchona bark. You can make tea with that. It's a much more cost effective way to get quinine than buying tonic water is, and compared to HCQ, there are chemicals in the bark that support the desired effects of the quinine, and also make it harder for a virus to become resistant to that combination of chemicals, which might be important as the vaccines cause variants.

    ("The main plant chemicals found in quinine [cinchona] bark include: aricine, caffeic acid, cinchofulvic acid, cincholic acid, cinchonain, cinchonidine, cinchonine, cinchophyllamine, cinchotannic acid, cinchotine, conquinamine, cuscamidine, cuscamine, cusconidine, cusconine, epicatechin, javanine, paricine, proanthocyanidins, quinacimine, quinamine, quinic acid, quinicine, quinine, quininidine, quinovic acid, quinovin, and sucirubine.") (www.rain-tree.com/quinine.htm)

    General info, dosing, example of what to buy:



    HCQ vs quinine bark


    Risks of using the bark:


    Also useful: nigella sativa a.k.a. black cumin seed (grind it in a coffee grinder or mortar and pestle and make tea):

    Last edited: Aug 16, 2021
    Penny likes this.
  3. Dan2

    Dan2 Pedantic schlub

    You mentioned Povidone-Iodine.

    In that study you linked to...

    Screen shot 2021-06-22 at 11.44.19 AM.png
    Screen shot 2021-06-22 at 11.45.42 AM.png

    So to prevent infection from inhaled viral particles, they're putting it in the nose.

    I'm more confident about the ability of the variety of chemicals in "herbs" to prevent variant strains from becoming resistant to a treatment.

    So because of finding this info about black cumin seed...


    and black cumin seed oil can be bought... (example: https://mountainroseherbs.com/black-cumin-seed-oil )...

    and knowing that frankincense, myrrh, and other essential oils are good general antivirals...

    (good overview article: https://ifaroma.org/en_GB/home/blog/essential-oils-coronavirus-covid19 )

    (good places to buy essential oils: https://naturesgift.com/ , https://www.edenbotanicals.com/ )

    I mixed into a base of black cumin seed oil the essential oils of frankincense, myrrh, and spruce needle, and use an eyedropper to put it in my nose, as a preventative when I'm in public.
    Last edited: Jun 22, 2021
  4. Dan2

    Dan2 Pedantic schlub


    "Here, we show that EGCG has the ability to convert large, mature α-synuclein and amyloid-β fibrils into smaller, amorphous protein aggregates that are nontoxic to mammalian cells... Previous studies have shown that the polyphenol (-)-epi-gallocatechine gallate (EGCG), found in large amounts in green tea, has antiamyloidogenic properties and modulates the misfolding of disease proteins and prions (1–5). EGCG directly binds to unfolded polypeptide chains and inhibits β-sheet formation, an early event in the amyloid formation cascade (6). In the presence of EGCG, the assembly of a new type of unstructured, SDS-stable, nontoxic oligomer was observed, instead of the expected formation of β-sheet-rich aggregates. This suggested that the compound redirects aggregation prone polypeptides into off-pathway protein assemblies (6), as has since been confirmed for other flavonoids (7)."

    Probably other polyphenols in other kinds of tea would be complementary, like in oolong:


    Pu-erh is tea leaves prepared with another fermentation method.


    "Mutations in the copper/zinc superoxide dismutase (SOD1), TAR DNA-binding protein 43 (TDP-43), and FET family proteins are associated with the development of amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease... The results of this study revealed that components of a pu-erh tea extract (PTE) interacted with FET family proteins but not with TDP-43 or SOD1. PTE [pu-erh tea extract] induced the degradation of FET family proteins but had no effects on TDP-43 or SOD1. The most frequently occurring ALS-linked FUS/TLS mutant protein, R521C FUS/TLS, was also degraded in the presence of PTE [pu-erh tea extract].

    Tea is one of the most popular and widely consumed beverages in the world. Unlike green tea, pu-erh tea contains a number of compounds that are produced as the result of the preparation process. Human epidemiological and animal research experiments suggest that the pharmacological benefits of tea drinking may help protect the brain as we age. There is a growing body of evidence to indicate that polyphenol compounds have the ability to convert large, mature α-synuclein, and amyloid-β fibrils into smaller, amorphous protein aggregates that are nontoxic to mammalian cells [30–32]. Epigallocatechin gallate (EGCG) significantly reduces the aggregation and cytotoxicity of the Huntington protein containing polyglutamine (polyQ) in a yeast model of Huntington's disease [33]. It should also be noted that tea drinking has been shown to exert neuroprotective activities in a wide array of cellular and animal models of neurological disorders [34]. In this study, we prepared three different tea extracts Sepharose beads to screen the proteins strongly associated with PTE [pu-erh tea extract]. FUS/TLS was identified as a PTE-associated protein. Although FUS/TLS also could bind to GTE [green tea extract] and BTE [black tea extract], PTE [pu-erh tea extract] did have the greatest capacity to bind to FUS/TLS among those three different tea extracts. Perhaps this may account for the apparent absence of FUS/TLS in the proteins that bind to GTE or BTE Sepharose 6B beads in Coomassie brilliant staining. EGCG is the most abundant catechin in tea. EGCG is found mainly in green tea but, in smaller quantities, in black tea and Pu-erh Tea. We were not able to observe the degradation of FUS/TLS after treatment with EGCG (data not shown).

