Thank you, dear Walter! I got--and recovered from--longhaul covid (PASC) which I came down with in early 2020 and managed to clear by mid-2021. I attribute much of my success to being intuitively guided to start taking daily supplements of natural anti-amyloids. I felt huge improvement when I started taking Quercetin, and I also began taking Curcumin, Green Tea Extract, and Resveratrol. I chose to not add any more spike proteins to my body once I experienced hundreds of debilitating symptoms of longhaul covid--sometimes facing family, friends and neighbors demanding I 'protect myself' with the jab. I chose to not go that route, stating I'd already had far more than enough spike protein, thank you very much.
Here's an intriguing research article dating back pre-pandemic, sharing some natural anti-amyloid substances that can be good nutraceuticals we can include in our healthy diets (such as: Curcumin, Green Tea Extract, Quercetin, Resveratrol)
“However, I maintain the COVID-19 and Long COVID are both hyper-accelerated Amyloid Deposition Diseases. I believe the reason Minocycline may be a successful therapeutic for COVID-19 resides in the fact that the drug is also a potent ANTI-AMYLOID!”
. 2014 Jan 3;6(1):2. doi: 10.1186/alzrt232. eCollection 2014.
Photobiomodulation with near infrared light mitigates Alzheimer's disease-related pathology in cerebral cortex - evidence from two transgenic mouse models
Sivaraman Purushothuman 1, Daniel M Johnstone 1, Charith Nandasena 1, John Mitrofanis 2, Jonathan Stone 1
Introduction: Previous work has demonstrated the efficacy of irradiating tissue with red to infrared light in mitigating cerebral pathology and degeneration in animal models of stroke, traumatic brain injury, parkinsonism and Alzheimer's disease (AD). Using mouse models, we explored the neuroprotective effect of near infrared light (NIr) treatment, delivered at an age when substantial pathology is already present in the cerebral cortex.
Methods: We studied two mouse models with AD-related pathologies: the K369I tau transgenic model (K3), engineered to develop neurofibrillary tangles, and the APPswe/PSEN1dE9 transgenic model (APP/PS1), engineered to develop amyloid plaques. Mice were treated with NIr 20 times over a four-week period and histochemistry was used to quantify AD-related pathological hallmarks and other markers of cell damage in the neocortex and hippocampus.
Results: In the K3 mice, NIr treatment was associated with a reduction in hyperphosphorylated tau, neurofibrillary tangles and oxidative stress markers (4-hydroxynonenal and 8-hydroxy-2'-deoxyguanosine) to near wildtype levels in the neocortex and hippocampus, and with a restoration of expression of the mitochondrial marker cytochrome c oxidase in surviving neurons. In the APP/PS1 mice, NIr treatment was associated with a reduction in the size and number of amyloid-β plaques in the neocortex and hippocampus.
Conclusions: Our results, in two transgenic mouse models, suggest that NIr may have potential as an effective, minimally-invasive intervention for mitigating, and even reversing, progressive cerebral degenerations.
Walter do you think natural substances like Serrapeptase or Nattokinase would be helpful? I believe I've read that they both break down fibrin (or something to that effect).
Neuroprotective Effects of Quercetin in Alzheimer’s Disease
"... In addition to its antioxidant properties, it inhibits the fibril formation of amyloid-β proteins, counteracting cell lyses and inflammatory cascade pathways"
Quercetin binding accelerates prion fibrillation into proteinase sensitive and loosely structured amyloids
"...Prion diseases are carried out when accumulated PrPSc cannot be degraded efficiently. In human brain, PrPSc largely accumulates in astrocytes and microglia. The accumulated PrPSc can be cleared by phagocytosis. After PrPSc infection, microglia would enhance activity of phagocytosis by astrocyte-derived milk fat globule-epidermal growth factor 8 to remove PrPSc. When PrPSc clearance by microglia is inefficient, microglia would be activated by accumulated PrPSc and would consequently produce proinflammatory mediators resulting in neuron damage. As we found that quercetin binds to PrP and enhances the proteinase sensitivity of PrP fibrils, quercetin can potentially increase the clearance of PrPSc to prevent microglia activation and following neuroinflammation."
Quercetin Shows the Pharmacological Activity to Simultaneously Downregulate the Inflammatory and Fibrotic Responses to Tissue Injury in Association with its Ability to Target Multi-Kinases
Loving your constant research, dear Walter.
Keep it up!
Thank you, dear Walter! I got--and recovered from--longhaul covid (PASC) which I came down with in early 2020 and managed to clear by mid-2021. I attribute much of my success to being intuitively guided to start taking daily supplements of natural anti-amyloids. I felt huge improvement when I started taking Quercetin, and I also began taking Curcumin, Green Tea Extract, and Resveratrol. I chose to not add any more spike proteins to my body once I experienced hundreds of debilitating symptoms of longhaul covid--sometimes facing family, friends and neighbors demanding I 'protect myself' with the jab. I chose to not go that route, stating I'd already had far more than enough spike protein, thank you very much.
Here's an intriguing research article dating back pre-pandemic, sharing some natural anti-amyloid substances that can be good nutraceuticals we can include in our healthy diets (such as: Curcumin, Green Tea Extract, Quercetin, Resveratrol)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5841551/
“However, I maintain the COVID-19 and Long COVID are both hyper-accelerated Amyloid Deposition Diseases. I believe the reason Minocycline may be a successful therapeutic for COVID-19 resides in the fact that the drug is also a potent ANTI-AMYLOID!”
