Neuroinflammation and degenerative & cognitive diseases

[Guest guest]

Hmmm, thanks for that link . Neuroinflammation isn't something I've really looked at much before. (I've looked more at ICP.) But there are a zillion papers on it. Especially linking it to alzheimers as well as autism. Here's a quote from just one paper on the subject of NI and Alzheimers: "Inflammatory processes may play a critical role in the pathogenesis of the degenerative changes and cognitive impairments associated with Alzheimer's disease (AD). In the present study, lipopolysaccharide (LPS) from the cell wall of gram-negative bacteria was used to produce chronic, global inflammation within the brain of young rats." http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=10051200 & dopt=Citation In study after study, the method used to induce the inflammatory process in the brains of rats is by administering the endotoxin, lipopolysaccharides (LPS), which is derived from the cell wall of gram negative bacteria. I mean...give me a break. Isn't this what we've been saying all along? We're chronically sick and inflammed due to endotoxins produced by gram negative bacteria that are being ignored by the medical community??? Here's another: It has been postulated that

neuroinflammation plays a critical role in the pathogenesis of Alzheimer's disease (AD). To directly test whether an inflammatory stimulus can accelerate amyloid deposition in vivo, we chronically administered the bacterial endotoxin, lipopolysaccharide http://www.blackwell-synergy.com/links/doi/10.1046/j.0953-816x.2001.01666.x And in other papers, minocycline is regularly cited as helping with certain neuro degenerative disorders due to it's "anti-inflammatory properties". (same with Rheumatoid Arthritis). So we know that gram negative bacteria easily induces inflammation because they use it in research. So why can't they make the connection that minocyline's anti inflammatory properties might possibly have something to do with the fact that it kills some of the bacteria that produces

the toxins that create the inflammation????. Is it because no one wants to acknowledge the bacteria's existence and destructive capabilities in the first place? penny Windsor <rwindsor@...> wrote: Dear Rich Slim pickings for a quickie http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstract & list_uids=16401547 & query_hl=1 & itool=pubmed_docsum Very hard to tease out stuff from Goldberg though. Regards Windsor

[Guest guest]

I just got so frustrated by researcher's inability to see the bigger picture or connect the dots, that I went and vented to my husband, who's a scientist himself. I asked him why he thinks researchers are so slow to at least consider what seems to be obvious connections. He said he sees it all the time. Not only are researchers one track minded due to the monetary impact on their research if it goes "off track", they also have egoic involvement. But he says he also thinks it's mainly the way the majority of scientist's minds seem to work. He said he thinks of a scientist's mind as being like a big spinning hamster wheel. The wheel is comprised of a certain amount of information that defines his "known" universe, and he spins that wheel over and over attempting to make better sense of it. Anything that tries to enter the spinning hamster wheel that is not already related

to the defined universe will just bounce right off. But very gradually, the new piece of information sometimes starts to spin alongside the hamster wheel. At first it spins out of sync, but eventually it spins in sync with the wheel. At that point, the new information can jump on board and become part of the scientist's defined universe. But apparently it takes a very long time for the average scientist or research community to allow new information on board, especially if that information at first goes against what they already "know" to be "true". I suppose it was this frustration at this kind of thinking that compelled Barry Marshall to infect himself inducing ulcers just to prove that they're caused by "bacteria" not stress. Of course, what makes it even more difficult to counter this kind of thinking is the fact

that scientists are by nature very intelligent and articulate and can easily convince others of the "logic" that supports their positions. This is why we need to start funding our own research, because we'll probably all be dead before the medical establishment starts taking microorganisms seriously (other than flesh eating, polio, tb, etc., etc.,) I truly think that we HAVE to get people to start looking at the most destructive and damaging part of our disease first. The big problem has to be acknowledged before we start trying to figure out how to tinker with our immune systems to combat it. Seriously, how successfully can we combat an unknown enemy? It's imperative that we identify the enemy, then work on the strategies to fight it. Right now, everything is the opposite, we keep developing strategies to bolster our defenses. And all that does is lead us in

circles around the enemy but we never actually take the offense or penetrate its front line. I ask for the bazillionth time, why is it that you can look at almost any autoimmune, cognitive or degenerative disorder and find numerous research articles linking it to bacteria in some way and yet no one ever says that perhaps the bacteria itself is the CAUSE of the disorder? How can researchers talk about minocycline's and other antibiotics' anti-inflammatory properties and never even consider that perhaps its anti-inflammatory abilities have something to do with the fact that it's killing an organism that creates the endotoxin which results in inflammation????? It's mind blowing to me. penny p.s. I'm going to start asking every doctor this question who suggests the relief I'm getting from an antibiotic is due to it's