    ...PTE [pu-erh tea extract] may prevent protein aggregation and enable cells to function normally with normal levels of FET family proteins. There are currently no FET family protein-targeted therapies available for the treatment of ALS. The decreased levels of a toxic FET family proteins or mutant FET family proteins might be efficacious for FET family protein-associated ALS. Further studies are required to assess whether the PTE-induced reduction in FET family proteins is also observed in in vivo FET family proteins proteinopathies models."



    "Sheng, or “raw” pu-erhs are so named because they are fermented naturally over a long aging period. This is a lot like the ripening of cheese, rather than the fermentation of alcohol. Typically pressed into discs, or otherwise packed for storage, these teas must be aged for at least 10 years before they are considered “drinkable”...

    This naturally fermented style is rumored to have roots in the Tibetan tea trade, dating back to the Tang Dynasty. For portability, teas from Yunnan were pressed into bricks or cakes, and fermented naturally during the months-long journey to Tibet. On the steppe, the fermented teas were stewed and combined with yak butter to create a nutritionally valuable beverage.

    In the 1980s, demand for pu-erh teas began to outpace the supply from traditional aging processes. To keep up, tea makers developed a technique to accelerate fermentation and imitate well-aged sheng teas. This new style was called shou, or “cooked” pu-erh.

    To make shou pu-erh, the green maocha is heaped into a large pile. Tea makers often mix in a small amount of a previous batch of tea to introduce desirable microbes, and then the leaves are left to ferment. This process works a lot like composting, with the dense pile producing heat that encourages fermentation. The leaves are then turned regularly until they are fully fermented, at which point they may be pressed into cakes, already ready to drink.

    Shou pu-erhs are best viewed with a critical eye, since most mass produced pu-erhs are made using this method. Low quality leaves are often grown with heavy use of pesticides, and can leave a tea tasting flat, while poorly managed production and storage can result in the aforementioned fishy quality, or even dangerous mold. With the market for these teas booming, misinformation abounds, and few vendors are willing or able to navigate the remote regions where these teas are made."
    Last edited: Jun 25, 2021
    DebraGM likes this.
  5. Dan2

    Dan2 Pedantic schlub

    About the binding affinities of plant chemicals that bind to the ACE2 receptor, details of black cumin seed chemical composition, blood brain barrier permeability of chemicals in black cumin seed oil and effects on protein receptors that affect neurodegeneration







    Comparing practicality and reliability of black cumin seed oil, cinchona bark, HCQ, and chloroquine; also comparisons of binding affinities of Ivermectin, HCQ, and chloroquine:


    Cold-pressed black cumin seed oil vs. CO2 extract, essential oils


    Details of blending essential oils into a carrier oil (like black cumin seed oil) so they can be safely put in the nose or (depending on which essential oil, sometimes) ingested


    Dosages of thymoquinone in black cumin seeds or oil, and what are safe dosages

    Last edited: Jul 1, 2021
    Penny and DebraGM like this.
  6. Dan2

    Dan2 Pedantic schlub

    Ivermectin prescription vs. horse dewormer paste? Calculating an Ivermectin dosing schedule for your miniature horse


    Quinine and HCQ have different half-lives so how to dose an amount of quinine in cinchona bark similarly to Zelenko's prophylaxis protocol HCQ doses; risks of cinchona bark compared to synthetic derivatives


    (about cinchona and HCQ continued in post # 29)
    Last edited: Aug 23, 2021
  7. Jeremy Fox

    Jeremy Fox Silver

    Has anyone thought about methylene blue as a prophylactic against prions? I posted on Twitter and someone responded with methylene blue, without explanation.
  8. Dan2

    Dan2 Pedantic schlub

    @Jeremy Fox
    Have you learned more about that since you asked that?
    Last edited: Nov 13, 2021
  9. Dan2

    Dan2 Pedantic schlub

    Continuation of post # 26 about HCQ and cinchona bark...

    A picture of 2 grams of cinchona bark so people who don't have a scale can eyeball their dose estimate better than I did (so they don't get cinchonism symptoms)


    Uncertainties of mine about how to compare Zelenko's recommended HCQ doses with safe cinchona bark doses, considering that cinchona bark has lots of other chemicals in it that interact with the quinine effects

  10. Dan2

    Dan2 Pedantic schlub


    "...Prions, the brain proteins whose alteration seems to be responsible for BSE, are, Purdey argues, designed to protect the brain from the oxidising properties of chemicals activated by dangerous agents such as ultraviolet light. When, he suggests, the prion proteins are exposed to too little copper and too much manganese, the manganese takes the place of the copper the prion normally binds to, with the result that the protein becomes distorted and loses its function.

