Topic: Article: Alzheimer's caused by Bacterial Infection?
Vermont_Lymie
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When will the medical establishment wake up from the IDSA-induced coma and recognize the full impact of lyme and tick-borne diseases?
********** March 8, 2010
Infection Defense May Spur Alzheimer's
By GINA KOLATA
For years, a prevailing theory has been that one of the chief villains in Alzheimer's disease has no real function other than as a waste product that the brain never properly disposed of.
The material, a protein called beta amyloid, or A-beta, piles up into tough plaques that destroy signals between nerves. When that happens, people lose their memory, their personality changes and they stop recognizing friends and family.
But now researchers at Harvard suggest that the protein has a real and unexpected function -- it may be part of the brain's normal defenses against invading bacteria and other microbes.
Other Alzheimer's researchers say the findings, reported in the current issue of the journal PLoS One, are intriguing, though it is not clear whether they will lead to new ways of preventing or treating the disease.
The new hypothesis got its start late one Friday evening in the summer of 2007 in a laboratory at Harvard Medical School. The lead researcher, Rudolph E. Tanzi, a neurology professor who is also director of the genetics and aging unit at Massachusetts General Hospital, said he had been looking at a list of genes that seemed to be associated with Alzheimer's disease.
To his surprise, many looked just like genes associated with the so-called innate immune system, a set of proteins the body uses to fight infections. The system is particularly important in the brain, because antibodies cannot get through the blood-brain barrier, the membrane that protects the brain. When the brain is infected, it relies on the innate immune system to protect it.
That evening, after the lab's usual end-of-the-week beer hour, Dr. Tanzi wandered into the office of a junior faculty member, Robert D. Moir, and mentioned what he had seen. As Dr. Tanzi recalled, Dr. Moir turned to him and said, ``Yeah, well, look at this.''
He handed Dr. Tanzi a spreadsheet. It was a comparison of A-beta and a well-known protein of the innate immune system, LL-37. The likenesses were uncanny.
Among other things, the two proteins had similar structures. And like A-beta, LL-37 tends to clump into hard little balls.
In rodents, the protein that corresponds to LL-37 protects against brain infections. People who make low levels of LL-37 are at increased risk of serious infections and have higher levels of atherosclerotic plaques, arterial growths that impede blood flow.
The scientists could hardly wait to see if A-beta, like LL-37, killed microbes. They mixed A-beta with microbes that LL-37 is known to kill -- listeria, staphylococcus, pseudomonas. It killed 8 out of 12.
``We did the assays exactly as they have been done for years,'' Dr. Tanzi said. ``And A-beta was as potent or, in some cases, more potent than LL-37.''
Then the investigators exposed the yeast Candida albicans, a major cause of meningitis, to tissue from the hippocampal regions of brains from people who had died of Alzheimer's and from people of the same age who did not have dementia when they died.
Brain samples from Alzheimer's patients were 24 percent more active in killing the bacteria. But if the samples were first treated with an antibody that blocked A-beta, they were no better than brain tissue from nondemented people in killing the yeast.
The innate immune system is also set in motion by traumatic brain injuries and strokes and by atherosclerosis that causes reduced blood flow to the brain, Dr. Tanzi noted.
And the system is spurred by inflammation. It is known that patients with Alzheimer's disease have inflamed brains, but it has not been clear whether A-beta accumulation was a cause or an effect of the inflammation. Perhaps, Dr. Tanzi said, A-beta levels rise as a result of the innate immune system's response to inflammation; it may be a way the brain responds to a perceived infection.
But does that mean Alzheimer's disease is caused by an overly exuberant brain response to an infection?
That's one possible reason, along with responses to injuries and inflammation and the effects of genes that cause A-beta levels to be higher than normal, Dr. Tanzi said. However, some researchers say that all the pieces of the A-beta innate immune systems hypothesis are not in place.
Dr. Norman Relkin, director of the memory disorders program at NewYork-Presbyterian/Weill Cornell hospital, said that although the idea was ``unquestionably fascinating,'' the evidence for it was ``a bit tenuous.''
