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Prof Trevor Marshall
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As I read the latest article in PLOSone describing how Amyloid-beta protein, the supposed cause of Alzheimers, is an antimicrobial peptide of the innate immune system, related to LL-37 (Cathelicidin), I can't help but reflect how far the science has progressed these last few years.

Here is the Science Daily article:

http://www.sciencedaily.com/releases/2010/03/100302201656.htm

And here is the PLOSone article:

http://tinyurl.com/ydzs53p
"Now we need to figure out what is triggering the innate immune system, particularly as we age, and what genes control A-beta's role in the innate response," says Moir, who is an assistant professor of Neurology at Harvard Medical School (HMS). "If we can identify which pathogens are more likely to trigger A-beta plaque aggregation, we might develop ways to prevent or control that response, for example by immunization."
All you need is Google, Moir... Google (or PubMed)...
 
..Trevor..
 

Bane
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WOW!

The inflammatory aspects of Chlamydia pneumoniae-induced brain infection.

http://www.ncbi.nlm.nih.gov/pubmed/20011709

 

Role of infection in the pathogenesis of Alzheimer's disease: implications for treatment.

http://www.ncbi.nlm.nih.gov/pubmed/19958038

 

Chronic inflammation and amyloidogenesis in Alzheimer's disease -- role of Spirochetes.

http://www.ncbi.nlm.nih.gov/pubmed/18487847

"Recent observations showed that bacteria, including spirochetes contain amyloidogenic proteins and also that Abeta deposition and tau phosphorylation can be induced in or in vivo following exposure to bacteria or LPS. Bacteria or their poorly degradable debris are powerful inflammatory cytokine inducers, activate complement, affect vascular permeability, generate nitric oxide and free radicals, induce apoptosis and are amyloidogenic. All these processes are involved in the pathogenesis of AD. Old and new observations, reviewed here, indicate that to consider the possibility that bacteria, including several types of spirochetes highly prevalent in the population at large or their persisting debris may initiate cascade of events leading to chronic inflammation and amyloid deposition in AD is important, as appropriate antibacterial and antiinflammatory therapy would be available to prevent dementia."


Reduction of vitamin D hormone receptor mRNA levels in Alzheimer as compared to Huntington hippocampus: correlation with calbindin-28k mRNA levels.

http://www.ncbi.nlm.nih.gov/pubmed/1317496

"These results show that in Alzheimer hippocampal CA1 cells, VDR mRNA pool size is downregulated"

 

Amyloid-beta peptide degradation in cell cultures by mycoplasma contaminants

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2527505/

Guess they wanna protect themself?

Last edited on Wed Mar 3rd, 2010 02:44 by Bane

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This makes me think about the origin of Prion proteins. :)

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Enhancing the Innate Immune System may help to protect brain agains Alzheimer.

http://www.sciencedaily.com/releases/2005/06/050612112041.htm

was published already in 2005.

Alex

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1alpha,25-dihydroxyvitamin D3 interacts with curcuminoids to stimulate amyloid-beta clearance by macrophages of Alzheimer's disease patients.

http://www.ncbi.nlm.nih.gov/pubmed/19433889

"In silico, 1,25D3 showed preferential binding to the genomic pocket of the vitamin D receptor, whereas bisdemethoxycurcumin showed preference for the non-genomic pocket."

Comment from Trevor: These researchers have no credibility. They have not published a credible location or function of this "non-genomic binding pocket" and previous publications have dealt with the benefits of high-dose Vitamin D. Circumin actually binds well into the normal ligand binding domain.

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Wow.. indeed!  Thanks Dr Marshall for keeping us so well informed on these papers and new findings!

This interesting finding, that is totally consistent with Dr Marshall's research, hopefully means that perhaps mainstream medicine is getting closer to figuring out that PATHOGENS cause many of these neurodegenerative diseases!

It is not a large leap of faith, even for some of these stubborn researchers to make, to conclude that: if pathogens trigger the AMP's that then cause a neurodegenerative disease like Alzheimer's... the same mechanism could be the causal factor in many other neurodegenerative diseases... like ALS!!!

And it is tragic that these researchers are not building on the revolutionary findings of Dr Marshall along these same lines of research.  Like Trevor said ... all they need is Google for crying out loud! 

I certainly will pass this information on to my neurologist and get her opinion. 

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Microglia Activation and Anti-inflammatory Regulation in Alzheimer's Disease.

http://www.ncbi.nlm.nih.gov/pubmed/20195797

http://en.wikipedia.org/wiki/Microglia

Inflammatory regulators, including endogenous anti-inflammatory systems, can down-regulate inflammation thus providing negative feedback. Chronic inflammation can result from imbalance between levels of inflammatory mediators and regulators during immune responses. As a consequence, there are heightened inflammatory responses and irreversible tissue damage associated with many age-related chronic diseases. Alzheimer's disease (AD) brain is marked by prominent inflammatory features, in which microglial activation is the driving force for the elaboration of an inflammatory cascade. How the regulation of inflammation loses its effectiveness during AD pathogenesis remains largely unclear. In this article, we will first review current knowledge of microglial activation and its association with AD pathology. We then discuss four examples of anti-inflammatory systems that could play a role in regulating microglial activation: CD200/CD200 receptor, vitamin D receptor, peroxisome proliferator-activated receptors, and soluble receptor for advanced glycation end products. Through this, we hope to illustrate the diverse aspects of inflammatory regulatory systems in brain and neurodegenerative diseases such as AD. We also propose the importance of neuronal defense systems, because they are part of the integral inflammatory and anti-inflammatory systems. Augmenting the anti-inflammatory defenses of neurons can be included in the strategy for restoration of balanced immune responses during aging and neurodegenerative diseases.

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Independent component analysis of Alzheimer's DNA microarray gene expression data

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2646728/

Significant genes found by ICA
 
"Even though the immune system tends to work less effectively in older adults than in younger ones, the elderly are prone to neuroinflammation. In fact, even though recent studies have indicated that certain aspects of the inflammatory response may have therapeutic potential [22-24], neuroinflammation is commonly believed to be a culprit in AD pathogenesis. Associated with this robust inflammatory response is the extracellular deposition of amyloid β-protein (Aβ) [25] that together are the characteristic pathological features of AD. are To validate the strong link between neuroinflammation and AD, we found that many inflammation-related genes are highly expressed, such as AMIGO2, BTG1, CD24, CD44, CDC42EP4, IFITM1, IFITM2, IRF7, FI44L, IL4R, IRAK1, NFKBIA, as Table 1 shows."
 
"Our ICA selected results exhibited NF-κB (NFKBIA) at a high expression in severe AD (see Table 1). NF-κB plays a key role in regulating the immune response to infection. Consistent with this role, incorrect regulation of NF-κB has been linked to cancer, inflammatory and autoimmune diseases, septic shock, viral infection, and improper immune development. NF-κB has also been implicated in processes of synaptic plasticity and memory. The NF-κB activation provides the potential link between inflammation and hyperplasia."

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Use of angiotensin receptor blockers and risk of dementia in a predominantly male population: prospective cohort analysis.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2806632/

Objective To investigate whether angiotensin receptor blockers protect against Alzheimer’s disease and dementia or reduce the progression of both diseases.

Conclusions Angiotensin receptor blockers are associated with a significant reduction in the incidence and progression of Alzheimer’s disease and dementia compared with angiotensin converting enzyme inhibitors or other cardiovascular drugs in a predominantly male population.




Last edited on Thu Mar 4th, 2010 11:55 by Bane

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Trevor said:
Circumin actually binds well into the normal ligand binding domain.
Do you know does it act as a VDR antagonist or if it could possibly activate the VDR?


Prof Trevor Marshall
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I docked circumin in the VDR and it looked as though it could be an agonist - it certainly had high affinity for the binding pocket. I didn't have the time to do the molecular dynamics necessary to make sure it is an agonist. It didn't seem as active as Olmesartan, though.

..trevor..

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Curcumin: a novel nutritionally derived ligand of the vitamin D receptor with implications for colon cancer chemoprevention

http://tinyurl.com/yg9gtmw

Prof Trevor Marshall
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The 'magic' of Olmesartan is not only its action in the VDR, but in a host of other receptors (and non-signaling proteins) as well. The sum total of which induces recovery from chronic disease :)
 

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So I wonder, why Amyloid-beta protein fails to eliminate infection ? It is not mis-folded protein after-all ?

Bane
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wrotek wrote: So I wonder, why Amyloid-beta protein fails to eliminate infection ? It is not mis-folded protein after-all ?

Maybe the Microglia loses track of the amount of amyloid-beta present in the brain because of failing TLR2. Which in turn also means that the Microglia can't mount a complete attack against pathogens???

 

 

Activation of Toll-like Receptor 2 on Microglia Promotes Cell Uptake of Alzheimer Disease-associated Amyloid β Peptide

http://www.jbc.org/content/281/6/3651.long

"The human G-protein-coupled formyl peptide receptor-like 1 (FPRL1) and its mouse homologue mFPR2 mediate the chemotactic activity of a variety of polypeptides associated with inflammation and bacterial infection, including the 42-amino acid form of amyloid β peptide (Aβ42), a pathogenic factor in Alzheimer disease. Because mFPR2 was inducible in mouse microglial cells by proinflammatory stimulants, such as bacterial lipopolysaccharide, a ligand for the Toll-like receptor 4 (TLR4), we investigated the role of TLR2 in the regulation of mFPR2. We found that a TLR2 agonist, peptidoglycan (PGN) derived from Gram-positive bacterium Staphylococcus aureus, induced considerable mFpr2 mRNA expression in a mouse microglial cell line and primary microglial cells. This was associated with a markedly increased chemotaxis of the cells in response to mFPR2 agonist peptides. In addition, activation of TLR2 markedly enhanced mFPR2-mediated uptake of Aβ42 by microglia."

 
http://en.wikipedia.org/wiki/Formyl_peptide_receptor

"The formyl peptide receptors (FPR) are a members of a class of G protein-coupled receptors involved in chemotaxis.[1][2] These receptors where originally identified by their ability to bind N-formyl peptides such as N-formylmethionine produced by the degradation of either bacterial or host cells.[3][4] Hence formyl peptide receptors are involved in mediating immune cell response to infection."