    BSE arose in British herds during the 1980s, Mark Purdey asserts, because the Ministry of Agriculture started forcing all cattle farmers to treat their animals with an organophosphate pesticide called phosmet, at far higher doses than are used elsewhere in the world. The pesticide had to be poured along the line of the spinal cord. Phosmet, Purdey has shown, captures copper. At the same time, cattle feed was, disgustingly, being supplemented with chicken manure, from birds dosed with manganese to increase their egg yield. The prion proteins in the cows’ brains were both deprived of copper and dosed with manganese. In France, the use of phosmet first became mandatory in Brittany. Twenty of the country’s initial 28 cases of BSE emerged there. BSE’s subsequent spread, Purdey maintains, mirrors the use of the pesticide.

    Poisoning by similar means may explain the distribution of the human form of the disease. Of the two main clusters in Britain, one, in Kent, is in the middle of a fruit and hop growing area where huge quantities of both organophosphates and manganese-based fungicides are used. The other is in Queniborough in Leicestershire, whose dyeworks (until they caught fire a few years ago, spraying chemicals over the village) used, he alleges, to dump some of their residues into the sewage system. The sewage was spread over the fields. Dyeworks use shedloads of manganese.

    Purdey has tested his theory in BSE and CJD clusters in Iceland, Colorado, Slovakia and Sardinia. In every case he found that people and animals had been exposed to deficiencies of copper and surfeits of manganese. Most of the clusters, intriguingly, are in mountainous areas, where levels of ultraviolet light are high. But the most compelling evidence in support of his hypothesis comes from a paper published by a team of biochemists at Cambridge this year. They found that when copper was substituted by manganese in prion proteins, the prions adopted precisely the distinguishing features which identify the infective agent in BSE..."
    Beasol and Jeremy Fox like this.
  11. Dan2

    Dan2 Pedantic schlub

    Intervew by Patrick Timpone with Stephanie Seneff and Greg Nigh
    June 16, 2021



    "Show highlights:

    These injections are disrupting a special enzyme that is critical to virtually all major organs

    We asked both guests “compared to three months ago are you less, the same, or more concerned about these injections?”

    The potential auto immune issues that may erupt in those who take this may be massive

    Three years or so from now no one will connect the dots between the injections and increased diseases.

    Guests explain how this prion protein also known as mad cow is involved.

    Dr. Seneff explains exactly what spike proteins are.

    They are using computer modeling to created the injections and predict outcomes, no real testing on humans.

    The fat lipids being used as an adjuvant is quite toxic

    We discuss what we know of shedding

    Both Dr. Seneff and Dr. Nigh have direct contact with some women who’s menses have been affected by being near injected women."
    Last edited: Aug 25, 2021
  12. Dan2

    Dan2 Pedantic schlub

    For blood clotting problems from the spike proteins, this is probably just a band-aid but ginkgo tea might prevent clots from developing much. But it also affects platelets


    and I don't know enough about how low platelets (which can be an effect of the spike proteins) and clotting interact to know if ginkgo would help prevent clotting but be a problem for platelets because of how the spike proteins dysregulate so many things making unusual effects.

    I've still been drinking tea of milk thistle seeds, black cumin seeds, licorice, ginger, curry spices, and green/oolong tea (which, without the spike proteins, would usually be a pretty harmless combination to drink consistently) as a ham-fisted hoping-it-combines-to-not-make-too-much-of-one-specific-unusual-problem-with-the-spike-protein's-variety-of-effects (like ginkgo usually not affecting platelets dangerously when used at doses that help prevent clots, but with the spike protein, yeah probably contraindicated against itself) prophylactic in the meantime until I learn more about the spike protein effects, and recently started including ginkgo. (Considering that I told you guys about including ginkgo while being lazy to not research it more carefully first, if I stop posting, probably safe to say I got lucky and accidentally made my platelets suddenly plummet.)

    edit: "Immune thrombocytopenia is characterized by both increased platelet destruction and reduced platelet production, and autoantibodies play a pivotal role."

    Ham-fisted. Where did that phrase come from? ...Some guy was going to war, and they asked him, "So, Bob, what do you think? You want a sniper rifle? Or at least something with a scope?" And Bob looks into the distance contemplatively for a moment, slowly raises his fists, and says, "No... I think I'm gonna stick my fists into some hams... Can't be too careful."
    Last edited: Sep 3, 2021
  13. Jeremy Fox

    Jeremy Fox Silver

    Here is a short report on a man who developed prion disease, apparently due to vaccine shedding as he was not vaccinated himself. He traveled a lot on airplanes. Adam Gaertner posted this on Twitter.

    We need a protocol to prevent the escalation of prion disease, assuming everyone, vaccinated or not, has been infected by some amount of prions due to vaccine shedding.

    Attached Files:

  14. Dan2

    Dan2 Pedantic schlub

    A message I sent to Jeremy:

    About the prion protocol, there's been a lot of lab research about Ayurvedic neuroprotective herbs, that I think could be helpful for preventing or reverting prions. I'll look through studies I've saved soon and get back to you with better leads about that. Some of the most likely ones to help, I think, will be celastrus paniculatus seed (a.k.a. jyotishmati) (which isn't very popular outside of India compared to other Ayurvedic nootropic herbs but in my experience is powerful with small doses if the seeds are fresh (and to preserve them, when ground into paste they tincture in 190 proof alcohol well)), bacopa monnieri leaf (a.k.a. brahmi), centella asiatica (a.k.a. gotu kola), black cumin seed, evolvulus alsinoides (or convolvulus pluricaulis) (a.k.a. shankhapushpi (I love the sound of some of these Indian words)), and acorus calamus (a.k.a. vacha). And moreso common from Chinese medicine is huperzia serrata (Chinese club moss), which in my experience was such a powerful memory enhancement that I got concerned about long-term neurotransmitter imbalances and stopped using it.