As for the link with infections, Dr. Steven T. DeKosky, an Alzheimer's researcher who is vice president and dean of the University of Virginia School of Medicine, noted that scientists have long looked for evidence linking infections to Alzheimer's and have come up mostly empty-handed.
But if Dr. Tanzi is correct about A-beta being part of the innate immune system, that would raise questions about the search for treatments to eliminate the protein from the brain.
``It means you don't want to hit A-beta with a sledgehammer,'' Dr. Tanzi said. ``It says what we need is the equivalent of a statin for the brain so you can dial it down but not turn it off.'' (Dr. Tanzi is a co-founder of two companies, Prana Biotechnology and Neurogenetic Pharmaceutical, that are trying to dial down A-beta.)
Dr. Relkin said that even if A-beta were not part of the innate immune system, it might not be a good idea to remove it all, along with the hard balls of plaque it makes in the brain.
In the past, Dr. Relkin said, scientists assumed ``that the pathology was the plaque.'' Now, he likens removing plaque to digging up bullets at the Gettysburg battlefield.
The more bullets in an area, the more intense the fighting was. But ``digging up bullets will not change the outcome of the battle,'' he said. ``Most of us don't believe that removing plaque from the brain is the end-all.''
But other scientists not connected with the discovery said they were impressed by the new findings.
``It changes our thinking about Alzheimer's disease,'' said Dr. Eliezer Masliah, who heads the experimental neuropathology laboratory at the University of California, San Diego. ``I don't think we ever thought about that possibility for A-beta.''
Dr. Masliah is intrigued by the idea that aggregates of A-beta may be killing bacteria and brain cells by the same mechanism. He noted that Dr. Tanzi had a track record of coming up with unusual ideas about Alzheimer's disease that later turn out to be correct.
``I think he's onto something important,'' Dr. Masliah said.
[ 03-09-2010, 06:57 AM: Message edited by: Vermont_Lymie ]
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Rivendell
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In the book "Cure Unknown" (about Lyme Disease written by a science journalist), the author talks about the link between Lyme Disease and Alzheimer's. In fact, I think that my foggy brain remembers her saying that a Harvard researcher did an autopsy on 10 brains from alzheimer's patients and found Lyme Disease in 7 of the brains.
I'm hoping that research such as this, plus the research that is being done on Morgellon's disease will eventually lead to better diagnostic tools and better treatments for Lyme Disease.
Just how long can greed and power keep us down?
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D Bergy
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Some other, related research.
Prion Found to Damage Brain Arteries
Scientists investigating how prion diseases destroy the brain have observed a new form of the disease in mice that doesn't cause the sponge-like brain deterioration typically seen in these disorders. Instead, they found damage to brain arteries that resembled a disease related to human Alzheimer's disease.
TerryK
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Good find!
Why does anyone think that the Harvard researchers are the first to find a possible association with infection? Don't they have access to a computer so they can look at other research? LOL
MacDonald tried to get someone to listen regarding spirochetes and Alzheimers years ago. MacDonald is the one who found spirochetes in 7 of 10 alzheimer brains. I'm not sure if he found borrelia or some unknown spirochete.
From the book "Cure Unknown", apparently MacDonald tracked a DNA sequence in 7 of 10 Alzheimer's brains that were part human, part spirochete. He asserts that this is a "transfection", in which the proteins causing illness are no longer manufactured by Bb but by the genes of the patients themselves.
Terry
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Pinelady
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Alzheimers caused by Genetics-----Citing that 1 in 10 Whites,
1 in 4 Blacks and 1 in 3 Hispanics will get Alzheimers...
It is in refute to that article but most people will not see it is labor related----Not Genetic!
It is the people who are most closely involved with tick territories. I had a whole crew of
Mexican tree trimmers here wading around in the weeds I cautioned. Think how many migrant workers
work in the fields. And labor for road crews etc.
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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posted
Thank you, Pinelady. Always good to know the source of the article.