 

Toll-Like Receptor 2 Acts as a Natural Innate Immune Receptor to Clear Amyloid β1–42 and Delay the Cognitive Decline in a Mouse Model of Alzheimer's Disease

http://www.jneurosci.org/cgi/content/full/28/22/5784

"TLR2 deficiency accelerated spatial and contextual memory impairments, which correlated with increased levels of Aβ1–42 and transforming growth factor β1 in the brain."

 

Fibrillar Amyloid-β Peptides Activate Microglia via TLR2: Implications for Alzheimer’s Disease

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2701549/

"The present study underlines the importance of TLR2 in mediating Aβ peptide-induced activation of microglia. Fibrillar Aβ1–42 peptides induced the expression of inducible NO synthase, proinflammatory cytokines (TNF-α, IL-1β, and IL-6), and integrin markers (CD11b, CD11c, and CD68) in mouse primary microglia and BV-2 microglial cells. However, either antisense knockdown of TLR2 or functional blocking Abs against TLR2 suppressed Aβ1–42-induced expression of proinflammatory molecules and integrin markers in microglia. Aβ1–42 peptides were also unable to induce the expression of proinflammatory molecules and increase the expression of CD11b in microglia isolated from TLR2−/− mice. Finally, the inability of Aβ1–42 peptides to induce the expression of inducible NO synthase and to stimulate the expression of CD11b in vivo in the cortex of TLR2−/− mice highlights the importance of TLR2 in Aβ-induced microglial activation. In addition, ligation of TLR2 alone was also sufficient to induce microglial activation."

 

 

 


Last edited on Fri Mar 5th, 2010 10:24 by Bane

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The Lipoprotein Receptor LR11 Regulates Amyloid  Production and Amyloid Precursor Protein Traffic in Endosomal Compartments

http://www.jneurosci.org/cgi/content/full/26/5/1596

"Here, we show neuronal expression of the lipoprotein receptor LR11 in control brain in regions vulnerable to AD neuropathology and marked reduction of LR11 expression in these regions in AD brains before cell death." 

 

Last edited on Fri Mar 5th, 2010 07:20 by Bane

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Could Amyloid A be Antimicrobial??? http://en.wikipedia.org/wiki/Amyloid

 

Serum amyloid A regulates granulomatous inflammation in sarcoidosis through Toll-like receptor-2.

http://www.ncbi.nlm.nih.gov/pubmed/19910611

"Serum amyloid A activated NF-kappaB in Toll-like receptor-2-expressing human cell lines; regulated experimental Th1-mediated granulomatous inflammation through IFN-gamma, tumor necrosis factor, IL-10, and Toll-like receptor-2; and stimulated production of tumor necrosis factor, IL-10, and IL-18 in lung cells from patients with sarcoidosis, effects inhibited by blocking Toll-like receptor-2."

 

Serum amyloid A protein binds to outer membrane protein A of gram-negative bacteria.

http://www.jbc.org/content/280/19/18562.long

"Further studies will be needed to determine whether this interaction has a role in innate immunity."

 

Serum amyloid A is an innate immune opsonin for Gram-negative bacteria

http://bloodjournal.hematologylibrary.org/cgi/content/full/108/5/1751

"In this report we have shown that SAA not only binds to many Gram-negative bacteria but, when it has done so, can induce a number of responses from both macrophages and neutrophils, which are responsible for rapid killing of invading bacterial pathogens."

 

Comparison of serum amyloid A concentrations with those of C-reactive protein and procalcitonin in diagnosis and follow-up of neonatal sepsis in premature infants.

http://www.ncbi.nlm.nih.gov/pubmed/19078972

"SAA is an accurate and reliable marker for diagnosis and follow-up of neonatal sepsis. It is especially useful at the onset of inflammation for rapid diagnosis of neonatal sepsis and can be safely and accurately used in combination with other sepsis markers such as CRP and PCT in diagnosis and follow-up of neonatal sepsis in preterm infants."

 

Human Serum Amyloid A Protein Inhibits Hepatitis C Virus Entry into Cells

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1900255/

"Serum amyloid A (SAA) is an acute-phase protein induced by a variety of inflammatory stimuli, including bacterial and viral infections. SAA was recently found to function as an opsonin for gram-negative bacteria."

 

Serum amyloid A mediates human neutrophil production of reactive oxygen species through a receptor independent of formyl peptide receptor like-1

http://www.jleukbio.org/cgi/content/full/83/2/245

"Serum amyloid A (SAA) is one of the acute-phase reactants, a group of plasma proteins that increases immensely in concentration during microbial infections and inflammatory conditions, and a close relationship between SAA levels and disease activity in rheumatoid arthritis (RA) has been observed.

 

Mechanisms of the Hepatic Acute-Phase Response during Bacterial Pneumonia

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2687329/

"During bacterial pneumonia, APPs correlate with the severity of disease, serve as biomarkers, and are functionally significant."



 

Last edited on Wed Mar 10th, 2010 02:45 by Bane

wrotek
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Coffee increases SAA  http://findarticles.com/p/articles/mi_m0887/is_11_23/ai_n7578036/ Compared with coffee nondrinkers, men who consumed >200 mL coffee/d had 50% higher IL-6,30% higher CRP, 12% higher SAA, and 28% higher TNF- [alpha] concentrations and 3% higher WBC counts (all: P < 0.05). Women who consumed >200 mL coffee/d had 54% higher IL-6, 38% higher CRP, 28% higher SAA, and 28% higher TNF- [alpha] concentrations and 4% higher WBC counts (all: P < 0.05) than did non coffee drinkers.

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wrotek wrote: Coffee increases SAA  http://findarticles.com/p/articles/mi_m0887/is_11_23/ai_n7578036/ Compared with coffee nondrinkers, men who consumed >200 mL coffee/d had 50% higher IL-6,30% higher CRP, 12% higher SAA, and 28% higher TNF- [alpha] concentrations and 3% higher WBC counts (all: P < 0.05). Women who consumed >200 mL coffee/d had 54% higher IL-6, 38% higher CRP, 28% higher SAA, and 28% higher TNF- [alpha] concentrations and 4% higher WBC counts (all: P < 0.05) than did non coffee drinkers.

 

I guess the question is, were they drinking coffee for it's immunosuppressive effects? Meaning the reason they had higher inflammatory markers wasn't because of drinking coffee, but that people that drink a lot of coffee happen to do so because their prone to TH1, maybe??;)

Associations between coffee consumption and inflammatory markers in healthy persons: the ATTICA study

http://www.ajcn.org/cgi/content/full/80/4/862#SEC2

Last edited on Wed Mar 10th, 2010 11:03 by Bane

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http://iospress.metapress.com/content/k457101686r62685/
1α,25-dihydroxyvitamin D_{3} Interacts with Curcuminoids to Stimulate Amyloid-β Clearance by Macrophages of Alzheimer's Disease Patients I wonder what expresses beta amyloid, since vdr is blocked, it is something else right  ?

Bane, I think that coffee is immunosupressive and immune stimulating at the same time. There is coffeeforum where ppl express their experience with drinking coffee and when they quit, pain decreases in arthritics for example. But what good is inflammation if it is not directed into real threat, it only damages your body.

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wrotek wrote:
I wonder what expresses beta amyloid, since vdr is blocked, it is something else right?

This video makes a suggestion that might shed some light.
http://www.scivee.tv/node/7266

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Good find, Lottis :)
 

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Found this today on amylase-A and sarcoidosis.  How do I make sense of it?

http://www.medicalnewstoday.com/articles/187493.php

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It says that Sarcoidosis is a Th1 disease, that TLR2 is important, and Nuclear factor kappaB. All of which we already knew.

But it also implies that Amyloid-A, like Amyloid-beta in Alzheimers, is performing an antimicrobial function (based on the cytokines it induces). Which is interesting indeed.

So basically this is nothing really new, but confirmation of what we had already figured out :)

I am in Ljubljana, and very busy, but hopefully others can fill in the detail for you :)
 

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Very interesting, since coffee also raises it.

Dr Marshall, is this protein expressed by VDR ?

wrotek
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No, it cannot be expressed by vdr since it raises when VDR is blocked :)

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Long-term TNF-alpha blockade in patients with amyloid A amyloidosis complicating rheumatic diseases.

http://www.ncbi.nlm.nih.gov/pubmed/20399323

Most adverse events were similar in both groups, although the number of infections was 3 times higher in amyloid A amyloidosis cases. CONCLUSION: Anti-tumor necrosis factor drugs are effective in treating amyloid A amyloidosis, although they might increase the risk of infection.

 

The acute phase reactant response to respiratory infection with Chlamydia pneumoniae: Implications for the pathogenesis of atherosclerosis.

http://www.ncbi.nlm.nih.gov/pubmed/20417302

A single intranasal inoculation stimulated statistically significant increases in the plasma levels of IL-2, IL-5, IL-6, IL-10, IL-12, GM-CSF, IFN-gamma, and serum amyloid A but not TNF-alpha, IL-1beta, IL-4 and serum amyloid P.

 

Hepatic gene expression changes in pigs experimentally infected with the lung pathogen Actinobacillus pleuropneumoniae as analysed with an innate immunity focused microarray.

http://www.ncbi.nlm.nih.gov/pubmed/19710094

The microarray analysis of liver tissue established that 51 genes were differentially expressed. A large group of these genes encoded proteins involved in the acute phase response, including serum amyloid A, C-reactive protein, fibrinogen, haptoglobin and tumor necrosis factor-alpha the expression of which were all found to be up-regulated and glutathione S-transferase, transthyretin, transferrin and albumin which were down-regulated.

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http://www.physorg.com/news192255677.html

Spouses of dementia sufferers have a 6-fold increased risk of dementia onset

 

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That last would be a good study to add to this KB article:
   http://mpkb.org/home/pathogenesis/familial_aggregation

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Infection Defense May Spur Alzheimer’s
 
http://www.nytimes.com/2010/03/09/health/09alzh.html?ref=science

Diesel

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Hello Diesel,

this thread has started with this!

Take care,
Titta

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Hi all,

Just ran into this on sciencedaily:

Harmful Amyloid Interferes With Trash Pickup for Cells in Alzheimer's Disease

http://www.sciencedaily.com/releases/2010/09/100908094924.htm

So: microbiota-> inflammation -> amyloid beta -> proteasome hi-jacked ?

Best, Frans

Lottis
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Yes :) maybe

    1- microbiota

    2- amyloid

    3- interferes with the processing of other proteins by competing for access

    4- inhibits the proteasome.

