Amyloids

[Kritters]

Insights into fibers' structure could aid studies of Alzheimer's, more - MIT News Office


Fibers unknown and being researched. I was researching bio-engineering and came across this collection of research projects by MIT today. The list is really impressive. One thing I came across is the word, "amyloid". It's a fiber. Is it a prion? Is it a protein?

What is amazing to me right now is that, here we are doing this research to figure out what our fibers are, and I have no doubt in my mind, feeble as it is, that the connection, although possibly broad in scope, is still a connection. And as I said, here we are struggling to figure this out with our microscopes, drawings, photos......and to find that there are students who are making it a project to figure out what SHOULD have been figured out by the people who are being PAID by the government!! Okay, these are grants for that purpose, but they are being financed by pharmaceutical companies.

So what is so very wrong with this picture? Everyone's out to make a buck.

Aside from that, check out amyloids, proteins, amyloid (fiber)construction on google. I will as well, but I just had to post this to get it started. I'm researching while watching the presidential debates right now but I will get back to it to see if there may be any connection between OUR fibers and AMYLOID fibers.

Hey, here's an idea: let's get a government grant to support NON PHARMACEUTICAL research regarding Morgellons. hey, let's get a PRIVATE grant! then we'll have more control. Anyone have Bill Gates for dinner lately? Hey how about Prince Charles?

On the one hand this shows how sad it is that so little is known about the construction of disease structures. On the other hand, when WE figure it out, it will be done.

Kritters

[Kritters]

Check out the 'yeast' prions.

Notice ALL the diseases named which are associated with this FIBER which is an enigma to scientists today.

Kritters

[pat]

'Krishnan was able to identify the precise segment at which the prions interact--something that no one had done before him with a real prion. To do this, he took a variety of yeast prion strains and modified them in such a way that if particular designated regions came into contact with each other, they would emit a fluorescent signal, allowing him to map the pattern by which the different strains of prions interacted with each other'

Well he had to modify them and found fluorescent signals.I haven't had to modify anything to see the fluorescence on the things that came out of my body and lungs,as I'm sure many others on here have found.
You would think that ALL these people with ALL the brain power they have between them would have seen the similarities to what we are suffering from.In fact if they read this forum and all the investigative work thats been done by members it would put them on the right road.
I'm no brainbox ,but saw my mum start with 'alzeimers' followed by most of the other symptoms associated with morgs-although I didn't know about morgs then.She started with 'brain fog' being forgetful,etc.Its said the victims of alzeimers are getting younger,usual case of 'they don't know why',but why the reluctance to look at this fibre connection?
These fibres we see are I'm sure behind quite a few diseases that the meds 'don't know why or what causes it'.And the biggest mystery is why there isn't ONE researcher/scientist interested in looking at the connection.Unless they are just waiting for someone on here to provide the answer and grab it for themselves.

[Kritters]

Pat,
Looks like you get my drift as usual. I also am wondering if it's a case of not seeing the forest for the trees (or in this case the fibers for the disease) and aren't aware of what is really going on with diseases (autoimmune esp.) because those who do the research are not perusing the web for blogs, and will certainly not get fed info. You'd think discerning research scientists would be aware of Morgellons by now, since the CDC has reluctantly acknowledged it, but of course, everyone is concerned about his/her job, aren’t they. Yes, I think those who are researching on forums will certainly lend a clue if there isn’t one.
Kritts xo

[Kritters]

There is no question in my mind that fundamental and extensive knowledge is free-flowing amongst the scientific research communities for more than one goal. The smelly stench of science for profit vs. science for the purpose of saving lives as opposed to making bigpharma even bigger is becoming overwhelming to me.

Oh no!!! The average person on the street is able to research and find out our secret information! You know for sure that it won't be long before our internet searching capabilities will be squenched.

In a perfect world, research for profit wouldn't exist, at least to the extent it has today. Let's just hope there are more of us than them and we will collectively be able to shame them into submission by our research. To quote an excerpt:

"While the results of this research are clearly of interest to scientists investigating conditions such as Alzheimer's, it's also relevant to scientists studying nanotechnology. In March of 2003, Lindquist published a paper in which she described how amyloid fibers can become the core of nanoscale electrical wires, opening the possibility of one day incorporating them into integrated circuits. "

These Amyloid fibers could VERY WELL be our Morgellons fibers. How on earth can we expect Kaiser Permanente to figure out what our Morgellons fibers are if no one in the scientific community can figure out what the so called amyloid fibers are?

give me a break.