Posts: 822 | From midwest | Registered: Apr 2009
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D Bergy
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More information regarding prions and an alternative explanation as to why they become destructive. Not directly related to Alzheimer's but possibly relevant.
You be the judge.
1.) Prions are naturally-occurring proteins, involved in protecting tissues (such as the eyes) from harmful UV radiation. 2.) When exposed to both organophosphates and manganese, prions change from copper-tipped to manganese-tipped, and cause a chain reaction of prions switching to manganese "tips". (The organophosphate may serve as a chelating agent or catalyst.) Manganese-tipped prions are virtually indestructible, surviving disinfectants, autoclaves, and incineration.
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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posted
To quote pinelady "Alzheimers caused by Genetics-----Citing that 1 in 10 Whites,
1 in 4 Blacks and 1 in 3 Hispanics will get Alzheimers..."
Also, it is harder to see a bullseye on darker skin. So, Blacks and Hispanics would be less likely to see the bullseye and catch LD in its early, treatable stages compared to Whites.
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Pinelady
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Dbergy you may be right with the recent meat packers being
shut down due to allowing downer cows in the food
chain. But I would still bet on ticks causing the
most incidence.
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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D Bergy
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I actually was looking for some old research that indicated that prions were part of the life cycle of some type of Spirochete. I think it was a German Guy, but my memory is not that great either.
I cannot find it, but I know I read it once. I stumbled on to this, so I posted it.
I am not promoting any particular theory. I am just throwing stuff out there, seeing if any of it sticks.
Dan
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Pinelady
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I think the article you speak of was a comparison of how they were related. Not sure as I don't know where it is either.
Here is a 2006 Alzheimer article that is very relevant. If you put this all together In my opinion one should treat and treat for as long as it takes.
The processes, which drive this host reaction are unknown. To determine whether an analogous host reaction to that occurring in AD could be
induced by infectious agents, we exposed mammalian glial and neuronal cells in vitro to Borrelia burgdorferi spirochetes and to the inflammatory bacterial lipopolysaccharide (LPS).
Morphological changes analogous to the amyloid deposits of AD brain were observed following 2-8 weeks of exposure to the spirochetes. Increased
levels of β-amyloid presursor protein (AβPP) and hyperphosphorylated tau were also detected by Western blots of extracts of cultured cells that
had been treated with spirochetes or LPS. These observations indicate that, by exposure to bacteria or to their toxic products, host
responses similar in nature to those observed in AD may be induced.
I know one thing for sure....We do not have near enough LLMD's to treat....
Allie that is so true! And those groups would also be less likely to seek medical treatment for a bug bite.
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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map1131
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It's not just ticks. That is why this has gotten into the epidemic stage. I don't know how long it's going to take for the "big picture" to come to be.
I've been waiting 10 yrs and hundreds of thousands, maybe millions of ill people later. But I haven't given up hope. It's got to be soon.
Pam
PS: What was it that Dr B said about 8 out of 10 Alzheimers brains tested were positive for lyme disease? I'm pretty sure that was his quote.
-------------------- "Never, never, never, never, never give up" Winston Churchill Posts: 6478 | From Louisville, Ky | Registered: Jan 2002
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Vermont_Lymie
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Terry, that was sure the scariest section of "Cure Unknown" for me! That transinfection concept, which McDonald seems to have shown by his DNA sequencing, is the thing that keeps me up at night!
Thanks Pinelady for the NYTimes link; somehow that source was cut off.
Pam, I definitely agree that it is not just ticks (or not just lyme); my cognitive issues with Babesia were profound before treatment.
You have to wonder why the IDSA is so incurious about this fascinating and important stuff....
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Pinelady
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If you get a chance see the news for the protests going on today in the news.
It looked like thousands there protesting peaceably.
The only one reported arrested were the ones trying to get in the building the exec.s were in to arrest them.
The people actually tried to make citizens arrests to Ins. Co. Exec's.
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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Pinelady
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Wow. MSM shut that down like a bomb. Did anyone else see it?
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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