MS is not an immune system dysfunction, but disease of BBB?

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MS is not an immune system dysfunction, but disease of BBB?

Postby CureOrBust » Sun Jan 28, 2007 1:50 am

If you don’t like conspiracy theories or half baked ideas, you can stop reading now, its long. However, if you enjoy to pick the threads from a poorly made suit, read on, I welcome the exchange.

Two points to start with:
1. Now, PRECEED EVERY SENTENCE WITH A "MAYBE", "POSSIBLY" or finish it with a "?" (as appropriate)
2. Read point 1 again.

* The BBB is in simple terms, the walls of capillaries http://www.daviddarling.info/encyclopedia/B/blood-brain_barrier.html
A key aspect of the blood-brain barrier are the thin, flat cells known as endothelial cells which form the walls of capillaries


* All people produce MRTC's weather they have or will get MS or not.http://www.thisisms.com/ftopict-3543.html (and Klein et al., 2000; Bruno et al., 2002)

* Steroids work so well on relapses because they block the BBB http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1619410&dopt=Citation
* Steroids stop working after some time of continued use, but they keep working for transplant patients (ie Immune down regulation doesn’t appear to fail, well I have never heard of it anyway but lets assumed it is accepted)
* EAE is a disease model based on creating MRTC's, not BBB permeability (read point 1 again...)
* A lot of MS treatments are 100% effective in EAE, but not that great on MS
* Tysabri works by latching onto T-cells making the BBB impermeable to them. ie It kind of stops BBB permeability, and is currently the highest rated "approved" treatment.

There are two main paths of pathology for the damage
a) "Anti-Brain Factor 1" (lets say this is MRTC's) (ABF1)
b) "Anti-Brain factor 2" (this is the unknown) (ABF2)

In case you didnt notice, I made up the term "Anti-Brain factor"...

Now, it’s ABF2 that is unknown, and I propose is why all the immune modulatory treatments do not work 100%. Now under ABF2's, as an unknown, I would imply in all, that it would be more than one. And if you
consider that the BBB is permeable, the reason its there is to keep stuff that shouldn’t be there, out. Such as MRTC's as well as ABF2's. Now, these things may be fine in the general blood stream, but are ABF's in the CSF.

All the 100% effective on EAE are effective in EAE because they work on ABF1. Things like Helminthes are ALMOST but not completely effective against MS, as they also work on ABF1 but, they may help against ABF2's as well. We don’t know yet.

It kind of has also been proposed, that ABF2 (ie the unknown) causes death of nerve cells (Myelin, oligodendrocytes or neurons take your pick) and it’s the ABF1 that comes in and tries to clear the damage, however causes further damage.(Prineas and Barrett, but they were too scared to come up with a catchy title like "Anti-Brain Factor")

Now Tovaxin only attacks the MRTC's, but we have only seen the high short term effectiveness of it to stop relapses. Has anyone tried it on PPMS or SPMS? Maybe that’s the difference between RRMS and the other two. RRMS is a disease mediated by ANBF1 and PPMS is a disease mediated by ABF2's.

Many believe in a contagious factor. CPn (and probably many other microbes both bacteria and virus) is known to love and cause damage to blood vessels. ie the BBB? Could this explain the Faroe islands? When vanderbuilt checked the CSF for CPn they only found it in a percentage of samples. Has anyone actually checked the BBB for CPn etc? Vanderbuilt were checking the fluid only if I got it right.

Vit D is said to strengthen the BBB. Could this explain the expression between the equator and poles?

Could the various diets that have worked for many, actually be strengthening the BBN?
Could the various diets that have worked for many actually reduce the toxins (ie ABF2's) in the blood stream, and hence cross over into our CSF?

Statins appear to be working for many. They have been found to decrease BBB permeability.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16729291&query_hl=1&itool=pubmed_docsum (posted by dignan at
http://www.thisisms.com/ftopicp-15681.html

Uric acid appears to reduce but not remove the risk of MS. Could it be fighting (a losing battle) against the ABF2's (or it the damage caused by ABF1's & 2's) that have made it into the CSF. But in the thread link provided below, jimmylegs found it may also hel0p with BBB permeability

There are a lot of holes in these ramblings, but they have been accumulating over the months to the point where I had to put them in words. Remember, I am not proposing any of the above as an absolute, just a possibility to be discussed.