Kritters

[chester]

And this elongated worm is repeted over and over inside the beans that i find. I have phases of it...before it elongates, and after it elongates. I have tiny ones elongating in their tiny orbs, and large ones in large bean orbs. This production is for a reason, and the reason has nothing to do with us. This is a freak side show going on inside us, and inside each bean orb. How i long to know what this is and have it long gone!

[Kritters]

any way we can keep threads relevant here?

[Niels]

I posted some info about the amyloid/morgellons connection, unfortunately, I'm not allowed to post the links as i've not posted enough... so i've de-linkified my links paste to your browser, remove the space ' ' character,and then submit....

alzheimer's fibers destroyed by DAPH
http: // lymebusters.proboards39.com/index.cgi ? action=display & board=rash & thread=10851 & page=1
Is Morgellons Alzheimer's of the Skin?
http: // lymebusters.proboards39.com/index.cgi ? action=display & board=theories & thread=10841 & page=1

[Niels]

FYI, CPN and Alz (still can't post links)
http :// www . tangledneuron . info / the_tangled_neuron/2007/06/chlamydia-pneum.html

Chlamydia Pneumoniae and Alzheimer's

Summary: Infection with a common bacterium called Chlamydia pneumoniae may increase the risk of developing Alzheimer’s. The bacterium has already been linked to heart disease and hardening of the arteries. Work to investigate the role of viruses and bacteria such as Chlamydia pneumoniae in chronic diseases is in the early stages, but researchers hope it will help identify and treat the underlying causes of Alzheimer’s.

More study is needed to confirm the bacterium’s relationship with dementia, and rigorous clinical trials would be necessary before any treatments based on this research could be recommended.

I’ve written before about how viruses and bacteria can contribute to chronic diseases not previously linked to infections. It is now accepted that a type of bacteria contributes to ulcers, and that human papillomaviruses are the major cause of cervical cancer. A common bacterium called Chlamydia pneumoniae (also called Chlamydophila pneumoniae and C. pneumoniae) has been linked to atherosclerosis (hardening of the arteries) and other chronic diseases.

Dr. Brian Balin, a professor at the Philadelphia College of Osteopathic Medicine and Basic Science Director of the school’s Center for Chronic Disorders of Aging thinks that same bacterium may also contribute to many cases of Alzheimer’s. As the name indicates, the bacterium causes a type of pneumonia - it’s not the same as the sexually transmitted type of Chlamydia.

Although the link between C. pneumoniae and Alzheimer’s is not well-accepted, Dr. Balin has been researching the relationship for years. At a 1995 meeting he attended, talk turned to the possible link between the bacterium, hardening of the arteries and heart disease.

“I asked whether anyone had ever looked for the organism in brain tissue,” he remembers. “My background in neuropathology dealt with the blood brain barrier, and I had for some time believed that damage to the blood vessels in the brain could be involved in Alzheimer’s disease. My beliefs were not widely held….”

“Anyway, after asking the question, I performed a search of the literature and found that no one had ever looked in brain tissues for the presence of this infection.... So, I went to our -80 C freezers and pulled out frozen brain tissues from both AD [Alzheimer’s disease] and non-AD brains. I sent these samples in a coded or blinded fashion to Dr. Alan Hudson for analysis by polymerase chain reaction (PCR), which is a way of testing whether the DNA of the organism was in the tissue samples.” [Dr. Hudson is a Wayne State University School of Medicine professor whose lab focuses on Chlamydia research.]

It turned out that the AD tissue samples contained the DNA from the bacterium, while the non-AD tissues did not. The two researchers repeated the experiment with different samples, and got the same results.

“This then led to our expanded experiments to determine whether C. pneumoniae could be detected using a variety of methods,” says Dr. Balin. “All in all, we used six different techniques which gave consistent results. The first publication of our work was in 1998 in Medical Microbiology and Immunology.”
[ ... ]

How Chlamydia Pneumoniae May Trigger Alzheimer’s

How could a type of pneumonia affect the brain? “My group has found that C. pneumoniae, once inhaled, infects white blood cells, in particular the monocytes that circulate throughout the blood stream,” Dr. Balin explains. “These cells can enter through the walls of the blood vessels and can carry the organism into different tissues, including the brain.”

“We also have evidence that the cells in our upper noses known as the olfactory neuroepithelial cells (those cells controlling our sense of smell) are infected by C. pneumoniae.” The olfactory neuroepithelial cells are close to the olfactory bulb region of the brain and to the hippocampus, where short term memory is formed. These areas of the brain are among the first to be affected by Alzheimer’s. This suggests there may be a link between infection with C. pneumoniae and the reported association between the loss of sense of smell and the onset of Alzheimer’s.