    The problem I expect with the Ayurvedic neuroprotective research is that there probably aren't a lot of studies specifically about affecting prions, and I don't know enough about neurochemistry to infer how other studies about the uses for other conditions might hint at that.
    Last edited: Sep 7, 2021
  15. Dan2

    Dan2 Pedantic schlub

    Here are some posts I made about chemicals in black cumin seed affecting proteins in the brain involved with neurodegeneration and neuroprotection:


    "...the current study targets the proteins involved in deteriorating the BBB endothelium. These molecular protein markers increase BBB permeability by triggering the inflammation response, which causes immune cells and cytokines to infiltrate the barrier resulting in BBB endothelium degradation. The markers also upregulate other pathogen proteins to promote NNDs [neuropsychiatric and neurodegenerative disorders] onset [4,8–11]. These molecular targets revealed a new treatment strategy for NNDs; by inhibiting these targets, one can expedite BBB rehabilitation and possibly delay or prevent the onset of these disorders...

    The onset of neuropsychiatric and neurodegenerative disorders (NNDs) is related with the deterioration of blood–brain barrier (BBB) which is facilitated by five pathogenic proteins markers; human IFN-γ, IL-1β, TNF-α, resisitin, VCAM-1 and MMP-9, respectively.

    Thymohydroquinone is assumed to be active against different NNDs but has not been evaluated in BBB-associated NNDs...

    Our study revealed that thymohydroquinone is a potent inhibitor of the BBB-disrupting proteins and show adequate interaction with all molecular targets responsible for BBB-associated NNDs...

    All molecular drug targets including human IFN-γ, IL-1β, TNF-α, resisitin, VCAM-1 and MMP-9 demonstrated inhibitory interaction with thymohydroquinone...

    This compound possesses appreciable binding and ligand efficiency with a promising inhibitory constant value.

    It possesses BBB and central nervous system permeability..."

    (I don't know how those protein markers relate to prions, though.)


    "So if thymohydroquinone is BBB and CNS permeable, I'd guess that thymoquinone and other things in the black cumin seed oil are too. I'd also guess that the combination of chemicals in the oil would be complementary as to the effects on those protein receptors that were studied with thymohydroquinone (my previous post)."


    "More about blood brain barrier permeability of quinones in black cumin seed oil
    [The study this post is about is with] rats, and injected, but without the nanoparticle carriers almost as much of the thymoquinone did still cross the blood brain barrier (but not into the hippocampus)."
    Last edited: Sep 3, 2021
  16. Dan2

    Dan2 Pedantic schlub

    Post # 13 of this thread:

    "Interview and article with Mercola, Stephanie Seneff, and Judy Mikovits, posted June 13...

    ...To combat the toxicity of the spike protein, Seneff suggests optimizing autophagy, which may help digest and remove the spike proteins. Time-restricted eating will upregulate autophagy, while sauna therapy, which upregulates heat shock proteins, will help refold misfolded proteins. They also tag damaged proteins and target them for removal. It is important that your sauna is hot enough (around 170 degrees Fahrenheit) and does not have high magnetic or electric fields."


    About a chemical in Celastrus paniculatus seed (aka Jyotishmati (Sanskrit name used in Ayurveda)) that influences heat shock proteins

    (maybe lots of medicinal plant chemicals influence heat shock proteins as well or better than this; I haven't searched for papers about that more yet)
    (and I don't know how strong these effects are compared to sauna)

    Celastrol and its Role in Chronic Diseases
    Shivaprasad H. Venkatesha and Kamal D. Moudgil


    “Table 1.
    Celastrol-induced prevention/treatment of chronic diseases of diverse etiology

    Parkinson’s disease (PD)
    mouse model
    Targets/mechanisms of celastrol action:
    - Modulates pro-inflammatory cytokines, prevents the generation of ROS, lipid peroxidation, and mitochondrial membrane potential.
    - Protects against cellular injury and apoptotic cells death.

    Alzheimer’s disease
    mouse model
    Targets/mechanisms of celastrol action:
    - Inhibits pro-inflammatory cytokines and expression of MHC-II molecules.
    - Induces neuroprotective heat-shock proteins (Hsps).
    - Lowers oxidative stress and regulates BACE-1 expression level via an NF-κB-dependent mechanism.