Now I understand virtually every one here (well at least the vocal ones) have already been stating that’s it’s not an Auto-immune condition, so I am not looking for the "yeah, this is what I have been saying" posts. I hardly see posts regarding thee BBB except for the side mention and this thread http://www.thisisms.com/ftopicp-16313.html.

I remember one of the first diagnoses I had received was of CIDP (chronic inflammatory de-mylinating poly neuropathy). Basically non CNS MS. I remember when I first started searching on the net about it, and I kept hitting MS web sites, so I read, and got a little scared. I asked my immunologist who diagnosed me, that MS sounds like my condition with a leaky BBB; could I progress to MS. He assured me that would not happen (should have got that one in writing, with a money back guarantee)

I am not the only one or the first to push the BBB as the MAIN culprit (see http://www.thisisms.com/content-3.html), but I feel it doesn’t get discussed enough in research and discussion.

So let’s try it against the other twelve prepositions coined by the "Best bet diet guy":
1- It must be found throughout the world but be specific enough to affect only half or less of the susceptible individuals.
> BBB's are found around the world. And by definition I am saying that permeable ones occur around the world.

2- It must affect immigrant children more than it does immigrant adults. On the other hand it must affect susceptible identical twins mainly when they are adults rather than when they are children.
>huh? maybe the BBB lack of permeability is built mostly during childhood?

3- It must be much more common or effective in northwestern Europe, Canada, United States, Australia and New Zealand than in the rest of the world.
>This would be the Vit D link to BBB stability. Or there could be a genetic pre-disposition for a permeable BBB

4- It must be more common or effective in higher latitude areas so as to create a pronounced north/south gradient of MS prevalence.
>see point 3 and the great thing, I could include diet here as a cover all...

5- It must have enough variation so as to create significant MS prevalence and incidence differences within ethnically homogeneous populations over relatively short distances.
>again genetic pre-disposition for a permeable BBB

6- In Hawaii it must adversely affect those of Japanese origin whereas at the same time have a positive effect on Caucasians.
>again genetic pre-disposition for a permeable BBB. Also the effect of Vit D on BBB and the way different genetic groups react to it and other food items?

7- It must be transportable so as to explain the sudden increase in MS prevalence in the Faroes following British troop occupation during World War II.
>If bacterial or viral infections cause BBB permeability, it’s covered

8- It cannot be transmitted by either person to person contact or by a blood transfusion.
>covered. I am saying it’s not in the blood.

9- It must be increasingly more widespread and effective over the last 100 years.
>Change of diet, ummm... Reduced infection with helminthes which may have covered the incidents of BBB permeability

I know I have pulled a lot together to cover the one thing, but if it were simple, it would have been cured by now.

Anyway, this has gone on long enough. Remember its just thinking out load, but please feel free to shoot holes at will. Boy, that must be my longest post. Do i get bonus points?
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Postby TwistedHelix » Sun Jan 28, 2007 7:24 am

Ramblings?...Possibly. Fascinating?...Definitely! Here's a few snippets mentioning the BBB, none of them really new, but I just had to paste them so I could steal those 'longest post' points from you!!


NMDA- and endothelin-1-induced increases in blood-brain barrier permeability quantitated with Lucifer yellow.

* Miller RD,
* Monsul NT,
* Vender JR,
* Lehmann JC.

Department of Neurosurgery, Medical College of Pennsylvania, Philadelphia, USA.

At 48 h following intrastriatal injection of N-methyl-D-aspartate (NMDA; 100 nmol/microliter) or endothelin-1 (ET-1; 143 pmol/microliter), significant increases in brain penetration of the highly polar, fluorescent tracer Lucifer yellow were observed. The competitive NMDA receptor antagonist selfotel (CGS-19755; 30 nmol/microliter, i.c.) significantly reduced the NMDA-induced increases in blood-brain barrier permeability, but not those induced by ET-1. These results suggest that NMDA receptors can mediate increases in blood-brain barrier permeability but do not primarily mediate increases in blood-brain barrier permeability caused by ET-1. This is the first study to our knowledge investigating the relationship between excitotoxicity and disruption of the blood-brain barrier, a major pathophysiological event in stroke and traumatic brain injury.

