This is fascinating. Just think, as I donated My Russell's body to research
he is assisting in this research. He would be so proud.
----- Original Message -----
From: "ellicete" <[log in to unmask]>
To: <[log in to unmask]>
Sent: Saturday, September 23, 2006 3:19 PM
Subject: [catholic_culture] lzheimer's might share traits with prion
disorders
lzheimer's might share traits with prion disorders
Exposure to brain extracts sickens mice
By JOHN FAUBER
[log in to unmask]
Posted: Sept. 21, 2006
Scientists have been able to induce brain disease in mice by injecting
extracts of the brains of people who died of Alzheimer's disease, a finding
that suggests that Alzheimer's has some characteristics of prion brain
disorders such as mad cow disease and chronic wasting disease.
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The research also shows that under extreme laboratory circumstances, an
Alzheimer's-like disease can be transmitted.
Scientists not connected with the study said it points to important new ways
to look for the causes of Alzheimer's and potential new treatments.
"It's fabulous work," said Sam Gandy, an Alzheimer's researcher and director
of the Farber Institute for Neurosciences at Thomas Jefferson University.
"This is the first time a brain of a human with Alzheimer's has been used to
provoke pathology in another being."
The study by researchers in Europe and the United States is published today
in the journal Science.
During the 1970s, other researchers tried unsuccessfully to induce
Alzheimer's in chimps by injecting them with brain extracts from Alzheimer's
patients.
The study leaves open the possibility that something in the environment,
such as a toxin or even a tiny viral agent, might be involved along with a
key protein in causing Alzheimer's, said Gandy, who also is a spokesman for
the Alzheimer's Association, which partially funded the study.
The paper also showed for the first time that there can be different strains
of Alzheimer's.
"It's an extremely stimulating study," Gandy added.
Beta-amyloid is the protein that builds up in the brains of people with
Alzheimer's disease. There still is some debate about whether the protein
causes brain cells to die or whether it is a byproduct of some other disease
process.
All people make beta-amyloid in their brains, but in some it builds up,
probably beginning in midlife, and becomes the hallmark of Alzheimer's.
Many of the Alzheimer's drugs now being developed are designed to clear
beta-amyloid from the brain or prevent it from forming.
Extract speeds up disease
For the study, researchers used mice that were genetically engineered to
produce a human form of beta-amyloid in their brains.
Within about a year after birth, these transgenic mice normally would
develop clumps of beta-amyloid in their brains, much like what happens in
people with Alzheimer's disease.
However, when the mice were injected with brain extracts that contained
beta-amyloid from people who had died of Alzheimer's, the plaques appeared
within a few weeks.
The injections seemed to act as a seed that accelerated the disease process,
the researchers said. However, injections of brain material from patients
without known Alzheimer's disease failed to produce the lesions.
In addition, injections of synthetically made beta-amyloid also failed to
cause disease.
The researchers and others cautioned that there is no evidence that
Alzheimer's is transmissible in the way known prion diseases are spread.
"It's sort of a forced corruption (that was used in the study)," said
co-author Lary Walker, a research professor at Emory University. "It takes
the right molecule (of beta-amyloid) and the right molecule has to get into
the brain.
"Idiopathic Alzheimer's remains unexplained. What sets it in motion?"
Walker said his theory is that with the vast majority of Alzheimer's cases,
the seed is formed within the brain rather than from outside, "but we don't
know."
One possibility is that seeding protein molecules are shipped through axons,
the root-like appendages that emanate from neurons.
"They (axons) will transport things they are not supposed to," he said. "If
we could find a way to selectively block the transport, we might be able to
prevent it (Alzheimer's disease) from moving through the brain."
Mathias Jucker, senior author of the paper, said the work leaves open the
possibility of an environmental cause for Alzheimer's.
"I wouldn't be surprised, however, again, there is no evidence yet," said
Jucker, of the University of Tübingen in Germany.
One of the problems with the study is that it used homogenates of
beta-amyloid brain extract from Alzheimer's patients, said Piero Antuono, an
Alzheimer's specialist and professor of neurology at the Medical College of
Wisconsin.
"Who knows what's in that stuff?" he said. "It's basically like something
you throw in your Cuisinart."
Antuono noted that for years, researchers have known that beta-amyloid
builds up in misfolded clumps.
But in some Alzheimer's cases, beta-amyloid clumps are found along with tiny
holes in the brain known as spongiform lesions that are common to prion
diseases such as human mad cow disease.
"It could be two diseases," he said. "It's never been fully explained."
Based on the paper's findings, he speculated that clusters of Alzheimer's
cases found in families might not be entirely based on genetic causes as
some believe. They might be the result of some prion-like process, he said.
"This paper causes a shift, . . . a different place to look," he said.
The research clearly has a "prion flavor," said Judd Aiken, a prion
researcher at the University of Wisconsin-Madison.
But there is no evidence to suggest that Alzheimer's can be spread like
other prion diseases, he said.
In addition to prion diseases, several neurological disorders, including
Parkinson's, ALS, Huntington's and Alzheimer's, involve misfolded proteins,
Aiken said. But only prion diseases have been shown to be infectious, he
said.
From the Sept. 22, 2006 editions of the Milwaukee Journal Sentinel
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