Yang and postdoc Xiaobei Zhao showed that amyloid actually doesn't harm the proteasome.
Instead it interferes with the processing of other proteins by competing for access, they report in a forthcoming issue of the journal ACS Chemical Neuroscience.


And again I am tempted to give a tip about this paper on how amyloid like struktures might build up in the brain.
http://www.scivee.tv/node/7266

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...and Chlamydia again, at least they look for that....
Immunohistological detection of Chlamydia pneumoniae in the Alzheimer's disease brainhttp://www.biomedcentral.com/1471-2202/11/121/abstract

They have used anitbodies against this species.
I wonder when they systemically use their devices to look futher on.........probably first when they think further on......:(

Titta


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I do not know what happened.....when I wrote it it looked better. So another try.



http://www.biomedcentral.com/1471-2202/11/121/abstract



http://www.biomedcentral.com/content/pdf/1471-2202-11-121.pdf


Titta

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Alzheimer's Disease: Are Plaques and Tangles a Symptom, Not the Cause?

http://www.sciencedaily.com/releases/2010/12/101214181932.htm

The theory -- which holds that the beta-amyloid peptide is the key to the initiation and progression of the disease -- has had significant appeal as the peptide is the main ingredient of the disease-related plaques that are common in the brains of those affected.

Indeed, this persistent correlation has led researchers to spend many years and many millions of dollars looking for ways to prevent plaques as a way of treating, curing or preventing Alzheimer's. In recent years, however, dozens of human clinical trials based on this theory have failed.

Herrup, the chair of the Department of Cell Biology and Neuroscience at Rutgers University, suggests an alternative perspective, which he has set forth in a paper published December 14 in the Journal of Neuroscience. Pointing out that age is the most important risk factor in the disease, he suggests a new hypothesis with age as the starting point.

Age slows the brain's agility and blunts its responses to change; on their own, however, age-related changes lead only to a slow 'natural' decline in cognitive function, Herrup says. He posits that while these changes might increase one's risk of the Alzheimer's, they do not cause the disease.

Herrup believes three three key steps that are needed for an individual to progress from this natural path to the full spectrum of Alzheimer's clinical symptoms: an initiating injury that is probably vascular in nature; an inflammatory response that is both chronic and unique to Alzheimer's; and a cellular change of state, a one-way cell biological door that permanently alters the physiology of neurons and several other cell types in the Alzheimer's disease brain.

"The initiating injury might trigger a protective response in the brain cells," Herrup said. "But the real problem is that in the elderly the response doesn't know when to quit. It continues even after the injury itself subsides. In the end, the real damage is done by the persistence of the response and not by the injury, itself."

Herrup hopes his new theory will stimulate discussion and open the way to new experimental and diagnostic advances. "This new hypothesis, for example, emphasizes the value of anti-inflammatory approaches to the prevention of Alzheimer's disease," Herrup says.

He concedes that the individual components of the model aren't entirely new, but points out that by rearranging their order and shifting their priority, his view has enormous implications for modern Alzheimer's research.

"My hypothesis implies that beta-amyloid aggregation is not a central part of the biology of Alzheimer's disease," Herrup says. "It predicts that one can have plaques without having Alzheimer's and that one can have Alzheimer's without having plaques.

"Researchers should be cautious about following up these predictions, but since we've gone about as far as we can with our current hypothesis, we may have reached a point where too much caution is ill-advised. It's time to re-imagine Alzheimer's disease, so we can think creatively about treating it."

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A Novel Perspective for Alzheimer's Disease: Vitamin D Receptor Suppression by Amyloid-β and Preventing the Amyloid-β Induced Alterations by Vitamin D in Cortical Neurons

http://iospress.metapress.com/content/mg838747x7844354/



Amyloid-β (Aβ) is the core component of amyloid plaques of Alzheimer's disease (AD). The effects of Aβ include damage to neuronal plasma membrane, disruption of Ca2+ homeostasis, and alterations of neurotrophic factor levels. The aim of this study was to determine the effects of Aβ treatment on vitamin D receptor (VDR), L-type voltage sensitive calcium channels A1C (LVSCC A1C), NGF, and observing the effects of vitamin D treatment on Aβ induced alterations in primary cortical neurons. As to the latter, we aimed to test the suggested neuroprotective role of vitamin D as a neglected neurosteroid. The expressions of VDR and LVSCC A1C were studied with qRT-PCR and Western blotting. NGF and cytotoxicity levels were determined by ELISA. Apoptotic cell death was investigated with caspase-3 protein expression by Western blotting. Our results showed that the Aβ triggers neurodegeneration not only by inducing LVSCC A1C expression and NGF levels and but also by dramatically suppressing VDR expression. Administration of vitamin D to this model protected neurons by preventing cytotoxicity and apoptosis, and also by downregulating LVSCC A1C and upregulating VDR. Additionally, vitamin D brought NGF expression to a state of equilibrium and did not show its apoptosis inducing effects. Consequently, prevention of Aβ toxicity which was one of the major component of AD type pathology by vitamin D treatment and understanding how Aβ effects vitamin D related pathways, might open up new frontiers in clarifying molecular mechanisms of neurodegeneration and provide basis for novel perspectives in both preventing and treating AD.

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The Effects of Vitamin D Receptor Silencing on the Expression of LVSCC-A1C and LVSCC-A1D and the Release of NGF in Cortical Neurons.

http://www.ncbi.nlm.nih.gov/pubmed/21408608

CONCLUSIONS/SIGNIFICANCE: Our results indicate that suppression of VDR disrupts LVSCC-A1C and NGF production. In addition, when VDR is suppressed, neurons could be vulnerable to aging and neurodegeneration, and when combined with Aβ toxicity, it is possible to explain some of the events that occur during neurodegeneration.

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http://www.msnbc.msn.com/id/41971124/ns/health-alzheimers_disease/

Alzheimers may start in the liver.

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"The protein that forms plaques in the brains of people with Alzheimer's disease may have its origins in the liver, a new study in mice suggests. The researchers said that targeting the liver's production of this protein, called beta amyloid, may be a new way to treat Alzheimer's."

However, if beta amyloid is one of the body's anti-microbials (as I have read previously in this thread) then you are simply reducing the anti-microbial activity in the brain???

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I also wonder if the drug they used actually does not get past the blood-brain barrier!  This study seems very flawed.

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I think its interesting from the perspective that alzheimers appears to be very much a systemic disease, much like the rest of the chronic diseases (diabetes, RA, etc.)

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It all just points to how integrated the ENTIRE human body truly IS vs the brain being seen as a separate entity. 

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Vitamin D And Transporter Proteins Hold Key To Prevent Alzheimer's Disease

http://www.medicalnewstoday.com/articles/230829.php

http://www.fluidsbarrierscns.com/content/pdf/2045-8118-8-20.pdf

Conclusions:
Active form of vitamin D, 1,25(OH)2D3, appears to enhance brain-to-blood Ab(1-40) efflux transport at the BBB through both genomic and non-genomic actions. Compounds activating these pathways may be candidate agents for modulating Ab(1-40) elimination at the BBB.


Prof Tetsuya Terasaki said:

"Vitamin D appears to increase transport of amyloid beta across the blood brain barrier (BBB) by regulating protein expression, via the vitamin D receptor, and also by regulating cell signaling via the MEK pathway. These results lead the way towards new therapeutic targets in the search for prevention of Alzheimer's disease."

 

Prof Gerald Silverberg concluded:

"While increased production of transporter proteins at the blood CSF barrier may help amyloid beta removal from the older brain, production of these proteins eventually fails. This failure may be an important event in brain function as we age and for people with Alzheimer's disease."

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WOW! I wonder if these transporter protein pathways are the same in humans as in mice (the study was done on mice). If so, this is just more validation and corroboration of the MP's positive impact on the brain. I wonder if Olmesartan has the same "non-genomic" effects as 1,25D in the study (it should have the same "genomic" effects by activating the VDR - right?).

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Two quotes buried in the fulltext are interesting:

"Indeed, mice exhibited reduced body weight and abnormal behavior from day 4 during treatment with 1,25(OH)2D3 (1 µg/day, data not shown)."

"Paricalcitol, a vitamin D analogue, did not significantly enhance [125I]hAß(1-40) elimination from mouse brain (data not shown)"

So the situation is infinitely more complex than these investigators were capable of comprehending. Additionally, they made a common mistake in Molecular Biology, far too high a concentration of 1,25-D was used (hence the 'abnormal behavior' of the poor mice, I guess).

In any case, we have early data from Germany that Dementia patients respond to the MP, so maybe these researchers are close to a real solution. Which IMO is not, as they suggested in their paper, supplementing with Vitamin D in order to prevent Alzheimers :X :X
 

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New paper about spirochetal microbiome in Alzheimer disease

Abstract
http://www.jneuroinflammation.com/content/8/1/90/abstract

full paper
http://www.jneuroinflammation.com/content/pdf/1742-2094-8-90.pdf

Bar graphs,in the end of this paper show
that they have found other spirochaetes to be more prevalent, borrelia wasn't dominant.

Video of oral spirochetes
http://www.youtube.com/watch?v=oHETTEXpwu4

Lol is dental plaque a bacterial biofilm ?

Last edited on Sat Aug 6th, 2011 23:09 by wrotek

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Good find Wrotek! 

This is maybe more evidence that most of these neurological diseases of unknown etiology like ALS are caused by undetected pathogens.  I wonder if all my sexual dalliances in my younger years, and their were a few, caused a type of latent syphilis infection that is now manifesting decades later in ALS?  This idea dawned on me when I read about clusters of ALS in professional sports players ... and we know sports stars are pretty promiscuous. 

I remember Lida Mattman the famous bacteriologist thought that ALS was a form of late stage Lyme disease as she detected spirochetes in ALL the ALS patients she tested.  But I think Dr Marshall feels the spirochetes are just a part of the overall microbiota and would be found in most chronically ill patients.  I'll be curious on Dr Marshall's take on this new paper. 