PMID: 8815176 [PubMed - indexed for MEDLINE]
* Bolton SJ,
* Perry VH.

Department of Pharmacology, University of Oxford, United Kingdom.

Acute neuronal degeneration can be induced by intracerebral injections of the glutamate receptor agonists kainic acid (KA) and NMDA (N-methyl-D-aspartate). It is accompanied by an inflammatory response that has not yet been fully investigated. We have previously demonstrated that the juvenile rat brain is more susceptible to an inflammatory challenge when compared to adult rat brain. This study set out to investigate whether this also applied to the inflammatory response associated with acute neuronal degeneration. NMDA and kainic acid were injected into the rat striatum and lesion size, leucocyte recruitment, and blood-brain barrier (BBB) breakdown were assessed after 4, 8, 12, 24, 72, and 168 h. Both NMDA and KA induced lesions of similar volume at either age and apoptotic and necrotic nuclei could be detected. NMDA induced cellular loss by 4 h, whereas KA-injected rats did not show signs of neuronal loss until 8-12 h. The inflammatory response was characterized by an infiltration of neutrophils followed by macrophages. Juvenile rats showed a greater susceptibility to leucocyte recruitment compared to adult rats. BBB breakdown in response to NMDA injection occurred in the absence of cellular recruitment at 4 h in juveniles and was significantly greater in juvenile compared to adult rats at 8 h. BBB breakdown was minimal in KA-injected animals while at 7 days an influx of serum IgG coincided with a loss of astrocytic GFAP staining within the lesion.

PMID: 9875284 [PubMed - indexed for MEDLINE]
School of Psychology, University of St. Andrews, Fife, Scotland.

Excitotoxins have been widely used to make lesions in the brains of experimental animals because they have the ability to destroy neurones while sparing fibres of passage. Because loss of fibres of passage can confound the interpretation of lesion effects, this property is of considerable value. Recently, however, there have been reports indicating that excitotoxins acting at different sites within the rat CNS not only destroy neurones but also strip myelin from fibres and compromise the integrity of the blood-brain barrier. However, some reports also indicate that the myelin content of the lesioned area recovers. Excitotoxic lesions of the lateral hypothalamus have been shown to produce local demyelination. The present studies sought to investigate this effect further by (1) defining the time course of demyelination and possible remyelination after excitotoxic lesions of the lateral hypothalamus made with N-methyl-D-aspartate (NMDA); (2) establishing the relationships between neuronal loss, de- and remyelination after various doses of NMDA; and (3) examining the integrity of the blood-brain barrier using an immunohistochemical probe. Our data show that after injection of NMDA into the lateral hypothalamus there was neuronal loss, blood-brain barrier disruption (followed by recovery over approximately 12 days), triggering of reactive gliosis, invasion of the lesioned area by cells from outwith the CNS, demyelination over an area coexistent with but not exceeding the area of neuronal loss, and remyelination. Remyelination occurred over a period of 3 months following the production of the lesion and was associated initially with blood vessels. It occurred across the whole of the lesioned area, not by encroachment from the borders. All doses of NMDA that produced neuronal death also produced demyelination. These data confirm that excitotoxic lesions of the lateral hypothalamus demyelinate fibres, but show for the first time that remyelination occurs here. They are consistent with reports concerning excitotoxin actions at other CNS sites and indicate that de- and remyelination after excitotoxic lesions is a ubiquitous process. Consideration should be given to this when using excitotoxins to make fibre-sparing lesions.

PMID: 9250618 [PubMed - indexed for MEDLINE]Leloir Institute, Universiity of Buenos Aires, Buenos Aires, Argentina.