    Amyotrophic lateral sclerosis (ALS)
    mouse model
    Targets/mechanisms of celastrol action:
    - Blocks neuronal cell death, reduces TNF-α, iNOS, CD40, and GFAP immunoreactivity


    Heat-shock proteins (Hsps), also known as Stress proteins, can be induced by heat and other types of stimuli that cause cellular stress [98,99]. These are highly conserved proteins evolutionarily. Hsps can be categorized into different families based on their molecular mass (kD), for example, Hsp110, Hsp90, Hsp70, Hsp60, Hsp40, and small Hsps. One of the major functions of Hsps is to protect cells from damage under different types of stressful conditions [98,99]. Acting as chaperones, Hsps bind to cellular proteins, ensure proper folding of cellular proteins, attempt to repair defective proteins, and protect them against denaturation and other types of damage. Hsps are also involved in signal transduction and apoptosis. Thus, heat-shock response is cytoprotective under situations that otherwise would promote apoptosis of cells. Stress-inducible heat-shock transcription factor-1 (HSF1) plays an important regulatory role in response to environmental stress and pathophysiological conditions.

    Dysregulation of cellular stress pathways and protein folding can lead to intracellular accumulation of protein aggregates, which is turn can induce tissue pathology [100,101]. Many pathophysiological conditions including neurodegenerative disorders (e.g., Alzheimer’s disease, Parkinson’s disease), cardiovascular diseases, cancer, diabetes, and aging are associated with accumulation of misfolded and/or aggregated proteins within certain tissues, attributable in part to defective cellular stress response pathways [32,17,102,100,101]. In addition, inflammation and oxidant damage also contribute to the pathogenic processes in these disorders. Accordingly, pharmacological agents that possess anti-inflammatory and anti-oxidant activities, and can reset these defective pathways are increasingly being sought [32,17,102].

    Celastrol has been shown to have a cytoprotective effect in response to stress-induced cell death. Celastrol can induce the expression of various Hsps, for example, Hsp70, Hsp40, and Hsp27, by activation of HSF1 and these Hsps might contribute to its cytoprotective effect [103]. Celastrol’s anti-oxidant attributes can also contribute to its cytoprotective effects. As described under cell signaling, the anti-oxidant response involves transcription factors Nrf-2 and Atf4, and celastrol has been shown to activate both these transcription factors [17]. In one study, celastrol’s cytoprotective effect was shown to be mediated via induction of Hsp32 (also known as heme oxygenase-1; HO-1) [104]. This induction of Hsp32 was mediated via Nrf-2 instead of HSF-1, and Hsp32 in turn inhibited pro-apoptotic JNK. Besides the induction of Hsps mentioned above, inhibition of Hsp90 has been shown to have a therapeutic effect in certain neurodegenerative diseases; the latter effect is attributable to selective proteasomal degradation of Hsp90 client proteins [100]. Importantly, celastrol is an inhibitor of Hsp90 [105,106], and it can modulate several nuclear transcription factors that are Hsp90 clients, including the aryl hydrocarbon receptor (AhR) [105],[106]. The involvement of celastrol-induced inhibition of Hsp90 and its anti-cancer effect is discussed below.”

    [17]: Activation of heat shock and antioxidant responses by the natural product celastrol: transcriptional signatures of a thiol-targeted molecule.
    Trott A et al.

    [32]: Induction of heat shock proteins in differentiated human and rodent neurons by celastrol
    Chow AM, Brown IR

    [98]: The heat-shock proteins.
    Lindquist S, Craig, E A

    [99]: Heat-shock proteins can promote as well as regulate autoimmunity.
    Rajaiah R, Moudgil KD

    [100]: Heat shock proteins in neurodegenerative diseases: pathogenic roles and therapeutic implications.
    Adachi H et al.

    [101]: Heat shock proteins as suppressors of accumulation of toxic prefibrillar intermediates and misfolded proteins in neurodegenerative diseases.
    Arawaka S et al.

    [102]: Modulation of neurodegeneration by molecular chaperones.
    Muchowski PJ et al

    [103]: Celastrols as inducers of the heat shock response and cytoprotection.
    Westerheide SD et al.

    [104]: Celastrol inhibits aminoglycoside-induced ototoxicity via heat shock protein 32.
    Francis SP et al.

    [105]: Heat shock protein 90 inhibitors suppress aryl hydrocarbon receptor-mediated activation of CYP1A1 and CYP1B1 transcription and DNA adduct formation.
    Hughes D et al.

    [106]: Celastrol regulates multiple nuclear transcription factors belonging to HSP90's clients in a dose- and cell type-dependent way.
    Zhang D et al.


    References about prions, or prion-like proteins,
    (I haven't read these; I'm including them in case you want to read them before I do, @Jeremy Fox )

    Molecular Mechanisms in the Pathogenesis of Alzheimer’s disease and Tauopathies-Prion-Like Seeded Aggregation and Phosphorylation
    Masato Hasegawa


    "...evidence for the prion-like mechanism has now spread to the major intracellular abnormal proteins including tau, as nicely reviewed in several articles [20,21,22,23,24].”