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Chronic Inflammation and Amyloidogenesis in Alzheimer’s Disease: Putative Role of Bacterial Peptidoglycan, a Potent Inflammatory and Amyloidogenic Factor

http://www.lymenet.de/shgs/dietmars/ChronicInflammation.pdf

Summary
Glycosaminoglycans (GAGs), which occur in most organisms from bacteria to vertebrates, appear to be present
in all amyloid deposits, and may play an essential role in the pathogenesis of amyloidosis. It is well established
that senile plaques are the sites of chronic inflammation, but the factor activating the complement remain
unknown. Here, we analyzed whether the amyloidogenic bacterial peptidoglycan, a potent activator of complement
and of the GAG metabolic system is present in senile plaques. Neuropathologically analyzed 54 autopsied
brains were investigated. The 54 cases consisted of 32 Alzheimer's disease (AD) cases with severe AD-type
changes, 12 cases with low number of senile plaques and 10 cases without any AD-type changes. We have
found that in the 32 AD cases with high number of plaques and in the 12 cases with low number of plaques,
bacterial peptidoglycan was immunolocalized to senile plaques and on serial sections co-localized with betaamyloid
protein.
Bacterial peptidoglycan has a variety of biological actions in mammals. It is an inflammatory cytokine inducer,
activates complement of the classic pathway, affects vascular permeability, generates nitric oxide, induces
proteoglycan synthesis and apoptosis, in addition is amyloidogenic. It is well established that all these processes
are implicated in AD, suggesting that bacteria or bacterial debris may be one among probably several factors
which may trigger the cascade of events leading to chronic inflammation and amyloid deposition in AD.

Key words: Alzheimer’s disease, bacteria, bacterial peptidoglycan, beta-amyloid, chronic inflammation,


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Thanks Gene!  Another good paper that implicates bacterial involvement in AD.

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I couldn’t help but wonder why no one had thought to look at the role of inflammation in Alzheimer’s disease.

I began to think about IL-1 and inflammation as part of a cytokine feedback cycle, with the initiating insult coming from a variety of sources: genetic predisposition (e.g., inheritance of APOE ε4 allele or alleles), repeated injury (head trauma or epilepsy), or infection (HIV), and the wear and tear of time. Although inflammatory mechanisms probably help to clear damaged cells in limited situations, in the long term, chronic microglial activation and elevation of IL-1 becomes cyclical, leading to more neuronal damage and death and, as a consequence, more microglial activation. And this is followed by the production of βAPP, more microglial activation, further production of hyperphosphorylated tau and βAPP, favoring formation of neurofibrillary tangles, beta amyloid plaques, and Lewy bodies.
In neuroinflammation we had a viable suspect—and a potential therapeutic target—which everyone seemed to be ignoring.

http://the-scientist.com/2011/08/31/what-causes-alzheimer%E2%80%99s/

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Good article.

And here Chlamydia has been found in the Brain of Alzheimer Patients.


Immunohistological detection of Chlamydia pneumoniae in the Alzheimer's disease brain.
http://www.ncbi.nlm.nih.gov/pubmed/20863379


Anti-C. pneumoniae antibodies, obtained commercially, identified both typical intracellular and atypical extracellular C. pneumoniae antigens in frontal and temporal cortices of the AD brain. C. pneumoniae, amyloid deposits, and neurofibrillary tangles were present in the same regions of the brain in apposition to one another. Although additional studies are required to conclusively characterize the nature of Chlamydial immunoreactivity in the AD brain, these results further implicate C. pneumoniae infection with the pathogenesis of Alzheimer's disease.

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wrotek wrote: New paper about spirochetal microbiome in Alzheimer disease 

"spirochetes were observed in the brain in more than 90% of AD cases"

Well, I guess these observations were made after the death of the patients, as you don't normally take samples of brain from living people, and Dr. Marshall says that the CWD organisms reconstitute themselves into cell walled bacteria after death.  So, I guess that is why we have spirochetes in the brain in this study and not CWD bacteria.

Cynthia


 

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Sorry if this report has been posted already. I scrolled through the thread but could not comprehend much of it. This article was simplified enough that I could follow it:

http://www.foxnews.com/health/2011/10/04/can-catch-alzheimers-disease/

"For the current study, researchers injected the brain tissue of an Alzheimer's patient into mice and compared the results to those from injected tissue of a control without the disease.

"None of the mice injected with the control showed symptoms of Alzheimer's, while all of those injected with Alzheimer's brain extracts developed plaques and other brain changes associated with the disease.

"Researchers said the findings open the possibility that sporadic Alzheimer's cases may arise from infectious processes."

(Emphases mine.) It sounds like progress to me! :)

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Good One!!

Those researchers think that it opens some possibilities eh?

They should come to the Marshall Protocol website. Have a look around. See whats going on... and maybe get up to speed.

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I have received a reply from a dentist
http://www.youtube.com/watch?v=oHETTEXpwu4&feature=email&email=comment_reply_received

He has very interesting imput about oraz spirochetes ( post from under the movie and in commentaries).


These clusters of spirochetes are a strange phenomena. We do not know what this behavior is about. These spirochetes are microscopically indistinguishable from syphilis or lyme disease spirochetes. Oral spirochetes have been found in the brains of alzheimer's patients. We believe that oral spirochetes are the primary injurious agent in two other chronic diseases that plague man, heart disease and diabetes. These things breed by the trillions in the gingival sulcus and invade into the body by millions moving via the de-epitheliazed gingival sulcus into the blood stream then into cells found along the blood stream. Primarily the endothelial cells lining blood vessels, and the Islets of langerhans cells in the pancreas..
We have not seen anyone with heart disease or diabetes who are not infected with oral spirochetes. Recent papers have proven the alzeheimers plaques are created by these spirochetes which breed in the crevice between the tooth and the gum and under plaque bacteria. The use of tooth cleaning agents will not remove these spirochetes. The only effective methods we have found is Dakins solution. Vigorous rinses for at least two minutes with Dakins or Dakins in a WaterPic®. The use of the Dakins which is a 20:1 dilution of clorox bleach is by far the most effective technique for killing spirochetes in between the teeth as well as the more accessible areas. Tooth pastes are good for cleaning teeth! But this is a different problem entirely. Spirochetes form spores which require daily disinfection of the crevice between the tooth and gum. The only thing which will dissolve plaque(the vegetative bacteria which cause tooth decay) off a tooth surface without friction is clorox diluted in water at a 20:1 water/clorox ratio. This material is cheap effective and absolutely works but no one can sell it to you for a high price, so not one cent of marketing money will be spent to educate the public! This is tragic in the extreme. We have research grade microscopes to show the spirochetes. The only effective techniques involve using bactericidal materials such as clorox and high concentrations of baking soda... Other things such as hydrogen peroxide, povidone iodine, chlorhexidiene, and table salt have drawbacks in daily use. Tooth pastes are valuable in stopping and treating tooth decay, but flossing and brushing with tooth paste or oral rinses with items such as OTC mouth washes, will not guarantee a kill, and in comparison to clorox are very expensive over a lifetime. Patients wonder if clorox is toxic. While it tastes terrible, it is harmless when diluted to 0.3 percent, that is a 20:1 dilution of 6% clorox. Clorox turns into
table salt in the stomach if swallowed. There will be some initial stinging of the skin in the mouth when first used! That goes away when the skin heals after a few uses. Use at night before going to bed and do not rinse the mouth after. If irritation develops move to mornings. Use at night when saliva flow shuts down will keep the material killing for a longer time when not rinsed out.. Finally, we have tried them all and brushing with copious amounts of baking soda forcing it into the gums and in between the teeth one time daily and then using a WaterPic® with the dilute clorox solution will give the best results. What are those results? Absolutely no leakage of the seal where the tooth come out of the skin. The Gum is a specialized tissue designed to seal the skeleton where it come out thru the skin. The teeth are the only part of the skeleton which is out side the skin... So it cannot heal itself. Use of a good fluoride tooth paste at night will do much to stop tooth decay. Never eating sugar or carbohydrates between meals will assure no tooth decay in those with normal saliva.


Could it be that bacteria that live on teeth in biofilm colonies, like tooth stone/plaque, can reinfect the body over and over again causing chronic illness ? Because Immune system can't get to them there.

Last edited on Wed Oct 26th, 2011 03:07 by wrotek

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Why can't the immune system get to them there? Teeth are porous, at the level of the molecule...
 

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Really ? I did not know that.
Actually that would make sense. My mother developed paradontosis in a very quick period of time, after my grandmother died. From emotional stress.

Last edited on Wed Oct 26th, 2011 08:26 by wrotek

Russ
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Would the Clorox mouth rinse this dentist suggests be a good oral hygiene practice?

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We suggest that mouthwash using Cetylpyridinium Chloride works well, and that Baking Soda/Hydrogen Peroxide also seem effective.

http://mpkb.org/home/othertreatments/mouthwash
 

wrotek
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It is called Dakins sollution, used in dentistry when working on root canal treatment
http://doreen.mkbmemorial.com/NF/dakins.pdf

Well, this dentist ciaims it is safe, u can read it in his long post i quoted above.

Last edited on Wed Oct 26th, 2011 09:19 by wrotek

Cairo123
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Another interesting presentation along the same line.

http://www.youtube.com/watch?v=l3AKA46fbRw&feature=related

Last edited on Wed Oct 26th, 2011 10:49 by Cairo123

wrotek
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Yes i saw this movie before, but forgot about it.
It would be wonderful if special mouth washing could improve condition of patients.

But the movie says that husband had more oral spirochetes but less symptoms

Last edited on Wed Oct 26th, 2011 12:17 by wrotek

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But the movie says that husband had more oral spirochetes but less symptoms

That could be caused by what they considered to be 'symptoms'.  A slow growth of arterial plaque was probably not going to be noticed as a symptom.  We can assume that the husband and wife started with different metabiomes, so the varied results is to be expected. 

Nothing is linear in the TH1 situation, and not much is in a healthy body.

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I have tried Clorox, DISGUSTING :(
But i decreased the dose to just a little and I spread it with toothpaste, also I do not breathe through mouth, only nose, it seems to irritate lungs but i am not sure.

Dr Marshall, dentist advises Baking Soda as well.
You have mentioned Baking Soda/Hydrogen Peroxide .
How to use this combination ?

Last edited on Sat Oct 29th, 2011 22:32 by wrotek

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Wrotek,
What I have done is to use the baking soda for brushing and follow with dilute hydrogen peroxide as a mouth wash, similar to the clorox regimen.

I am afraid I am at some risk of becoming eccentric.:cool:
Best regards,
Mike
PS Too late...

wrotek
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Mvanwink5 did this approach help You with anything ? Teeth pain etc ?