Interleukin-1beta (IL-1) expression is associated with a spectrum of neuroinflammatory processes related to chronic neurodegenerative diseases. The single-bolus microinjection of IL-1 into the central nervous system (CNS) parenchyma gives rise to delayed and localized neutrophil recruitment, transient blood-brain barrier (BBB) breakdown, but no overt damage to CNS integrity. However, acute microinjections of IL-1 do not mimic the chronic IL-1 expression, which is a feature of many CNS diseases. To investigate the response of the CNS to chronic IL-1 expression, we injected a recombinant adenovirus expressing IL-1 into the striatum. At the peak of IL-1 expression (days 8 and 14 post-injection), there was a marked recruitment of neutrophils, vasodilatation, and breakdown of the BBB. Microglia and astrocyte activation was evident during the first 14 days post-injection. At days 8 and 14, extensive demyelination was observed but the number of neurons was not affected by any treatment. Finally, at 30 days, signs of inflammation were no longer present, there was evidence of tissue reorganization, the BBB was intact, and the process of remyelination was noticeable. In summary, our data show that chronic expression of IL-1, in contrast to its acute delivery, can reversibly damage CNS integrity and implicates this cytokine or downstream components as major mediators of demyelination in chronic inflammatory and demyelinating diseases.

PMID: 15509551 [PubMed - indexed for MEDLINE]
MANIPULATING THE BLOOD-BRAIN BARRIER—A REALISTIC THERAPEUTIC GOAL?

NEW ORLEANS— "It was 100 years ago that the anatomy of the blood-brain barrier was first shown. But it is only today that we begin to understand the relevance the barrier has for medicine and neurological disorders," said Damir Janigro, PhD, at the 25th International Stroke Conference. Currently, researchers are taking a new look at the blood-brain barrier, interested in how they might find ways to cross this seemingly insuperable obstacle to deliver drugs to the brain or, conversely, to protect the integrity of the barrier in hopes of preventing diseases such as multiple sclerosis, AIDS, Alzheimer's disease, and Parkinson's disease.

DETECTING PATHOLOGIC CHANGES

The blood-brain barrier is an exclusive component of the endothelium of the over 400 miles of cerebral capillaries, where tight junctions prevent substances in the blood from crossing between cells and into the brain, said Dr. Janigro, Director of Cerebrovascular Research at the Cleveland Clinic Foundation in Cleveland. These undesirable substances include "not only molecules but also cells, primarily inflammatory cells," he said. While some agents do cross the barrier, including antidepressants and recreational drugs like cocaine and ethyl alcohol, a variety of desirable drugs, including antitumor and antiviral agents, growth factors, and gene delivery systems do not, he noted.

Conversely, it is becoming evident that the barrier itself may be subject to loss, perhaps underlying the initiation of chronic disease. In stroke, for example, there is a transient loss of blood-brain barrier function that happens within minutes or hours of the event, he said. In other settings, there appears instead to be a "leakage" across the barrier that may be protracted over time, leading to chronic diseases such as multiple sclerosis or Alzheimer's disease. "There's plenty of evidence … that if you lose blood-brain barrier function—even a low fraction of its function but for an extended period of time—you may allow entry into the brain, [of] molecules or cells that cause the development of pathology," he said.

Work is ongoing to develop simple blood tests or diagnostic imaging techniques that may allow evaluation of the integrity of the blood-brain barrier, he said. For example, in stroke, the loss of integrity of the barrier may herald adverse bleeding events after the administration of tissue plasminogen activator (t-PA). The ability to visualize this loss might allow those with existing breaches of the barrier to be excluded from treatment.

"How … [many] of these changes that are seen in pathological situations really relate to the loss of barrier function, and how early can we detect these changes in chronic neurological disease?" Dr. Janigro asked. The answers may make it possible to aggressively treat the blood-brain barrier disease, thereby preventing the cascade of events that lead to full-blown pathology.


Plus, a link which makes me wonder if the cascade begins early in life:
http://cat.inist.fr/?aModele=afficheN&cpsidt=17304523

Dom.[/i]
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Postby Lyon » Sun Jan 28, 2007 8:52 am

Hi Cure,
I think this kind of speculation is exactly what this site is about. I've got....heck, we've all got different thoughts but thinking about and responding to the thoughts of others helps us all learn.