anti-inflammatory properties alone, not because it's actually combatting a toxin/inflammation producing infection. Penny Houle <pennyhoule@...> wrote: Hmmm, thanks for that link . Neuroinflammation isn't something I've really looked at much before. (I've looked more at ICP.) But there are a zillion papers on it. Especially linking it to alzheimers as well as autism. Here's a quote from just one paper on the subject of NI and Alzheimers: "Inflammatory processes may play a critical role in the pathogenesis of the degenerative changes and cognitive impairments associated with Alzheimer's

disease (AD). In the present study, lipopolysaccharide (LPS) from the cell wall of gram-negative bacteria was used to produce chronic, global inflammation within the brain of young rats." http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=10051200 & dopt=Citation In study after study, the method used to induce the inflammatory process in the brains of rats is by administering the endotoxin, lipopolysaccharides (LPS), which is derived from the cell wall of gram negative bacteria. I mean...give me a break. Isn't this what we've been saying all along? We're chronically sick and inflammed due to

endotoxins produced by gram negative bacteria that are being ignored by the medical community??? Here's another: It has been postulated that neuroinflammation plays a critical role in the pathogenesis of Alzheimer's disease (AD). To directly test whether an inflammatory stimulus can accelerate amyloid deposition in vivo, we chronically administered the bacterial endotoxin, lipopolysaccharide http://www.blackwell-synergy.com/links/doi/10.1046/j.0953-816x.2001.01666.x And in other papers, minocycline is regularly cited as helping with certain neuro degenerative disorders due to it's "anti-inflammatory properties". (same with Rheumatoid Arthritis). So we know that gram negative bacteria easily

induces inflammation because they use it in research. So why can't they make the connection that minocyline's anti inflammatory properties might possibly have something to do with the fact that it kills some of the bacteria that produces the toxins that create the inflammation????. Is it because no one wants to acknowledge the bacteria's existence and destructive capabilities in the first place? penny Windsor <rwindsor@...> wrote: Dear Rich Slim pickings for a quickie http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstract & list_uids=16401547 & query_hl=1 & itool=pubmed_docsum Very hard to tease out stuff from Goldberg though. Regards Windsor

[Guest guest]

One problem CFS has is a wheres-the- & ^%$ & ^-pathology problem.

If inflammations your suspicion, first thing you do is look for

leucocyte infiltrates. Theyve been seen in the CFS muscle, but theyre

very very light and only in a minority. Theres a bit of excess

leucocytes in the cerebrospinal fluid in some - again a minority.

Several other diseases have this problem.

Schizophrenia.

Narcolepsy (very very likely to be infection/immune-mediated, the

genetics show).

IBS.

Physiological depression, anxiety, etc.

Alzheimers is notable because there are no inflitrates. Theres just

gliosis (and the degenerative plaques, of course). This has been one

argument against it being an infectious disease. However,

neuroborreliosis (in the orthodox sense) is considered to

occasionally have no infiltrates.

Gliosis in CFS was suggested by the CSF protein findings in the

recent town study. A very important question we should

eventually try to answer is whether any CFS autopsy has ever done the

pathology (staining) needed to detect gliosis.

I wrote more about this here:

cfs_research/message/22035

[Guest guest]

That reminds me. I think we need to create an awareness campaign (and maybe a card to carry) requesting that our families order an autopsy, for research purposes, once we've died. Of course, we'd need someplace to send those autopsy results that wouldn't have a pre-existing agenda. penny <usenethod@...> wrote: One problem CFS has is a wheres-the- & ^%$ & ^-pathology problem. If inflammations your suspicion, first thing you do is look for leucocyte infiltrates. Theyve been seen in the CFS muscle, but theyre very very light and only in a minority. Theres a bit of excess leucocytes in the cerebrospinal fluid in some - again a minority.Several other diseases have this problem. Schizophrenia. Narcolepsy (very

very likely to be infection/immune-mediated, the genetics show).IBS.Physiological depression, anxiety, etc.Alzheimers is notable because there are no inflitrates. Theres just gliosis (and the degenerative plaques, of course). This has been one argument against it being an infectious disease. However, neuroborreliosis (in the orthodox sense) is considered to occasionally have no infiltrates.Gliosis in CFS was suggested by the CSF protein findings in the recent town study. A very important question we should eventually try to answer is whether any CFS autopsy has ever done the pathology (staining) needed to detect gliosis. I wrote more about this here:cfs_research/message/22035

[Guest guest]

Its absolutely essential to try and find the gliosis if it hasnt been

directly looked for - and the town study didnt mention it

having been looked for.