Eccentrics are interesting people :)
But why teeth washing should be considered eccentric ?

Last edited on Sun Oct 30th, 2011 02:20 by wrotek

Russ
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wrotek wrote: Dr Marshall, dentist advises Baking Soda as well.
You have mentioned Baking Soda/Hydrogen Peroxide .
How to use this combination ?

Wrotek, there are some recipes at this link for homemade toothpaste and mouthwash that incorporate baking soda and hydrogen peroxide.

http://jennifer.hubpages.com/hub/Make_Your_Own_and_Save_-_Toothpaste_and_Mouthwash

Last edited on Sun Oct 30th, 2011 03:01 by Russ

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Great, thanks Russ.

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wrotek,
I use just baking soda for brushing and use the "Sonicare" brand vibrating tooth brush, and always floss. The brush has made a big difference over the last 15-20 years. I avoid commercial abrasive pastes. I used to use peroxide mixed with the grocery brand mouth wash, mixed, but have switched to the dilute clorox, at least for the present, as a test. I really want to keep my teeth and gums healthy. So far things are going fine, but I don't take my teeth for granted. It is a whole lot of trouble when care is not consistent, from my point of view, especially given the extra MP treatment avoidance needs.

Certain details such as consistent good dental care is worth the trouble.
Best regards,
Mike

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There are several commercial preparations of baking soda & peroxide available here in the USA.

http://www.colgate.com/app/Colgate/US/OC/Products/Toothpastes/ColgateBakingSodaAndPeroxide.cvsp

http://www.crest.com/crest-products/whitening-tartar-protection.aspx

These are made by large multi-national firms, so they might be available near you, or certainly by mail order.

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To all,

There is a commercial mouthwash that is based on chlorine dioxide in solution.  It is called CloSYS.  I have used it a while and it has a bearable taste.  It also has a mint flavoring in the box for optional use.  Pricey though.

Lou

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Mvanwink5 a tip for You, breath through nose while cloroxing Your teeth. And dont wash mouth with water after but this is mentioned under the youtube spirochete alzheimer video.

I just don't know how long should one use it.

Last edited on Thu Nov 3rd, 2011 08:54 by wrotek

wrotek
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Hmm could removing oral spirochetes help with systemic infection ? That is a question that interests me.

Here is a little clue

Skin problems disappeared after treatment of oral spirochetosis. The question is what skin, was it also somewhere further from the teeth ? Was it acne and just acne ? I always had an acne, even on my scalp i do have acne.

http://www.youtube.com/watch?v=xqXblUDan0k
http://www.youtube.com/watch?v=KJ3W7F4haLg

My poor grandmother, beside her osteoporosis and heart problems, she also had trigeminal neuralgia and half her teeth were removed(she had nerve blocks etc). If I just knew what i know today.

Later my mother, after grandmother died, had paradontosis and she could lose many teeth but some injections helped her - prescribed by very good dental surgeon.

I do have teeth pain(4 wisdom teeth removed surgically from gums) and TMJ aswell, it was my early symptom, just after back nerve pain.

Even if immune system can get to these spirochetes on teeth, there is not reason why we should not help the immune system fighting them. Especially because teeth are uncovered and accessible.

And there is another thing, patients are sensitive to oral epinephrine in dental anesthetic, right ? :) That is reeely interesting

Last edited on Mon Nov 7th, 2011 23:05 by wrotek

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wrotek,
I have been adjusting my view on innate immune system assistance to include the mouthwash regimen. It is simple, low tech, and not expensive. In a way, one could almost put daily dental care into the category of good first aide, and for people who have or have borderline periodontal disease, it is first aide care.

I really consider this topic essential for an MPr's expedited recovery. Thanks for opening my eyes on its importance (hat tip to Marion for her insights also). I find that I am not always the quickest off the mark and slow to see things, so I really appreciate the help here.

Best regards,
Mike

wrotek
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Yes, I am very excited by this topic also :)

But why would spirochetes like teeth so much ?

Last edited on Mon Nov 7th, 2011 23:10 by wrotek

Russ
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wrotek wrote: Yes, I am very excited by this topic also :)

But why would spirochetes like teeth so much ?

Maybe it is easier to build biofilms on teeth than other parts of the body?  Also the mouth area gives them easy access to food and nutrients.  The average kid who drinks milk, juice, and soda all day long is constantly filling his mouth with sugar to feed the bugs and vitamin D to suppress the immune system. 

mvanwink5
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Why the mouth? Reminds me of a 6 foot diameter patch of lavender colored wild flowers that grew in just this one roadside place and flowered there every year. I always wondered why there and not elsewhere? Why my left shoulder and not my right shoulder? Or right hand versus my left hand. These bugs are just picky eaters is all I can say.
Best regards,
Mike

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About a year ago I started to add a small amount of my disinfectant mouthwash (about 1:10 ratio) to the salt solution I use as a sinus neti pot flush.  I also started to use mucienex.  Over a period of about a month, my sinus congestion significantly improved.  I also noted that I no longer get the occasional bloody discharge when blowing my nose.

I think the idea of eliminating bugs from the mouth and sinus is a very good idea.  This may not work for everyone and I suggest caution at first if you try this.  As I remember it took awhile to get use to it. 

Gene

wrotek
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This could be potential treatment for acne, which I had for years, and i never used to brush teeth up/down (gum pockets) , only sideways . It hurts a little, but i will do it, to make mouthwash reach there.

P.s. I got used to clorox, it is not so bad after a while.

Last edited on Wed Nov 9th, 2011 00:32 by wrotek

wrotek
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I remember Dr Marshall discussed cigarette microbiome and human lung diseases - COPD, asthma .

I wonder, if mouth microbiome can contribute to these diseases.

Can mictobiota, or antigens, be inhaled from the mouth to the lungs ? And perpetuate inflammation ?

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Wrotek,
Any method that reduces bug colonies that does not involve immune suppressive chemicals is positive in my book and these ideas being suggested here sound good to me and I plan to incorporate them.

I want to point out something though. In the power plant where I worked for 30 years as an engineer, we had cooling water pipes carrying 115 F to 120 F water. It may be hard to imagine, but bacteria would form slime colonies on the inside of these pipes and eat right though the metal. So, we used biocides and a host of chemicals to try to control them. Even with the harshest chemicals and most potent industrial antibiotics, these slime colonies could not be eliminated. Eventually we had to start a project to replace the pipes.

I related the above industrial experience to give a reference point for what we are up against. The one thing we do have that the steel pipes did not and that is the innate immune system with its hundreds of different antimicrobial peptides.

Best regards,
Mike

wrotek
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Mvanwink5, have You tried ozone for pipes ?
It is used to clean air conditioning in cars.

You can even build an ozone machine Yourself, and close it while being turned on, with air conditioning turned on as well, inside the car and it does the job.

:) Little trick, if You don't want to pay for this in Auto-service.

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Wrotek,
I don't know what the engineers are doing now for their cooling water treatment as I retired a bit ago. They have snake oil like sales people that consult and make money from chemical sales, just like doctors have drug sales people that visit. I know that ozone has become more popular for pool water treatment. I do like your suggestion for the car. For making an ozonator, do you perhaps have a link you favor?

Best regards,
Mike

wrotek
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I dont have a link, but there is plenty ozonators available on the internet to buy.

You just need one that makes ozone from air, not from pure oxygen source.

My friend is electronic hobbyist so he can make his own ozonator.

Last edited on Fri Nov 11th, 2011 04:38 by wrotek

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wrotek wrote:
I remember Dr Marshall discussed cigarette microbiome and human lung diseases - COPD, asthma .

I wonder, if mouth microbiome can contribute to these diseases.

Can mictobiota, or antigens, be inhaled from the mouth to the lungs ? And perpetuate inflammation ?


My chest says yes, after having bad tooth pulled. From the lining of the mouth they can go to The upper gi as well.

Here ibuprofen helps Alzheimer knock out mice and humans
http://neuro.cjb.net/content/20/15/5709.full

It doesnt explain much but i prefer ibuprofeb over Tylenol. Palliation?

Last edited on Tue Nov 22nd, 2011 21:17 by jlunn247

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NSAIDs actually inhibit immune tolerance/suppression. Prostanoids are highly immuno-suppressive, in particular PGE2, which is also associated with pain perception, fever and tissue healing. NSAIDs inhibit the cyclo-oxygenases and in this manner limit the conversion of arachidonic acid into PGE2. Thus, NSAIDs can alleviate pain and fever but can also lead to further joint destruction, for example. On the other hand, they are associated with a lower of rate of alzheimers and a strikingly reduced rate of cancers, particularly the COX2 inhibitors. The smoker/celebrex user lung cancer rates are super low compared to non-COX inhibitor users.

The angiotensin receptors increase the expression of COX-2. I suspect this is one of the pathways that the ARBs work on, amongst others, which lead to a reduction in cancers and neurodegenerative disease.

Last edited on Wed Nov 23rd, 2011 11:13 by Phillyguy

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Do You think some people get darker teeth from minocycline, because they have bacteria in their mouth, that minocycline attacks ?

Some kind of reaction ?

Last edited on Thu Nov 24th, 2011 11:51 by wrotek

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wrotek wrote: Do You think some people get darker teeth from minocycline, because they have bacteria in the mouth, that minocycline attacks ?
Could be, but remember that minocycline has profound biochemical effects on the human body, including its actions as a PXR receptor agonist. So one of these more direct actions might be in play, who knows?
 

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Dr William D. Nordquist directed me to this website for my answers...

http://lifeguardyourhealth.com/

Many interesting materials, including videos, about mouth microbiome.

For example Helicobacter Pylori, beside spirochetes.
http://www.youtube.com/watch?v=IOalajsPBX8&feature=channel_video_title


It is a long website :) Just starting to read.

He also said he has written two books on the subject

The Stealth Killer: Is Oral Spirochetosis the Missing Link in the Dental and Heart Disease Labyrinth?

The Silent Saboteurs: Unmasking Our Own Oral Spirochetes as the Key to Saving Trillions in Health Care Costs


Dr Marshall, but many drugs target PXR, right ? Do they also make teeth darker ?

Last edited on Thu Nov 24th, 2011 12:03 by wrotek

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Excellent find wrotek.  It looks like folks are more and more finding a relationship between pathogens and chronic inflamatory disease.  I wonder when the tipping point will be reached to where the common therapy becomes immunostimulation versus immuno suppression.  I particularly noted the segment near the bottom connecting depression to an increase in inflamatory cytokines.   