    Alzheimer's and Parkinson's diseases: The prion concept in relation to assembled Aβ, tau, and α-synuclein
    Michel Goedert

    Prion-like properties of Tau protein: the importance of extracellular Tau as a therapeutic target
    Brandon B Holmes, Marc I Diamond

    Self-propagation of pathogenic protein aggregates in neurodegenerative diseases
    Mathias Jucker, Lary C Walker

    Biology and genetics of prions causing neurodegeneration
    Stanley B Prusiner

    Prion-like mechanisms in neurodegenerative diseases
    Bess Frost, Marc I Diamond

    Another I found searching for those:
    The role of prion‐like mechanisms in neurodegenerative diseases
    Jaunmuktane, Zane; Brandner, Sebastian

    and I found that Hasegawa paper from this

    Effects of medicinal plants on Alzheimer's disease and memory deficits
    Muhammad Akram, M.D. Ph.D., and Allah Nawaz

    “The main features of AD [Alzheimer’s Disease] are extracellular Aβ [amyloid beta] pathology and neurofibrillary tau pathology (tangles and threads). For 25 years, most studies have been conducted on the Aβ hypothesis of AD pathogenesis and progression (Pimplikar, 2009). But because of failure in clinical trials of Aβ-targeted treatment and the new concept of prion like propagation of intracellular abnormal proteins, tau has come back into the spotlight as a candidate therapeutic target in management of Alzheimer's disease. Tau pathologies are found in a range of neurodegenerative disorders, but extensive analyses of pathological tau in diseased brains has indicated that the abnormal tau protein in each disease is structurally distinct (Avila et al., 2004), supporting the concept that progression of the diverse but characteristic tau pathologies occur through prion like seed dependent aggregation. Therefore, intervention in the conversion of normal tau to abnormal forms and in cell-to-cell transmission of tau may be the key for development of disease modifying treatment of AD and other memory deficits (Hasegawa, 2016)..."
    Last edited: Sep 7, 2021
  17. Dan2

    Dan2 Pedantic schlub

    (I don't have a plan for the organization of these posts; I'm just posting excerpts that seem like it might be relevant as I read through stuff.)

    Role of medicinal plants in neurodegenerative diseases Greeshma Ratheesh et al.

    page 3:

    Celastrol (from Tripterygium wilfordi) [also in Celastrus paniculatus]… in mice...
    - Inhibit pro-inflammatory cytokines production, NO synthase peroxidation of lipid [4]
    - Ability to attenuate loss of dopaminergic neurons & dopamine depletion [30]

    Convolvulus pluricaulis [shankhapushpi] extract...
    - Inhibits the enzymatic activity of acetylcholine esterase
    - Helps in maintaining the level of various mRNA receptors such as M1 receptors, nerve growth-factor tyrosine kinase A receptor, choline acetyl transferase [21]

    page 6:

    ...The leaf extract of Ginkgo biloba contains active ingredient which is known for its antioxidant properties and it has a potent ability to inhibit aggregation of blood platelets… Neuronal apoptosis which is the root cause for neurodegenerative disease is said to be reduced by Ginkgo…
    This Chinese medicine is also known to improve the congnitive function and blood flow [85]. Yao et al. [142] investigated that the leaf extract of Ginkgo has the ability to inhibit the formation of Ab from b amyloid precursor protein in Alzheimer’s disease.”


    Nanoformulations of Herbal Extracts in Treatment of Neurodegenerative Disorders
    Seyed Zachariah Moradi et al.


    "In 2013, a nanodroplet formulation of pomegranate seed oil improved the Creutzfeldt Jacob disease (CJD). The results of the study exhibited that accumulation of scrapie isoform of the prion protein (PrPSc) did not show significant changes but neuronal loss and lipid oxidation relatively decreased, an indicative of neuroprotective function of pomegranate seed oil (Mizrahi et al., 2014). In mouse model of MS, nanodroplet formulation of pomegranate seed oil reduced the disease burden more than free pomegranate seed oil (Binyamin et al., 2015)…"


    Centella asiatica, an Ayurvedic Medicinal Plant, Prevents the Major Neurodegenerative and Neurotoxic Mechanisms Associated with Cognitive Impairment
    Agrawal, Dinesh Chandra et al.

    page 17 of the PDF file

    Gotu kola references table 1.png

    Gotu kola references table 2.png

    Gotu kola references table 3.png

    Gotu kola references table 4.png

    Gotu kola references table 5.png

    "In Sri Lanka it is common knowledge that elephants, who have a reputation of a long life and a great memory, eat the plant... Gotu kola could possibly be confused with... bacopa (Bacopa monnieri), [which is] often sold under the same Ayurvedic name 'brahmi' or 'mandukaparni'. However, gotu kola... is in an entirely different family than bacopa. These two plants [centella and bacopa] are confused however, because, in Ayurveda, they do have similar energetic characteristics... It is used in Ayurveda to soothe mental turbulence. It is one of those herbs that is tri-doshic or brings balance to all three of the Ayurvedic body types, vata, pitta, and kapha."
    Last edited: Sep 8, 2021
  18. Dan2

    Dan2 Pedantic schlub

    Review article: Herbal Medicine for the Treatment of Vascular Dementia: An Overview of Scientific Evidence

    Dennis Chang et al.