First, part of your subject title is almost surely correct. The permiable BBB is the first of the recognized steps in the MS disease process (the permiable bbb, inflammation, lesions, myelin loss, axon death and eventual atrophy) and even though I don't completely agree, at least one researcher has said that controlling the permiable bbb would control the MS process.

There are multiple truths which are self evident regarding MS but I don't think most people take the time to recognize them.

One is that, like the hunt for answers with most any disease, from the beginning this hunt for answers has been a "reverse engineering" process. In the beginning, 150 years ago or so, the only thing known about MS were the outward symptoms. Little by little with increased research and advancing tools, in the time since, we are now at the point in which the permiable bbb, inflammation, lesions, myelin loss, axon death and eventual atrophy have been identified.

These things are what the reverse engineering process has taught us to this point in time. No one is saying these things constitute the sum total of the MS disease process. In fact most researchers would probably say that these are just the final steps of a very long process and that we need to contiue to work our way back.

Yes it's true controlling any of these would result in improvements from the treatments we now have but anything resembling a real "cure" is going to have to come from knowledge of even earlier stages of the disease process which we have yet to identify.

I suppose that's why I'm so excited about the chance discovery of what seems to be a relationship between the loss of helminths and the subsequent rise in immune dysfunction.

We've reverse engineered and identified the final stages of the MS process but reverse engineering in itself is a tediously slow process and identifying the first step of the process would only require filling in the blanks between the two. I've got a pretty vivid imagination but I can't imagine anyone ever being able to come up with an incident leading to immune dysfunction which could be prior to the relationship between the human immune system and the parasites which have been with us and regulating our immune systems throughout our evolution.

OK, that's good enough for now!
Bob
Last edited by Lyon on Sun Jan 28, 2007 1:07 pm, edited 1 time in total.
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Postby Chris55 » Sun Jan 28, 2007 12:20 pm

I have been a member of "Betty's" MS blog ever since my daughter was diagnosed. She is a strong believer in strenghtening the BBB. She practices everything she preaches. She has not had a relapse in 20 years. Impressive! (Her doctors are REALLY impressed!) And please don't tell me it's because her case is benign--it's not. She has just worked on it every single day.
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Postby Chris55 » Sun Jan 28, 2007 12:26 pm

A "P.S." here....first, one of the mysteries about MS is the T cell's ability to cross the BBB because NOTHING is supposed to be able to get through. However, very recently it was found that the pneumonia bacteria can cross the BBB and when it does, it attacks the neurons.

My BIGGEST problem with all of the MS drugs, including Tysabri. Stopping the T cells from crossing the BBB may or may not effect the relapse rate but it appears to do nothing for damage. One's disability keeps on keeping on. Thus one of my theories..the T cells are attacking for a reason. Inflammation first, then attack--not inflammation caused by the attack. A subject they are still struggling with--what came first, the chicken or the egg.

Wish WE were researchers! Great information and thanks so much for sharing.
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Postby robbie » Sun Jan 28, 2007 1:53 pm

And please don't tell me it's because her case is benign--it's not.

chances are it's benign-chances are it's Betty's work ethic which is it? obvious for some not so for others. thats the great thing about this we all have our own opinions !!


Wish WE were researchers!

i wish u were all researchers too we would all be better off..Image
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Postby Lyon » Sun Jan 28, 2007 2:37 pm

Chris55 wrote:A "P.S." here....first, one of the mysteries about MS is the T cell's ability to cross the BBB because NOTHING is supposed to be able to get through.
Sadly Chris, although I thought the same in the beginning, things aren't quite that simple.

With further research I found that there are certain things under a certain size which can go in through even a healthy bbb and when there is problem the immune system is allowed to go in after them.

Things got so complicated in trying to determine what should and shouldn't be allowed through the bbb that I recognized that the whole thing was above my ability to completely understand and I gave up, but in truth things do and some things are intended to go through the bbb, even a healthy one.