This should be front page news.
Very interesting
The tetracycline family comes through again. Miracle workers. Thank you, Walter.
Thank you for your brilliant research!
How about photobiomodulation?
Alzheimers Res Ther
. 2014 Jan 3;6(1):2. doi: 10.1186/alzrt232. eCollection 2014.
Photobiomodulation with near infrared light mitigates Alzheimer's disease-related pathology in cerebral cortex - evidence from two transgenic mouse models
Sivaraman Purushothuman 1, Daniel M Johnstone 1, Charith Nandasena 1, John Mitrofanis 2, Jonathan Stone 1
Affiliations expand
PMID: 24387311 PMCID: PMC3978916 DOI: 10.1186/alzrt232
Free PMC article
Abstract
Introduction: Previous work has demonstrated the efficacy of irradiating tissue with red to infrared light in mitigating cerebral pathology and degeneration in animal models of stroke, traumatic brain injury, parkinsonism and Alzheimer's disease (AD). Using mouse models, we explored the neuroprotective effect of near infrared light (NIr) treatment, delivered at an age when substantial pathology is already present in the cerebral cortex.
Methods: We studied two mouse models with AD-related pathologies: the K369I tau transgenic model (K3), engineered to develop neurofibrillary tangles, and the APPswe/PSEN1dE9 transgenic model (APP/PS1), engineered to develop amyloid plaques. Mice were treated with NIr 20 times over a four-week period and histochemistry was used to quantify AD-related pathological hallmarks and other markers of cell damage in the neocortex and hippocampus.
Results: In the K3 mice, NIr treatment was associated with a reduction in hyperphosphorylated tau, neurofibrillary tangles and oxidative stress markers (4-hydroxynonenal and 8-hydroxy-2'-deoxyguanosine) to near wildtype levels in the neocortex and hippocampus, and with a restoration of expression of the mitochondrial marker cytochrome c oxidase in surviving neurons. In the APP/PS1 mice, NIr treatment was associated with a reduction in the size and number of amyloid-β plaques in the neocortex and hippocampus.
Conclusions: Our results, in two transgenic mouse models, suggest that NIr may have potential as an effective, minimally-invasive intervention for mitigating, and even reversing, progressive cerebral degenerations.
This is wild! I had no idea tetracycline antibiotics could have anti-amyloidogenic effects. Hope there is some further digging on this, and soon
Walter do you think natural substances like Serrapeptase or Nattokinase would be helpful? I believe I've read that they both break down fibrin (or something to that effect).
https://www.news-medical.net/news/20210521/Can-SARS-CoV-2-trigger-amyloidosis.aspx
Missing you on twitter, but happy I found you on here
Bromelain also possible?
Has Dr Resia Pretorius tried this yet?
Impact of the Flavonoid Quercetin on β-Amyloid Aggregation Revealed by Intrinsic Fluorescence
https://pubs.acs.org/doi/full/10.1021/acs.jpcb.2c02763
Neuroprotective Effects of Quercetin in Alzheimer’s Disease
"... In addition to its antioxidant properties, it inhibits the fibril formation of amyloid-β proteins, counteracting cell lyses and inflammatory cascade pathways"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7023116/
Quercetin binding accelerates prion fibrillation into proteinase sensitive and loosely structured amyloids
"...Prion diseases are carried out when accumulated PrPSc cannot be degraded efficiently. In human brain, PrPSc largely accumulates in astrocytes and microglia. The accumulated PrPSc can be cleared by phagocytosis. After PrPSc infection, microglia would enhance activity of phagocytosis by astrocyte-derived milk fat globule-epidermal growth factor 8 to remove PrPSc. When PrPSc clearance by microglia is inefficient, microglia would be activated by accumulated PrPSc and would consequently produce proinflammatory mediators resulting in neuron damage. As we found that quercetin binds to PrP and enhances the proteinase sensitivity of PrP fibrils, quercetin can potentially increase the clearance of PrPSc to prevent microglia activation and following neuroinflammation."
https://www.sciencedirect.com/science/article/pii/S0753332222005662
Quercetin inhibits amyloid fibrillation of bovine insulin and destabilizes preformed fibrils
https://www.sciencedirect.com/science/article/abs/pii/S0006291X11019693
A further investigation concerning correlation between anti-fibrotic effect of liposomal quercetin and inflammatory cytokines in pulmonary fibrosis
https://pubmed.ncbi.nlm.nih.gov/20510684/
Anti-fibrosis activity of quercetin attenuates rabbit tracheal stenosis via the TGF-β/AKT/mTOR signaling pathway
https://pubmed.ncbi.nlm.nih.gov/32179074/
The dietary antioxidant quercetin reduces hallmarks of bleomycin-induced lung fibrogenesis in mice
https://bmcpulmmed.biomedcentral.com/articles/10.1186/s12890-020-1142-x
Quercetin Enhances Ligand-induced Apoptosis in Senescent Idiopathic Pulmonary Fibrosis Fibroblasts and Reduces Lung Fibrosis In Vivo
https://www.atsjournals.org/doi/full/10.1165/rcmb.2017-0289OC
Quercetin Shows the Pharmacological Activity to Simultaneously Downregulate the Inflammatory and Fibrotic Responses to Tissue Injury in Association with its Ability to Target Multi-Kinases
https://www.karger.com/Article/Abstract/490417
Doxycycline has been tried in cardiac amyloidosis and it is much more widely available.
I wonder if minocycline is much more effective than doxycycline.
where do you see it is being used in China?