Its 100% clear that the brain can be affected by peripheral cytokines

in a big way. Nevertheless it seems very likely to me that something

is really wrong in the brain in most CFS, because so many neurologic

symptoms are often so extreme. I dont get significant photophobia,

significant hyperacusis, near-total insomnia, severe hyperactive

mentation, severe anxiety, or extreme brain fog from even the

lousiest flu, but I had all those from CFS, as so many people do.

The weird thing is, I was able to find out about a couple autopsies,

but there is NONE in the modern literature. I found one statement on

the web that no consistent autopsy findings have been found. Thats

not a shock. But not every autopsy can have every possible procedure.

Therefore, for gods sake, a disease needs to have a formal autopsy

series done and the protocols reported in the literature - even if

there is no expectation of consistent positive findings and there

dont in fact turn out to be any. That way it would be possible to

find out whether gliosis (etc etc etc) had ever been looked for, and

if so, how. Or, at least, case reports should be filed on all CFS

autopsies in the case report literature. Five zillion case reports

are published every year in dedicated journals about the most obscure

medical details and oddities you can imagine.

One autopsy was done early last century in an epidemic case and was

quite abnormal in the brain (source, Hydes book).

>

> That reminds me. I think we need to create an awareness campaign

(and maybe a card to carry) requesting that our families order an

autopsy, for research purposes, once we've died. Of course, we'd need

someplace to send those autopsy results that wouldn't have a pre-

existing agenda.

>

> penny

[Guest guest]

Wow, great post, Penny.

I expect all of you know that Pat Fero started a tissue bank for cfs after the

death of her son. Her problem is, though, who is going to test those tissues

and what for?

Personally, I would love to see IgeneX

testing for borrelia. I would like to see this testing also done on brains from

deceased Alzheimer’s patients. This would be just a start, but it might

begin to see how much borrelia is a factor.

I guess we can all get our names on Pat’s

list. Does anyone know if we can???

a

Carnes

I just got so frustrated by researcher's inability to see the

bigger picture or connect the dots, that I went and vented to my husband,

who's a scientist himself. I asked him why he thinks researchers are so slow to

at least consider what seems to be obvious connections.

He said he sees it all the time. Not only are researchers one

track minded due to the monetary impact on their research if it goes

" off track " , they also have egoic involvement. But he says

he also thinks it's mainly the way the majority of scientist's minds seem

to work. He said he thinks of a scientist's mind as being like a big

spinning hamster wheel. The wheel is comprised of a certain amount of

information that defines his " known " universe, and he spins that

wheel over and over attempting to make better sense of it. Anything

that tries to enter the spinning hamster wheel that is not already related to

the defined universe will just bounce right off. But very gradually,

the new piece of information sometimes starts to spin alongside the

hamster wheel. At first it spins out of sync, but eventually it

spins in sync with the wheel. At that point, the new information can jump

on board and become part of the scientist's defined universe.

But apparently it takes a very long time for the

average scientist or research community to allow new information on

board, especially if that information at first goes against what

they already " know " to be " true " . I suppose it was this frustration

at this kind of thinking that compelled Barry Marshall to infect

himself inducing ulcers just to prove that they're caused by

" bacteria " not stress.

Of course, what makes it even more difficult to counter this kind

of thinking is the fact that scientists are by nature very intelligent and

articulate and can easily convince others of the " logic " that

supports their positions.

This is why we need to start funding our own research, because we'll

probably all be dead before the medical establishment starts

taking microorganisms seriously (other than flesh eating, polio, tb,

etc., etc.,)

I truly think that we HAVE to get people to start looking at the most

destructive and damaging part of our disease first. The big

problem has to be acknowledged before we start trying to figure out how to

tinker with our immune systems to combat it. Seriously, how successfully can we

combat an unknown enemy? It's imperative that we identify the enemy, then

work on the strategies to fight it. Right now, everything is the opposite, we

keep developing strategies to bolster our defenses. And all that does

is lead us in circles around the enemy but we never

actually take the offense or penetrate its front line.