A better term in regards to the bbb and MS would be "increased permiability" of the bbb rather than currently used term of "permiable" because that implies that a healthy bbb isn't permiable.

Bob
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Postby CureOrBust » Mon Jan 29, 2007 1:45 am

lyon wrote:First, part of your subject title is almost surely correct. The permiable BBB is the first of the recognized steps in the MS disease process (the permiable bbb, inflammation, lesions, myelin loss, axon death and eventual atrophy) and even though I don't completely agree, at least one researcher has said that controlling the permiable bbb would control the MS process.
I dont necessarily think its the first. Its possible that MS is really a condition where our bodies undergo something that causes the BBB to become degraded. eg by infection, genetics or both etc etc etc. It may be this trigger as the "first" event. Any neuro that prescribes steroids for a relapse to me is saying that closinbg the BBB will stop MS in its tracks (for a while).

lyon wrote:There are multiple truths which are self evident regarding MS ...
I have NEVER herd anyone say that someone can have MS but a healthy BBB. So it would appear to be the only un-argued "truth". I'm stating it this way so someone will prove me wrong :)

lyon wrote:Yes it's true controlling any of these would result in improvements from the treatments we now have but anything resembling a real "cure" is going to have to come from knowledge of even earlier stages of the disease process which we have yet to identify.
Now, a lot of current treatments do work on most of these MS disease paths. Steroids SHUTS the BBB and is known to STOP MS in its tracks (at least in the begining). Now, what else has been shown to provide this effect? What else do they give you during a relapse (ie when MS is at its most active)? How does this other agent work? Helminths have never been shown to stop a relapse in it tracks. ;)

lyon wrote:I can't imagine anyone ever being able to come up with an incident leading to immune dysfunction which could be prior to the relationship between the human immune system and the parasites which have been with us and regulating our immune systems throughout our evolution.
Hey, get your own thread! this one is about it NOT being an immune system dysfunction but a BBB dysfunction. Close the BBB and no pig worms would be needed. I implied these parasites may have been covering the effects of an overly permeable BBB, this doesnt meen we shouldnt be looking for a way to remove the need for the critters.

Chris55 wrote:She practices everything she preaches. She has not had a relapse in 20 years. Impressive!
A result of 1 is not that impressive at all. The CRABs work 100% for at least one person in the world. Even if it supports my ramblings :)

Chris55 wrote:A "P.S." here....first, one of the mysteries about MS is the T cell's ability to cross the BBB because NOTHING is supposed to be able to get through.
Oxygen? water? sugars? etc etc. It is suppose to be permeable, just not allow "Anti brain factors" 1 or 2 get in in any great numbers. Cancer Dr's have an issue because some of their effective drugs do not (or not enough) cross the BBB. I read once that they found if they injected them with sugar, the BBB opened up enough to allow chemo through, into the brain for brain cancer treatments.

Chris55 wrote:Stopping the T cells from crossing the BBB may or may not effect the relapse rate but it appears to do nothing for damage
Yeah, thats "Anti Brain Factor 2" The unknown. But fix the BBB and it doesnt get to the brain, so who cares what it is. See steroids effects on acute relapses.

Robbie, I LUUUURVE the animated GIF!

lyon wrote:With further research I found that there are certain things under a certain size which can go in through even a healthy bbb and when there is problem the immune system is allowed to go in after them.


The following is from the first link in my original post. It implies its simply a size issue, however, I have seen various tovaxin animations which imply its more than size which determines what gets through and what doesnt.
http://www.daviddarling.info/encyclopedia/B/blood-brain_barrier.html wrote:A mechanism that controls the passage of substances from the blood into the cerobrospinal fluid and thus into the brain and spinal cord. The blood-brain barrier (BBB) lets essential metabolites, such as oxygen and glucose, pass from the blood to the brain and central nervous system (CNS) but blocks most molecules that are more massive than about 500 Daltons. This is a low mass in biomolecular terms and means that everything from hormones and neurotransmitters to viruses and bacteria are refused access to the brain by the BBB. It also means that many drugs, which would otherwise be capable of treating disorders of the CNS, are denied access to the very regions where they would be affective.