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Yes depression, and generally feeling bad from cytokines really interests me.

Because if one has wide body inflammation it is like having source of their pain spread throughout the whole body.


I wonder, if cytokines can act stimulatory on sympathetic nervous system. Can they make you focus and alert and not sleepy ?

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Here is a recipe for making your own dental bleach as prescribed by Dr. Clark.
Recommended after tooth extractions to kill clostridium:

http://livingnetwork.co.za/drclarknetwork/recipes/dental-bleach-lugols-iodine/


She also suggests adding oregano oil to baking soda for toothpaste.




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Sean, I don't agree with the need for any mouthwash more potent that the Hydrogen Peroxide-Baking Soda combination. Cetylpyridinium Chloride 0.07% is a less aggressive, but acceptable substitute (eg Crest 'Pro-Health' mouthwash).

I would actively discourage members from following the formulation suggested in the Dr Clark link (above) :)
 

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I understand.  I was actually trying to nudge folks away from using clorox.  

Last edited on Sun Dec 4th, 2011 20:29 by seanc

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The Alzheimer's disease-associated beta-amyloid protein is an antimicrobial peptide with a redox mechanism of action

by Soscia, Stephanie J., Ph.D., BOSTON UNIVERSITY, 2011, 151 pages; 3463283

The ?-amyloid protein (A?) is believed to be a key factor underlying Alzheimer's disease (AD) pathology. The physiochemical and cytotoxic activity of A? has been the subject of intense study for over 25 years. However, few studies have addressed the normal role of A? in cell biology. At present A? is most often characterized as an accidental pathological product of catabolism with no normal function. Here, for the first time, we provide strong evidence that A? normally functions as an antimicrobial peptide (AMP) of the innate immune system. A? has potent antimicrobial activity equivalent to, and in some cases greater than, that of the archetypical human AMP LL-37. Furthermore, AD brain homogenates show increased A?-mediated AMP activity compared to age-matched controls.

A?/copper complexes that catalytically generate reactive oxygen species (ROS) cause lipid peroxidation in vivo . To date, A?-mediated ROS generation has been considered a pathological and likely accidental consequence of the peptide's metal binding. However, the second part of this study suggests ROS generated by A?/Cu may serve to increase the peptide's antimicrobial action. A? causes lipid peroxidation in microbial cells and induces a protective response in Staphylococcus aureus that is a marker for oxidative stress. Furthermore, catalase deficient S. aureus mutants are more sensitive to A? compared to wild type bacteria. These findings raise the possibility that while A? redox activity is cytotoxic, this action may normally be directed against pathogens and play a protective role. Selecting for redox active AMPs may be a novel strategy for enhancing the efficacy of these agents in therapeutic settings.

The final part of this study aims to analyze the toxicity profiles of soluble, covalently cross-linked A? protein species (CAPS). CAPS, particularly dimeric forms, are emerging as key pathological agents in AD pathology and appear to have increased redox activity. Methods for generating and purifying synthetic CAPS were developed. The synthetic CAPS were then used to study A?-mediated membrane disruption. The data suggest membrane permeabilization by CAPS is strongly modulated by the composition of the lipid bilayer and the peptide's access to metals. Future research will determine if redox-mediated oligomerization increases AMP activity.

--------------------------------------------------------------

Note:  ARBs block the expression of beta amyloid in mice.  The ATII receptor probably has a role in innate immunity.

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Phillyguy wrote: Note:  ARBs block the expression of beta amyloid in mice.  The ATII receptor probably has a role in innate immunity.

Wouldn't that be a bad thing, if beta amyloid is an anti-microbial peptide and part of the innate immune system?

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Russ,

if -- if -- if - and mice.

Too many variables to answer your question definitively :) In addition, Mice may well have totally different transcription of the Amyloid-beta genes. We just don't know.

It is good to see this type of research being done, however :) Gives me a nice warm feeling in this Holiday season...
 
 
 
(Thanks Phillyguy :) )

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Autophagy and the VDR:

http://www.cell.com/cell-host-microbe/abstract/S1931-3128%2809%2900283-2

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This 10 minutes TED talk is from 2008, but gives us more good arguments why the world must try the MP

Biochemist Gregory Petsko makes a convincing argument that, in the next 50 years, we'll see an epidemic of neurological diseases, such as Alzheimer's, as the world population ages. His solution: more research into the brain and its functions.

http://www.ted.com/talks/gregory_petsko_on_the_coming_neurological_epidemic.html

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I went to a conference at the Salk a couple of years ago. It focused on how the brain works - there were lots of videos of poor animals running around with wires into their brains. Ugggh. In any case, it turns out the brain responds most to waves, ergo, it probably communicates with waves, alternating current, not direct ON/OFF currents like Medicine currently thinks. Neurons are viewed as if they were something like Digital computers, but they are more like analog computers, with a complexity beyond anything we could devise to measure them, I think.

So the scientists can research as much as they like - they have a life's vocation ahead of them. It is most unlikely the brain will ever be decoded beyond the outer layers, those which fire and directly stimulate muscles. The cognition and memory layers are hidden deep below that superficial, but easily observed, functionality. And it is those layers which make us human.
 

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Lottis, IMO the neuro epidemic has kicked in well and truly, which is why I no longer necessarily vote for age and experience in elections: age and experience make you truly dangerous if you are going nuts like many dictators have done

Trevor, the downside of my broadband is that (short of big house modifications) the gadget is less than 2m from my bed. Fortunate not to spend as much "down time" as many of the old hands here, but the penny dropped late that I really do not know if it is retarding my recovery.
I now switch of the transmitter thingy in the evening and switch it back on in the morning for phone calls. We did not replace the last Microwave oven either

Last edited on Sat Jan 21st, 2012 13:06 by Sallie Q

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Sallie, I have seen nothing which would make me think that WiFi energy, or the leakage from a microwave oven, is going to retard healing.

A few members are especially sensitive to radiation, but that is a symptom, and would not retard healing, as far as I can see :)

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Thankyou for passing on your knowledge of physics
I know my older son is hugely sensitive to radiation and perhaps does not talk about it much because can be regarded as a delusion :(
I know he is healthier and happier after moving from a flat near high voltage transmitter, which of course, is a different kettle than ovens and domestic communications.
Sallie Q

btw
Alzheimer's disease is forecast to affect nearly 75,000 New Zealanders by 2026http://www.stuff.co.nz/the-press/news/6296012/Kiwis-at-edge-of-brain-study

A blood test aimed at the early detection of Alzheimer's disease is being developed by researchers at the University of Otago.but does not say what they are looking out for, only " Plasma molecules would then be screened using biochemical and molecular techniques"
The team leader, Professor Cliff Abrahams, said treatments for the disease would probably be developed in the near future,
watch that space, any of you kiwis skilled in PR??

Last edited on Sat Jan 21st, 2012 14:46 by Sallie Q

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Sallie Q wrote:
I know my older son is hugely sensitive to radiation and perhaps does not talk about it much because can be regarded as a delusion :(
I know he is healthier and happier after moving from a flat near high voltage transmitter, which of course, is a different kettle than ovens and domestic communications.

This page lists as symptoms of EM sensitivity a lot of th1 diseases:

http://emfsensitivity.com/

This is an article from last year about the conductivity of biofilms:

http://physicsworld.com/cws/article/news/46821

So it seems possible that th1 disease could make people sensitive to EM radiation.  I have noticed feeling rough myself after a couple of hours sitting next to a wifi transmitter although I don't know that I would be able to pick it out in a double blind study.

I know somebody who has what is almost certainly a th1 disease who is so electrosensitive that she moved from her flat in Paris to a farmhouse in a hamlet in the countryside outside Toulouse, I have tried to tell her to look for the underlying issue in her health but as yet to no avail.

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Yes, it is the underlying issues which need to be addressed. Generally there is an underlying Th1 inflammatory problem which has not yet been recognized.

Only after one's brain starts to really heal, is it possible to understand the profound nature of the delusions which a Th1 patient has to deal with. I look back on so many over my life.

There is no doubt that super-high frequency waves (upwards of 50GHz) have the potential to alter the way that biological molecules function. Not only do my in-silico emulations indicate atomic dynamics at those frequencies, but there have been numerous reports of problems with those ultra-high frequencies. Many molecules have resonances up above 50GHz.

Do any molecules have resonances at WiFi frequencies? Probably, but WiFi energy is low, and does not penetrate the skin very far. Additionally, they would need to be larger molecules, which are already subject to many other forces in-vivo, and have thus developed a resistance to damage.

..Trevor..
 

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kudos for the interest in electrical functions.
Didn't Tesla have a "vision" of how his ac motor worked?
What a nut job a real "Einstein". :D

So also cell towers cannot hurt brain function ever?
Even if turned up to 11?

Last edited on Sun Jan 22nd, 2012 13:52 by jlunn247

jlunn247
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NickBowler wrote:
Autophagy and the VDR:

http://www.cell.com/cell-host-microbe/abstract/S1931-3128%2809%2900283-2


Jees try breaking down Cathelicidin and understanding the connections between anti microbial cells as they mature.
hows that riddle go? "What walks in the morning on all 4 legs? in the afternoon ect.

bzzt there goes another synapse connection, hope it was in piano lessons. And not where i remember good stuff. I dont care if i remember some music.

Last edited on Sun Jan 22nd, 2012 14:34 by jlunn247

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jlunn247 wrote: So also cell towers cannot hurt brain function ever? Even if turned up to 11?
Well, when I was at High School I was a Ham Radio operator (VK5ZTM) using 'ultra-high frequencies' (576MHz) so I designed some "turned up to 11" transmitters for setting the distance records (one of which stands to this day LOL).

I was already very sick by then, and standing right in front of these large antenna arrays didn't seem to make me any worse... the shadows were already on my lung X-rays. Yes, there was some heat, and yes, you could strike a 40 Watt fluorescent tube from the energy, and hold it lighted in your hand.

So I am  hard to convince that RF energy is so causative of harm. All that I suffered from was from misfiring neurons, later in life :)

I was going to say that my brain went progressively wrong later in life, but who but a deranged lunatic would light a 40W bulb from RF in their hands and stand in an RF field to show it off :)

..trevor..
 