Finally, there is some tantalizing evidence that the bacterium may actually trigger the formation of the amyloid plaques characteristic of Alzheimer’s brains. When mice in Dr. Balin’s lab were infected with C. pneumoniae, they developed amyloid plaques in their brains. Adding to the evidence of the link between the bacterium and Alzheimer’s pathology, the bacterium was found near plaques and tangles in human Alzheimer’s brains studied in his lab.

C. Pneumoniae – Another Piece of the Dementia Puzzle?

Dr. Balin points out that the connection between C. pneumoniae and Alzheimer’s is consistent with other research on the disease. Some scientists think inflammation causes the brain damage seen in Alzheimer’s. “Quite possibly the inflammatory response due to a chronic persistent infection with C. pneumoniae and/or other infectants causes much of the cellular damage in the brain,” he says. “Also, genetic risk factors such as having the ApoE 4 variant which has been correlated with Alzheimer’s disease may actually increase one’s risk for being infected with C. pneumoniae and other infectants such as Herpes Simplex Virus 1. The interrelationship of ApoE with infectants may be how this variation confers greater risk for getting both infections and Alzheimer’s disease. Our data have shown that Alzheimer’s brains that express the ApoE4 variation actually have greater concentrations of C. pneumoniae than Alzheimer’s brains not expressing the variant.”

He thinks the connection between C. pneumoniae and hardening of the arteries may also be relevant to dementia. Of course, arteries are a type of blood vessel. Once white blood cells infected with C. pneumoniae reach the brain, Dr. Balin theorizes, they may damage the blood vessel walls there. This would contribute to vascular dementia and brain tissue damage.

But if exposure to Chlamydia pneumoniae is common, as indicated by the antibodies in many people’s blood, why don’t we all develop Alzheimer’s? “Exposure to an infectious agent does not necessarily translate into a specific disease,” says Dr. Balin. “There are many other factors, both genetic and environmental, that would dictate why some get a disease and others do not, even when you have a large percentage of the population exposed to the infectious agent. One example is exposure to the common cold viruses, which are very ubiquitous. Not everyone exposed gets a cold. …so, not everyone exposed to C. pneumoniae would develop Alzheimer’s, but the potential for the disease would be ever-present.”

Potential Treatments for Alzheimer’s and Dementia

Dr. Balin cautions against rushing to treat Alzheimer’s based on the possibility that C. pneumoniae could trigger the disease. “The dilemma that we face is that without current long-term effective treatments for AD, many people may want to try, even experimentally, other types of drug regimens based on the work that we and others are doing with infection,” he says. “Obviously, without clinical trials first, we cannot know for sure who would be most likely to benefit. We have to determine who is infected with which organism(s) and try to treat appropriately. This is why we really need a concerted effort to develop controlled clinical trials.”

He’s done some thinking about what types of therapies a clinical trial could test. “We know that Herpes Simplex Virus 1 may be involved in a significant number of AD cases and this may also have to be considered in a therapeutic regimen. All in all, I think that infection data (even at this point in time), suggests that using combination therapy of an anti-inflammatory, anti-chlamydial and an anti-viral for Herpes could be beneficial."

The “cocktail” he is proposing for trials includes anti-inflammatory medicines or NSAIDs (non-steroidal anti-inflammatory drugs such as aspirin and ibuprofen). Although some population studies have shown a link between NSAID use and decreased risk of Alzheimer’s, evidence from clinical trials using NSAIDs to slow progression of the disease is not very encouraging. If inflammation is caused by infection with C. pneumoniae, Dr. Balin says, it’s unlikely that it could be controlled in the long run by NSAIDs alone.

Antibiotics targeted to Chlamydia bacteria are also part of the proposed cocktail. At least one study has shown antibiotics may slow progression of mild to moderate Alzheimer’s, but more research is needed. “Our research suggests that treating individuals who have Mild Cognitive Impairment, and those who have newly diagnosed and/or existing Mild AD, with anti-chlamydial antibiotics may have a positive effect by either stopping a trigger for the disease or preventing disease onset in the case of MCI,” Dr. Balin says.

But antibiotics don’t always wipe out C. pneumoniae, and as with other infectious disease, there are worries that the bacterium will become resistant to treatment. These worries have scientists searching for alternative therapies, Dr. Balin says. “The use of more novel anti-infection compounds, and potentially the development of a vaccine for these infectants could result in combating dementia-causing organisms.”

[...]

[Jo]

Thanks Niels, great threads.

I've been reading some journals which state that the amyloid fibre deposits are the cause of at least 17 human diseases.

I'm also trying to understand fruit fly protein (GAGA factor), in relation to amyloid fibre formation...

IngentaConnect The glutamine-rich domain of the Drosophila GAGA factor is necess...

Any help, would be gratefully received.

Jo