Interesting that you say "when there is a problem" more is allowed to go through. Relapse point! and steroids again, close the BBB and stop the relapse. Now for the past 10years whenever I get an infection (cold/flu) I have a relapse, and steroids (prednisone) is the only agent that stops it.

As for the term "permeable" word, I think its used as its assumed permeable otherwise the brain wouldnt get oxygen, so stating its permeable implies an excess I think, so i am not bothered by it. When I first herd it, I went into auto pilot and understood what they meant, generally.
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Postby TwistedHelix » Mon Jan 29, 2007 6:03 am

Hello Cure,

A thought has just occurred to me: if the BBB becomes excessively permeable, is it just a one-way street? I mean, could peptides or proteins leak OUT of the brain and into the bloodstream where they shouldn't be, cause a reaction, then lymphocytes moves back IN to do their dirty work? Just a thought.

Dom.
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Postby Chris55 » Mon Jan 29, 2007 8:17 am

Just went back and checked my "Betty Iams" MS site. She was diagnosed with SPMS 20+ years ago. I knew it was not benign..just could not remember which stage.
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Postby Chris55 » Mon Jan 29, 2007 8:19 am

"With further research I found that there are certain things under a certain size which can go in through even a healthy bbb and when there is problem the immune system is allowed to go in after them. "

Lyon--what are they going after???
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Postby Chris55 » Mon Jan 29, 2007 8:29 am

Chris55 wrote:
A "P.S." here....first, one of the mysteries about MS is the T cell's ability to cross the BBB because NOTHING is supposed to be able to get through.
Sadly Chris, although I thought the same in the beginning, things aren't quite that simple.

Yes Lyon, that is a very "simplistic" statement; however, for the sake of argument, the MS community states that is one of the mysteries of the disease. Tysabri is geared towards stopping that very action. Again, perhaps there is a REASON they are going to the CNS. They know there is inflammation, the prompt for immune attack. They simply don't know if it is coming from the immune attack or if the cells are attacking inflammation that was there first. I think these consider SERIOUS consideration when researching/preparing new drugs for this disease.
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Postby Lyon » Mon Jan 29, 2007 9:26 am

Hi Chris,

I'm at work and don't have my bookmarks with me but in reading about the bbb earlier (months ago) the way I read it seemed that the researcher was saying that neither bacteria or viruses nor the immune system were supposed to go through the bbb but if/when bacteria and viruses did get through and cause problem, certain aspects of the immune system were also "allowed" in. That is in the case of a healthy bbb because the paper I read wasn't specific to MS and was an explanation of how the bbb is supposed to work.

CURE...your response is to in depth for me to respond to at work but we agree on more than you think. I think you must be female because you're arguing with me even though we are in agreement.

I think the only thing we disagree on is whether or not you are going to drink helminths. I'm pretty sneaky and I genetically altered a batch to they taste like bloody mary. A stick of celery, a couple of jumbo olives, I leave the glass sitting where you normally leave your drink...Voila! Oh, gosh.....what if I've already done it??

Bob
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Postby Chris55 » Mon Jan 29, 2007 10:31 am

I think you must be female because you're arguing with me even though we are in agreement. Oh god, can you hear me laughing??? On an American Idol blog last night someone told me I was "condescending". Now--that hurt!


I think the only thing we disagree on is whether or not you are going to drink helminths. I'm pretty sneaky and I genetically altered a batch to they taste like bloody mary. A stick of celery, a couple of jumbo olives, I leave the glass sitting where you normally leave your drink...Voila! Oh, gosh.....what if I've already done it?? Actually, I'm a Pina Colata girl myself!
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Postby robbie » Mon Jan 29, 2007 11:11 am

Chriss you must know alot about ms with all the research u do. Are relapses still happening with spms?, this is what i have and the relapses have stopped. You said that Betty has had spms for 20 years but hasn"t had a relapse in 20 years. So she just hasn't gotten worse in 20 years , could this still not be a benign form of ms, Please tell me how i'm wrong.
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robbie
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