NYT: Spirochetes, et al, in the brain could cause Alzheimer's
Mort Zuckerman
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Subject: NYT: Spirochetes, et al, in the brain could cause Alzheimer's
Date: Mar 9, 2010 3:35 AM
NYT ARTICLE BELOW
HEEeeey! I know. Spirochetes in
the brain - since we know they're permanent
brain infections according to CDC officer
Alan Barbour and IDSA -
http://www.actionlyme.org/BRAIN_PERMANENT.htm
could cause Alzheimers!!
Hey, I know. I could write that up and be
famous!!
Here's one written by DENTISTS which show
the high association between spirochetes in
the brain and Alzheimers:
http://www.actionlyme.org/BRAIN_PERMANENT.htm
(Number 22)
And on my homepage now in rebuttal to the
insane IDSA "guidelines" is a reference to
making NO FUNGAL ANTIBODIES against fungal
antigens like OspA or HIV gp120 vaccine
antigens amplified with OspA or Pam3Cys
I discuss how you won't be making antibodies
against these same type of fungal antigens
in Candida... not to mention the activation
of Opportunistics (The Cause of the New
Great Imitators):
http://www.actionlyme.org/Pam3Cys_Version15.htm
Some day I will become a famous scientist
and make a discovery.
LOL.
I'm trying to think ... How long have I
been screaming about OspA as an immune
suppressor and Lyme as a permanent
brain infection?
10 years?
Oh.
In between I had to go to jail for being
a "dangerously intelligent Unabomber Chemist"
to be saying such things, because after all
spirochetes and penises are almost identical
and are easy to mistake for each other :)))
"Hey, I think she's onto something"
ROTFLMAO.
KMDickson
http://www.actionlyme.org
==================================
http://www.nytimes.com/2010/03/09/health/09alzh.html?hpw
Infection Defense May Spur Alzheimer’s
By GINA KOLATA
Published: March 8, 2010
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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.
Enlarge This Image
Lee Goldstein, Robert Moir, Rudy Tanzi
COMMON VILLAIN Bacteria being attacked by beta amyloid, in this image
enlarged 18,500 times.
Related
*
Health Guide: Alzheimer's Disease
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.
"[Real] scientists are *fiercely* independent. That's the good
news."-- NIH's Top Fool, Anthony Fauci