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who but a deranged lunatic would light a 40W bulb from RF in their hands and stand in an RF field to show it off :)
You WERE a daredevil in your younger days!!  :D

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looking in to photon output of diff elements.
Does that possibly affect internal vit d production?
vicious circle of mal absorption in diet as well?
And or also "In physics, absorption of electromagnetic radiation is the way by which the energy of a photon is taken up by matter, typically the electrons of an atom."
We dont all share the same body chemistry some bodies are cokes others are pepsis. Although we probably all taste the same.

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http://www.reproduction-online.org/content/14/3/355.short
Darn ageing process are not sperm the shortest living human cells?
Thought it was about more than just a tanning booth experiment.
:)

Last edited on Mon Jan 23rd, 2012 07:31 by jlunn247

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Hi,

This study is getting alot of attention today:

http://news.yahoo.com/mouse-study-suggests-alzheimers-spreads-brain-infection-190410018.html

THURSDAY, Feb. 2 (HealthDay News) -- Alzheimer's disease appears to spread through the brain, traveling from neuron to neuron in much the same way that an infection or cancer moves through the body, new research with mice suggests.

Scientists reported Thursday that their work indicates that abnormal tau protein -- already identified in the brains of those with Alzheimer's -- starts in one region of the brain and spreads along linked cellular circuits.

Identification of this tau pathway could influence the direction of future research and treatment of the mind-wasting disease, the study authors and other experts said.

"This opens up a whole new area of biology that has direct relevance for Alzheimer's disease. We now have a whole new set of targets that perhaps we can develop drugs for," said study lead author Karen Duff, a professor of pathology at Columbia University's Taub Institute for Research on Alzheimer's Disease and the Aging Brain...

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Rosie,
It sounds like another dead-end to me. Just like the prion diseases. Remember the prions that were supposed to be at the root of neuromuscular diseases?

It is very difficult to do experiments in animals and tissue culture, and to be able to extrapolate them to the clinic. I go to a lot of conferences, meet a lot of these researchers.

My assessment is that these researchers drew an incorrect conclusion from an inadequate model. It is up to them to show that their discovery can induce recovery in human beings. I don't give them a chance in Hades of being successful at that.

But then, here at the MP site, we have seen stuff these researchers could only dream of. Since they clearly haven't Googled, I guess dreaming is their best bet :) :)

Thanks for the link, though :) :)

..Trevor..
 

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Toxins from diseased brain cells make diseases of the brain even worse

http://news.ku.dk/all_news/2012/2012.2/toxins_from_brain_cells/

"If the NADHP Oxidase does not work in the macrophages, patients become so ill that they die".

This is because if the macrophages do not remove foreign bodies, the immune system decides instead to encapsulate viruses, bacteria, fungus and parasites in special shells. These granulomata accumulate in the body until they kill the patient before the latter has reached the age of thirty. This disease is known as Chronic granulomatous disease.


"Things have to be in balance", says Associate Professor Vilhardt. "In neurodegenerative diseases such as Alzheimer's and dementia the level of free radicals in the brain is out of balance: it is too high"

Last edited on Thu Feb 23rd, 2012 08:22 by Bane

wrotek
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Still, there is a belief that free radicals are bad and antioxidants are sold... If not for free radicals, immune cells would not clean our bodies, kill pathogens.

Very nice article, beside h202 body also produces ozone... That was discovered relatively recently.

Last edited on Thu Feb 23rd, 2012 16:43 by wrotek

wrotek
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Here is an interesting enzyme - indoleamine 2 3-dioxygenase, it supresses intracellular pathogens and produces ozone and hydrogen peroxide, to kill pathogens, from tryptophan  (could the lack of tryptophan caused by this process,from which serotonin is produced, result in a depression ? ) and from other indoleamines.

Some articles about it

http://www.ncbi.nlm.nih.gov/pubmed/1907934
http://bloodjournal.hematologylibrary.org/content/113/11/2394.full

Infections Early studies have demonstrated a role for IDO in the inhibition of viruses and intracellular pathogens, such as Toxoplasma gondii and Chlamydia psittaci.44,45 Moreover, the activity of IDO on the induction of a specific inhibitory environment during chronic infection has recently been revisited. In particular, IFN-dependent expression of IDO by different cell subsets, including DCs, is often seen during infections and represents an innate mechanism of pathogen elimination.46 Listeria monocytogenes infection of the mouse placenta, which leads to granulomatous disease, results in the induction of IDO, which, in turn, plays a role in counteracting the bacterial infection while maintaining a barrier to T cells to prevent fetal rejection.47 Similar observations were made with other granulomatous infections caused by Bartonella henselae and Mycobacterium tuberculosis, where IDO-expressing APCs prevent T cell–mediated granuloma destruction and subsequent pathogen dissemination.48 More recently, a critical role for IDO has been found in the generation of immunologic resistance to fungal infections, including candidiasis and aspergillosis. In this setting, DC expression of IDO, tryptophan catabolites, and Tregs all cooperate in regulating the fine balance between inflammation, which is required for protection, especially at the early pathogen encounter phase, and tolerance, which is necessary to down-modulate potentially overwhelming inflammatory responses.41,49


I have heard about this enzyme from Foreydoon Batmanghelidj ,MD, and his hydration protocol. He says that this pathway is suppressed, when there is dehydration in the body.




Last edited on Fri Feb 24th, 2012 05:15 by wrotek

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UCLA scientists pinpoint how vitamin D may help clear amyloid plaques found in Alzheimer's

http://www.eurekalert.org/pub_releases/2012-03/uoc--usp030612.php

A team of academic researchers has identified the intracellular mechanisms regulated by vitamin D3 that may help the body clear the brain of amyloid beta, the main component of plaques associated with Alzheimer's disease.

Published in the March 6 issue of the Journal of Alzheimer's Disease, the early findings show that vitamin D3 may activate key genes and cellular signaling networks to help stimulate the immune system to clear the amyloid-beta protein.


Previous laboratory work by the team demonstrated that specific types of immune cells in Alzheimer's patients may respond to therapy with vitamin D3 and curcumin, a chemical found in turmeric spice, by stimulating the innate immune system to clear amyloid beta. But the researchers didn't know how it worked.


"This new study helped clarify the key mechanisms involved, which will help us better understand the usefulness of vitamin D3 and curcumin as possible therapies for Alzheimer's disease," said study author Dr. Milan Fiala, a researcher at the David Geffen School of Medicine at UCLA and the Veterans Affairs Greater Los Angeles Healthcare System.


For the study, scientists drew blood samples from Alzheimer's patients and healthy controls and then isolated critical immune cells from the blood called macrophages, which are responsible for gobbling up amyloid beta and other waste products in the brain and body.


The team incubated the immune cells overnight with amyloid beta. An active form of vitamin D3 called 1a,25–dihydroxyvitamin D3, which is made in the body by enzymatic conversion in the liver and kidneys, was added to some of the cells to gauge the effect it had on amyloid beta absorption.


Previous work by the team, based on the function of Alzheimer's patients' macrophages, showed that there are at least two types of patients and macrophages: Type I macrophages are improved by addition of 1a,25–dihydroxyvitamin D3 and curcuminoids (a synthetic form of curcumin), while Type II macrophages are improved only by adding 1a,25–dihydroxyvitamin D3.


Researchers found that in both Type I and Type II macrophages, the added 1a,25–dihydroxyvitamin D3 played a key role in opening a specific chloride channel called "chloride channel 3 (CLC3)," which is important in supporting the uptake of amyloid beta through the process known as phagocytosis. Curcuminoids activated this chloride channel only in Type I macrophages.


The scientists also found that 1a,25–dihydroxyvitamin D3 strongly helped trigger the genetic transcription of the chloride channel and the receptor for 1a,25–dihydroxyvitamin D3 in Type II macrophages. Transcription is the first step leading to gene expression.


The mechanisms behind the effects of 1a,25–dihydroxyvitamin D3 on phagocytosis were complex and dependent on calcium and signaling by the "MAPK" pathway, which helps communicate a signal from the vitamin D3 receptor located on the surface of a cell to the DNA in the cell's nucleus.


The pivotal effect of 1a,25–dihydroxyvitamin D3 was shown in a collaboration between Dr. Patrick R. Griffin from the Scripps Research Institute and Dr. Mathew T. Mizwicki from UC Riverside. They utilized a technique based on mass spectrometry, which showed that 1a,25–dihydroxyvitamin D3 stabilized many more critical sites on the vitamin D receptor than did the curcuminoids.


"Our findings demonstrate that active forms of vitamin D3 may be an important regulator of immune activities of macrophages in helping to clear amyloid plaques by directly regulating the expression of genes, as well as the structural physical workings of the cells," said study author Mizwicki, who was an assistant research biochemist in the department of biochemistry at UC Riverside when the study was conducted.


According to the team, one of the next stages of research would be a clinical trial with vitamin D3 to assess the impact on Alzheimer's disease patients. Previous studies by other teams have shown that a low serum level of 25–hydroxyvitamin D3 may be associated with cognitive decline. It is too early to recommend a definitive dosage of vitamin D3 to help with Alzheimer's disease and brain health, the researchers said. They add that ongoing studies are showing that vitamin D3 may be beneficial in reducing the incidence of a growing number of human diseases.



Curcumin: a novel nutritionally derived ligand of the vitamin D receptor with implications for colon cancer chemoprevention.

http://www.ncbi.nlm.nih.gov/pubmed/20153625


Vitamin D receptor: molecular signaling and actions of nutritional ligands in disease prevention.

http://www.ncbi.nlm.nih.gov/pubmed/18844852


Last edited on Tue Mar 6th, 2012 09:11 by Bane

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I have chatted casually with Pat Griffin several times, and I can't recall one time he has asked whether I might be able to suggest possible pitfalls in their use of in-vitro analysis of in-vivo disease activity. Usually all these guys want to talk about is the weather :) :)

Nor do any of them Google for ideas, or pick up the telephone to chat about their work. It is just mind-boggling the gap which has opened up between these scientific research groups at the very time they could be closely coordinating their activities...

Oh well. IMO this will delay the solution for Dementia and Alzheimers patients by a decade. First they will try them all on high-dose Vitamin-D supplements, and after a few years, even higher dose vitamin-D supplements. Only then will they begin to notice the bodies accumulating :X

I just hope they leave the autistic kids alone..

..Trevor..
 