    “There are numerous types of dementia, among which vascular dementia (VaD) is the second most common cause after Alzheimer’s disease (AD). Other common forms of dementia include Parkinson’s disease, dementia with Lewy bodies, frontotemporal dementia, Huntington’s disease, and alcoholrelated dementia. VaD is associated with cerebrovascular and cardiovascular diseases and constitutes 10-15% of dementia cases in western countries. In developing countries, the prevalence of VaD is higher, accounting for around 30% of the dementia prevalence, which is partially due to poorer control of cardiovascular risk factors [4]. VaD often coexists with other forms of dementia especially AD. Indeed, postmortem studies reveal that over 40% of clinically diagnosed VaD cases also have AD type of neurodegenerative pathology, which is the most common type of mixed dementia [5].

    There is a long history of herbal medicine use to boost memory and cognitive functions and manage behavioral and psychological symptoms associated with dementia/VaD. Some of the most commonly used and studied herbs include Ginkgo biloba, Huperzia serrata, Curcuma longa, Panax ginseng, Panax notoginseng, Bacopa monnieri, Salvia miltiorrhiza, Crocus sativus, and Camellia sinensis...

    Recognising the lack of therapeutic options for the treatment of VaD, a combined team from the China Academy of Chinese Medical Sciences and Western Sydney University (authors of this article have contributed to the project in various ways) has been working together to develop a standardized complex herbal formulation, SLT (Sailuotong, previously known as WNK) for the treatment of VaD...

    SLT formula consists of specific dosages of standardized Ginkgo biloba (ginkgo), Panax ginseng (ginseng), and Crocus sativus (saffron) extracts, designed for the treatment of VaD. The herbs were selected based on their traditional use and existing clinical and pharmacological evidence (as summarised in Sections 3.1, 3.4, and 3.6). A number of bioactive components have been identified in ginseng, ginkgo, and affron that have a variety of pharmacological effects associated with VaD. The effects of these key bioactive components of SLT formula are summarised in Table 2.”

    Herbs vascuar dementia Chang Table 2 ginseng, ginkgo, saffron.png

    Table 1 – “...mechanisms of action of commonly used herbs for VaD” was rotated, so fixed-rotated PDF attached of Tables 1 and 2

    sample of Table 1:

    Herbs vascular dementia Chang Table 1 example.png

    Attached Files:

    Last edited: Sep 8, 2021
  19. Dan2

    Dan2 Pedantic schlub

    Another message I sent to Jeremy:

    Other stuff that might be helpful about prions
    (I haven't found things specifically about these and prions; something for you to consider while I research the neuroprotective herbs papers more)

    Brown's Gas and molecular hydrogen




    I have one of George Wiseman's AquaCure AC50 Brown's Gas machines, and one of the most noticeable ways I know it's something powerful is I can chain smoke cigarettes and then inhale BG for a few hours and my lungs feel pretty much as good again as if I'd gone hiking instead. It also helps with exercise endurance (exercising while inhaling it is noticeably easier), so I guess it's improving the efficiency of hormetic stress pathways (related to the heat shock protein stuff). The BG and molecular hydrogen machines are usually $1000+ to buy a pre-made good one though, so it's not a very practical recommendation to a lot of people. BG is popular in China as a fuel for welding and other things (drinking bleach, smoking cigarettes, and inhaling welding fuel -- the true American patriot way of medicine) (and I'm not sure if China uses BG or molecular hydrogen more for health, but one or the other is more popular there than in the west), there are molecular hydrogen inhalation cafes in Japan it's so popular there, and there are some papers from those countries about molecular hydrogen or BG for treating SARS-CoV-2 (George Wiseman could point you toward those).

    Milky oats tincture


    "milky oats tincture. Milky oats tincture is the best plant medicine I know of for generally strengthening the nerves (I don't know if it would stimulate neurotrophic factors in the brain though, or if it does, if it'd be much compared to iboga). It was common in the 1800s and early 1900s among not just herbalists but doctors too for neurasthenia and pretty much all nerve weakness conditions, still popular with herbalists nowadays. In herbal medicine it's considered a "trophorestorative", meaning it's more like a food than a medicine that has to be carefully dosed and not used too long. It can take weeks or months to start having a noticeable effect for someone who's very stressed and weak but it's safe to keep using for several months every day. For about a week each year, in the northern US usually early July, oats go through a growing stage where there's milky white sap-like stuff in them, and if you have an herb farmer nearby who grows them you buy those fresh during that week and have it shipped next day, then those can be blended gently with vodka, put in a jar to extract for a few months or more, and the liquid squeezed out of the mixture through cheese cloth to get just the liquid extract. The stuff sold in stores from HerbPharm is a translucent golden color, but if you get it from an herbalist who lets it extract sitting mixed together several months and it's good it'll be an opaque green-ish (maybe more golden, maybe more brown but opaque and milky). That'll be stronger than the HerbPharm kind. Buying it from a store it's about $10/oz; herbalists might charge a little less if you buy 4+ ounces. I make it each year by buying 2 lbs of fresh milky oats and 3 L of vodka (which is just enough for the 2 lbs), that costs me about $120, and I get about a half gallon of finished extract, so $2/oz. Then I put it in the 4 oz tincture bottles with eyedroppers, and dose it putting maybe 1/8-1/4 oz in a shot glass with water and shilajit. It works so well for me I get muscles that look like I've lifted weights some because of the increase of nerve strength supplying the muscle. It's also calming and helps with stress tolerance and sleep."
    Last edited: Sep 8, 2021
  20. Dan2

    Dan2 Pedantic schlub

    I posted about ginkgo being an anticoagulant.
    More about clotting...