I ask for the bazillionth time, why is it that you can look at

almost any autoimmune, cognitive or degenerative disorder and find numerous

research articles linking it to bacteria in some way and yet no one ever says

that perhaps the bacteria itself is the CAUSE of the disorder? How can

researchers talk about minocycline's and other antibiotics' anti-inflammatory

properties and never even consider that perhaps its anti-inflammatory abilities

have something to do with the fact that it's killing an organism that

creates the endotoxin which results in inflammation?????

It's mind blowing to me.

penny

p.s. I'm going to start asking every doctor this question who suggests

the relief I'm getting from an antibiotic is due to it's anti-inflammatory

properties alone, not because it's actually combatting a toxin/inflammation

producing infection.

Penny Houle <pennyhoule@...>

wrote:

Hmmm, thanks for that link . Neuroinflammation

isn't something I've really looked at much before. (I've looked more at

ICP.) But there are a zillion papers on it. Especially linking it to alzheimers

as well as autism. Here's a quote from just one paper on the subject of NI and

Alzheimers:

" Inflammatory processes may play a critical role in the

pathogenesis of the degenerative changes and cognitive impairments associated

with Alzheimer's disease (AD). In the present study, lipopolysaccharide (LPS) from the cell wall of

gram-negative bacteria was used to produce chronic, global inflammation

within the brain of young rats. "

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=10051200 & dopt=Citation

In study after study, the method used to induce the

inflammatory process in the brains of rats is by administering the

endotoxin, lipopolysaccharides (LPS), which is derived from the cell

wall of gram negative bacteria.

I mean...give me a break. Isn't this what we've been

saying all along? We're chronically sick and inflammed due to endotoxins

produced by gram negative bacteria that are being ignored by the medical

community???

Here's another:

It has been postulated that neuroinflammation plays a critical role in

the pathogenesis of Alzheimer's disease (AD). To directly test whether an

inflammatory stimulus can accelerate amyloid deposition in vivo, we chronically administered the

bacterial endotoxin, lipopolysaccharide

http://www.blackwell-synergy.com/links/doi/10.1046/j.0953-816x.2001.01666.x

And in other papers, minocycline is regularly

cited as helping with certain neuro degenerative disorders due to it's

" anti-inflammatory properties " . (same with Rheumatoid

Arthritis). So we know that gram negative bacteria easily induces

inflammation because they use it in research. So why can't they make the connection

that minocyline's anti inflammatory properties might possibly have something to

do with the fact that it kills some of the bacteria that produces the

toxins that create the inflammation????.

Is it because no one wants to acknowledge the bacteria's

existence and destructive capabilities in the first place?

penny

Windsor

<rwindsor@...> wrote:

Dear Rich

Slim pickings for a quickie

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstract & list_uids=16401547 & query_hl=1 & itool=pubmed_docsum

Very hard to tease out stuff from Goldberg though.

Regards

Windsor

[Guest guest]

I've offered my brain to Lloyd but he can't have it til I've finished with it

Regards

Windsor

Re: [infections] Re: Neuroinflammation and degenerative & cognitive diseases

That reminds me. I think we need to create an awareness campaign (and maybe a card to carry) requesting that our families order an autopsy, for research purposes, once we've died. Of course, we'd need someplace to send those autopsy results that wouldn't have a pre-existing agenda.

penny

<usenethod@...> wrote:

One problem CFS has is a wheres-the- & ^%$ & ^-pathology problem. If inflammations your suspicion, first thing you do is look for leucocyte infiltrates. Theyve been seen in the CFS muscle, but theyre very very light and only in a minority. Theres a bit of excess leucocytes in the cerebrospinal fluid in some - again a minority.Several other diseases have this problem. Schizophrenia. Narcolepsy (very very likely to be infection/immune-mediated, the genetics show).IBS.Physiological depression, anxiety, etc.Alzheimers is notable because there are no inflitrates. Theres just gliosis (and the degenerative plaques, of course). This has been one argument against it being an infectious disease. However, neuroborreliosis (in the orthodox sense) is considered to occasionally have no infiltrates.Gliosis in CFS was suggested by the CSF protein findings in the recent town study. A very important question we should eventually try to answer is whether any CFS autopsy has ever done the pathology (staining) needed to detect gliosis. I wrote more about this here:cfs_research/message/22035