Last edited on Tue Mar 6th, 2012 11:07 by Prof Trevor Marshall

wrotek
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So Curcumin does not work in VDR ? Or does it ?

Prof Trevor Marshall
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Who cares? And why?
 

wrotek
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Well if the study is badly done and curcumin actually shuts down VDR, we would know to avoid it.

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I thought we had already decided to avoid it, except in small quantities as a spice in foods??
 

wrotek
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Oh we did ? I did not know that. It never tasted good anyway, bitter dry sand. But i like Mustard ...

Last edited on Wed Mar 7th, 2012 01:37 by wrotek

Cynthia S
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If amyloid beta is an antimicrobial peptide, does it make any sense for macrophages to be gobbling it up?

Mustard comes under the heading of seasoning.  Tho I eat it in such quantities, I sometimes wonder.

Cynthia

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Cynthia,
Macrophages clean up general cellular junk and trash, and might perhaps clean up scraps of antimicrobial. In this case, whoever, the pathogens which caused the monocytes and macrophages to produce the amyloid-beta in the first place have almost certainly vanished in the process of the researchers trying to get access to the tissue, so all bets are off with respect to what actually might be happening a live human being :)
 

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I'm reminded of a paragraph on biotechnology by Wendell Berry in his book, Citizen Papers:

"Richard Strohman, of the University of California-Berkeley, has proposed that the problems of biotechnology arise, not because the science is new, but because it is old.  He sees it as a development of a now outdated paradigm according to which scientists have undertaken to supply simple solutions to complex problems, without due regard to the complexity of the problems.  The proper scientific response to this, he says, is to enlarge the context of the work."

lorenzo von matterhorn
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http://www.newsroom.ucla.edu/portal/ucla/scientists-pinpoint-how-vitamin-229702.aspx

macrophages gobbling up Amyloid Beta..

wrotek
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Interesting differences between curcumin and 1,25-D in this paper.

mvanwink5
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From the paperThe mechanisms behind the effects of 1a,25–dihydroxyvitamin D3 on phagocytosis were complex and dependent on calcium and signaling by the "MAPK" pathway, which helps communicate a signal from the vitamin D3 receptor located on the surface of a cell to the DNA in the cell's nucleus.I am not sure what they are saying here, are they really saying the VDR was on the cell surface membrane? These researchers need serious help in writing technical papers for clarity. I am not saying I am better, but I have never heard of the VDR being on the cell surface before.

The paper might have an interesting find if the difference in curcumin and 1,25D was only due to VDR stabilization differences as they assert, but I can't see that they showed that (though they seem to infer that). They utilized a technique based on mass spectrometry, which showed that 1a,25–dihydroxyvitamin D3 stabilized many more critical sites on the vitamin D receptor than did the curcuminoids.
Best regards,
Mike

PS Sometimes I wonder if these researchers would conclude police are the cause of crime because they are frequently found at the scene of crimes, and therefore we need to reduce how many policemen there are (amyloid beta is an amp)?

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mvanwink5 wrote: From the paperThe mechanisms behind the effects of 1a,25–dihydroxyvitamin D3 on phagocytosis were complex and dependent on calcium and signaling by the "MAPK" pathway, which helps communicate a signal from the vitamin D3 receptor located on the surface of a cell to the DNA in the cell's nucleus.
Is this implying that VDR activation is dependent on calcium? 

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Russ,
As I understanding the paper it is after the VDR agonist has docked that the Ca becomes involved.
Best regards,
Mike

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Don't dwell on these biology papers too much - this is a far more complex issue than any of these research groups have ever dreamed. Each only gives you a small glimpse into the actual mechanisms in play...
 

Russ
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Interesting.  Thanks.

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Study identifies new culprit that may make aging brains susceptible to neurodegenerative diseases

http://tiny.cc/ot2s1w

"The study, to be published Aug. 14 in the Journal of Neuroscience, reveals that with advancing age, a protein called C1q, well-known as a key initiator of immune response, increasingly lodges at contact points connecting nerve cells in the brain to one another. Elevated C1q concentrations at these contact points, or synapses, may render them prone to catastrophic destruction by brain-dwelling immune cells, triggered when a catalytic event such as brain injury, systemic infection or a series of small strokes unleashes a second set of substances on the synapses"

"No other protein has ever been shown to increase nearly so profoundly with normal brain aging," said Ben Barres, MD, PhD, professor and chair of neurobiology and senior author of the study. Examinations of mouse and human brain tissue showed as much as a 300-fold age-related buildup of C1q.


"The brain has its own set of immune cells, called microglia, which can secrete C1q. Still other brain cells, called astrocytes, secrete all of C1q's complement-system "teammates." The two cell types work analogously to the two tubes of an Epoxy kit, in which one tube contains the resin, the other a catalyst"

"
Most cells in the body have their own complement-inhibiting agents. This prevents the wholesale loss of healthy tissue during an immune attack on invading pathogens or debris from dead tissue during wound healing. But nerve cells lack their own supply of complement inhibitors. So, when astrocytes get activated, their ensuing release of C1q's teammates may set off a synapse-destroying rampage that spreads "like a fire burning through the brain," Barres said"

Last edited on Wed Aug 14th, 2013 03:19 by Bane

GillyB
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Maybe I'm stating the obvious, but the researcher is assuming that the buildup up is age-related.

"No other protein has ever been shown to increase nearly so profoundly with normal brain aging," said Ben Barres, MD, PhD, professor and chair of neurobiology and senior author of the study. Examinations of mouse and human brain tissue showed as much as a 300-fold age-related buildup of C1q.

Perhaps it's a consequence of immune system dysfunction instead.


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GillyB wrote:Perhaps it's a consequence of immune system dysfunction instead.
This:)

Bane
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Link between vitamin D, dementia risk confirmed

http://www.sciencedaily.com/releases/2014/08/140806161659.htm

"Similar results were recorded for Alzheimer's disease, with the moderately deficient group 69 per cent more likely to develop this type of dementia, jumping to a 122 per cent increased risk for those severely deficient"

"The study also found evidence that there is a threshold level of Vitamin D circulating in the bloodstream below which the risk of developing dementia and Alzheimer's disease increases. The team had previously hypothesized that this might lie in the region of 25-50 nmol/L, and their new findings confirm that vitamin D levels above 50 nmol/L are most strongly associated with good brain health"

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Alzheimer's Associated β-Amyloid Protein Inhibits Influenza A Virus and Modulates Viral Interactions with Phagocytes.

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0101364

Accumulation of β-Amyloid (βA) is a key pathogenetic factor in Alzheimer's disease; however, the normal function of βA is unknown. Recent studies have shown that βA can inhibit growth of bacteria and fungi. In this paper we show that βA also inhibits replication of seasonal and pandemic strains of H3N2 and H1N1 influenza A virus (IAV) in vitro. The 42 amino acid fragment of βA (βA42) had greater activity than the 40 amino acid fragment. Direct incubation of the virus with βA42 was needed to achieve optimal inhibition. Using quantitative PCR assays βA42 was shown to reduce viral uptake by epithelial cells after 45 minutes and to reduce supernatant virus at 24 hours post infection. βA42 caused aggregation of IAV particles as detected by light transmission assays and electron and confocal microscopy. βA42 did not stimulate neutrophil H2O2 production or extracellular trap formation on its own, but it increased both responses stimulated by IAV. In addition, βA42 increased uptake of IAV by neutrophils. βA42 reduced viral protein synthesis in monocytes and reduced IAV-induced interleukin-6 production by these cells. Hence, we demonstrate for the first time that βA has antiviral activity and modulates viral interactions with phagocytes.


Helicobacter pylori filtrate impairs spatial learning and memory in rats and increases β-amyloid by enhancing expression of presenilin-2

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3990046/

"Injection of H. pylori filtrate significantly increased Aβ42 both in the hippocampus and cortex, together with an increased level of presenilin-2 (PS-2), one key component of γ-secretase involved in Aβ production. Incubation of H. pylori filtrate with N2a cells which over-express amyloid precursor protein (APP) also resulted in increased PS-2 expression and Aβ42 overproduction"

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Down Syndrome helps researchers understand Alzheimer's disease

http://www.sciencedaily.com/releases/2014/09/140918150832.htm

http://brain.oxfordjournals.org/content/137/9/2556


"Our findings indicate that many adults with Down syndrome can tolerate amyloid-β deposition without deleterious effects on cognitive functioning."

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Human amyloid-beta acts as natural antibiotic in the brain: Alzheimer's-associated amyloid plaques may trap microbes

https://www.sciencedaily.com/releases/2016/05/160525161351.htm

"amyloid-beta protein -- which is deposited in the form of beta-amyloid plaques in the brains of patients with Alzheimer's disease -- is a normal part of the innate immune system, the body's first-line defense against infection"

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a normal part of the innate immune system, the body's first-line defense against infection
Oh man.
All the black-and-white or good-vs-bad polarity thinkers must be getting sea sick with all this news.

How will doctors explain it when someday they discover something similar about cholesterol?
I can see the headline now: "Breaking news: 'Bad Cholesterol", LDL, is found to be a normal part of the innate immune system, the body's first-line defense against infection." (note: this is not a real headline, just my imagined headline that may actually be real some day in the future.)

You sell more newspapers if things are billed as a conflict, right?

Life is a lot more like a network of factors all in tension I think. :D

wrotek
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Bane wrote:
Human amyloid-beta acts as natural antibiotic in the brain: Alzheimer's-associated amyloid plaques may trap microbes

https://www.sciencedaily.com/releases/2016/05/160525161351.htm

"amyloid-beta protein -- which is deposited in the form of beta-amyloid plaques in the brains of patients with Alzheimer's disease -- is a normal part of the innate immune system, the body's first-line defense against infection"


So why do these Amyloid peptides cannot erradicate infection ? Are there some other antimicrobial peptides supressed ?

RM
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Great question,

Not sure but just thinking aloud;

The immune system is compromised(the normal immune chain is broken somewhere down the line, and the amyloid is not the best response but the best the compromised immune can muster at the time.)?

In light of this wondering did anyone read the paper / have any thoughts on the amyloid response reported in sarcoid?( I know when I saw this Amyloid sarc paper & remembered the AD one I thought seems likely part of normal/reactive immune response).

So again wondering could `their` Amyloid sarc paper also be an indicator(backup) for active infection?

Last edited on Tue Oct 18th, 2016 21:00 by RM



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