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ChrisMavo
Member
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Posted: Fri Mar 18th, 2011 12:08 |
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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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PLS/ALS, speech difficulty, dizziness, leg weakness, overly emotional, Ph1Aug2609,11/2012 25D-12, 11/11: 25D-10, 04/11: 25D-11, 07/10: 25D-13, 05/10: 25D-15, 11/09: 25D-20, 9/09: 25D-27, 7/09: 25D-38, 1,25D-46, Mod Ph2Oct09, 100mg Mino
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Phillyguy
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Posted: Fri Mar 18th, 2011 12:21 |
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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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ChrisMavo
Member
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Posted: Fri Mar 18th, 2011 12:28 |
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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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PLS/ALS, speech difficulty, dizziness, leg weakness, overly emotional, Ph1Aug2609,11/2012 25D-12, 11/11: 25D-10, 04/11: 25D-11, 07/10: 25D-13, 05/10: 25D-15, 11/09: 25D-20, 9/09: 25D-27, 7/09: 25D-38, 1,25D-46, Mod Ph2Oct09, 100mg Mino
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Bane
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| Location: | Norway |
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Posted: Tue Jul 12th, 2011 03:18 |
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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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findinganswers
member
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Posted: Wed Jul 13th, 2011 08:57 |
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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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Diabetes type I hypothyroid IBS ADD GAD 125D37 25D12 Ph1Sept07 Ph2Jun08 ModPh2Nov08 25D8.5(June08) 25D<4(April2010) 25D5.5(Oct2010) 25D4(Jan2011) 25D7.4(Oct2011) 25D4(Feb2012) Levoxyl Lantus Humalog Cal/Mag Supp. qod Julbo Dolgan sunglasses light exp
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Prof Trevor Marshall
Foundation Staff
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Posted: Wed Jul 13th, 2011 09:19 |
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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 
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wrotek
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| Joined: | Thu Dec 30th, 2004 |
| Location: | Wroclaw, Poland |
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Posted: Sat Aug 6th, 2011 22:57 |
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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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Borreliosis(4 strains),Bartonella IgG only, reflux,headache TMJD ,chronic pain,chronic fatigue,depression 125D36 Ph1Sep05 Ph2Oct06 Ph3Apr07 in low lux NoIRs 25D<7 Oct06
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ChrisMavo
Member
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Posted: Sat Aug 6th, 2011 23:41 |
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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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PLS/ALS, speech difficulty, dizziness, leg weakness, overly emotional, Ph1Aug2609,11/2012 25D-12, 11/11: 25D-10, 04/11: 25D-11, 07/10: 25D-13, 05/10: 25D-15, 11/09: 25D-20, 9/09: 25D-27, 7/09: 25D-38, 1,25D-46, Mod Ph2Oct09, 100mg Mino
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edj2001
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| Location: | Allen, Texas USA |
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Posted: Sun Aug 7th, 2011 13:00 |
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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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Sarc98 A.Fib uveitis sk cancer basal/melanoma colon tmr bladder tmr bph| Benicar Propafenone Synthroid Proscar | 1,25D=50 10/05| 25D=7 4/08| =9 2012 | avd l&D|
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ChrisMavo
Member
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Posted: Sun Aug 7th, 2011 14:24 |
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Thanks Gene! Another good paper that implicates bacterial involvement in AD.
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PLS/ALS, speech difficulty, dizziness, leg weakness, overly emotional, Ph1Aug2609,11/2012 25D-12, 11/11: 25D-10, 04/11: 25D-11, 07/10: 25D-13, 05/10: 25D-15, 11/09: 25D-20, 9/09: 25D-27, 7/09: 25D-38, 1,25D-46, Mod Ph2Oct09, 100mg Mino
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Frenchie
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Posted: Tue Sep 27th, 2011 06:12 |
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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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Gulf War Syndrome, 1,25D 62 pg/ml Oct09, Ph1Jan10, 25D 9 ng/ml Mar 13
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Alejandro
Member
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Posted: Tue Sep 27th, 2011 08:15 |
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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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Skin Sarcoidosis (2004) 1,25 D3 : 46 pg/ml (was 63 pg/ml) 25 D :18 ng/ml (now increased in Summer, was 9 ng/ml). EBV
MP Dec 2009. Since around 2012 only Olm 40 mg daily
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Cynthia S
Foundation Staff
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Posted: Tue Sep 27th, 2011 08:59 |
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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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MP start 10/08,break 1/16 - 9/16, Spondylitis'97,early Diverticulosis'98,early AMD'08,Calcium anomaly'95,TypeII Diabetes(?)'02,Degenerative hip disease'12, 25D=10.8 May'18 (preMP 125D/25D=47/43) https://marshallprotocol.com/forum30/13911-2.html
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laura1814
Support Team
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Posted: Wed Oct 5th, 2011 07:28 |
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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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CFS, EBV, hypoglycemia, hyperlipidemia, MP 1/08; NoIRs, low lux home, ltd. outings, covered up; 25D=5ng/mL. Benicar q4h. XL doses Z+Q 4/18/20; Iv wkly 4/25; break 5/20; ZP 5.5mg 6/29; Iv 8/14 1/3 dose 2x/wk; 11/2 2/3; 11/24 11mg ZP; 1/5/21 3/3 Iv.
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Markt9452
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Posted: Wed Oct 5th, 2011 13:58 |
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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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MP Feb08 - light sensitivity, fatigue, confusion, muscle twitching, memory loss, dyslexia, skin lesions, sore feet, electrical sensations, vertigo, tinnitus, 125D20 D25<10 2008.Ivermectin topical 1 gram 7-10 days
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wrotek
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Posted: Wed Oct 26th, 2011 02:39 |
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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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Borreliosis(4 strains),Bartonella IgG only, reflux,headache TMJD ,chronic pain,chronic fatigue,depression 125D36 Ph1Sep05 Ph2Oct06 Ph3Apr07 in low lux NoIRs 25D<7 Oct06
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Prof Trevor Marshall
Foundation Staff
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Posted: Wed Oct 26th, 2011 06:07 |
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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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wrotek
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Posted: Wed Oct 26th, 2011 07:33 |
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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
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Borreliosis(4 strains),Bartonella IgG only, reflux,headache TMJD ,chronic pain,chronic fatigue,depression 125D36 Ph1Sep05 Ph2Oct06 Ph3Apr07 in low lux NoIRs 25D<7 Oct06
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Russ
Member
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Posted: Wed Oct 26th, 2011 09:03 |
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| Would the Clorox mouth rinse this dentist suggests be a good oral hygiene practice?
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Prof Trevor Marshall
Foundation Staff
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Posted: Wed Oct 26th, 2011 09:09 |
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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
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