    "Immune thrombocytopenia is characterized by both increased platelet destruction and reduced platelet production, and autoantibodies play a pivotal role."


    “...Dr Ochs has found interesting results: that people who have been vaccinated have a very high level of D-dimers, and a lot of physicians have been reporting blood clots forming with AstraZeneca.

    But those blood clots are very unusual. They are not the result of the normal thrombosis process, with all the cascades where you have fibrinogen being transformed, being triggered by the thrombin, into fibrin, and you have that in combination with platelets, and then you have the clots. [Rather,] here, with Covid-19, you have thrombocytopoenia, which means a very low level of platelets.

    So basically, it is coagulations, but that is not induced by the formation of platelets with fibrin as expected. Rather, it is induced by another process, of leukocytes acting with a protein which is on the surface of the endothelial cells of the arteries which is called E-selectin. So it’s the interactions of E-selectin with leukocytes [https://www.sciencedirect.com/science/article/pii/S0006497120342567 The role of leukocytes in thrombosis by Laura L.Swystun, Patricia C. Liaw] that’s forming these clots.

    For example, Dr Ochs prescribes Vitamin C and Ibuprofen to vaccinees who have a high level of D-dimers, a normal leukocyte level with a high level of C-reactive protein (CRP)—which is an indicator of inflammation processes—and a low level of platelets (thrombocytopoenia).

    This is very important, because some physicians have found that if you let the disease progress, some people will have clots forming in the occipital lobe, which is the back part of the brain, and if you give too much heparin or too much aspirin [to them], you will dissolve the clots. But then, if you drop below a certain level, if [the clots] are too freed, you start to have haemorrhaging, because you don’t have enough platelets.

    So it’s a very, very difficult symptom, and a complex disease, that evolves. And you should administer a given medicine at a certain time and at a certain dosage. The same medicine can either save lives or kill. So Ibuprofen, for example, is administered when there is a high level of D-dimers, a normal level of leukocytes, a high level of CRP, and a low level of platelets. In those conditions, you can administer Vitamin C and Ibuprofen, and the patients recover: the D-dimers come back to normal, and the clots disappear.

    So Ibuprofen is a treatment to dissolve the clots, but it should be administered with all the parameters [in place], if you like.”


    More from that article...

    “…whether the CDC or VAERS, all those official sites are reporting blood clots with AstraZeneca, and with Pfizer you have Bell's palsy.

    As Professor Perronne says, you can have myocarditis, especially among the young. That’s what Dr Hervé Seligmann said [Part 1| Part 2 of UK Column interview]: in Israel, they have seen young people getting myocarditis, especially men under 45. As Professor Perronne says, there is a correlation [between age and Covid vaccine mortality]: a lot of old people are dying and not young people.

    Why? Because [the young] have a high level of glutathione, and so they are not dying; they’re protected, compared with the oxidative stress induced by the vaccination [in the elderly].

    I want to emphasise that although I know we’re not talking about treatments, it’s very important [to point out] that people who have intravenous glutathione injections recover very well, because this liberates [them from] the oxidative stress-induced effects.

    The secondary adverse [reactions] are basically cytokine storm, which leads to organ failure. And it can be the heart, the brain, the lung or the kidney. You can have the process [in any of those organs]. The pulmonary disease progresses very rapidly, and when it develops to a certain stage, you have this inflammation process and these clots that then go everywhere, into your organs.

    If they go into your brain, you have [a thrombosis]; if it goes into your heart, of course, and you have all this inflammation process, this leaking of the water into the organ, then the organ [the heart] stops functioning.

    Basically, you’re being shut down; your vital functions are being shut down. And it can be very abrupt and very brutal, and it can all happen in 24 hours.

    And now, people have been discovering that there’s this graphene oxide: a Spanish team has been reporting [https://www.laquintacolumna.net] this graphene oxide [entering] the brain, that is also causing Guillain-Barré syndrome, and that is eating up the myelin, [the coating] on the nerves.

    One of the main [phenomena] being reported is the magnetic test at the site of vaccination: it sticks. People have been measuring these, and there’s an electromagnetic field that is engineered.

    People have been digging into this and have found that there’s a lipid nanoparticle [https://acuitastx.com/technology/lipid-nanoparticles/] that is being manufactured by this company called Aqua Therapeutics, who are providing [it to] Pfizer/BioNTech [and] Moderna.

    They [the lipid nanoparticles used to deliver Covid-19 vaccines] have three components: basically, first, phospholipids (a fat), cholesterol and polyethylene glycol (PEG200) [https://research.thea.ie/bitstream/handle/20.500.12065/3045/Cytotoxicity review priyanka2018.pdf] —but it also contains a ferric oxide [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6215243/} pegylation [polymer attachment] of graphene oxide which is inserted into the phospholipid layer.

    And that goes into your brain. It can cross the blood-brain barrier. Normally, it shouldn’t, but it can go and pass into your brain.”
    Last edited: Dec 13, 2021

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