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Alzheimer's, Dementia & Mental Health
Aging is the Critical Factor Allowing Alzheimer's to
Develop
Aging process plays an active role, too, in
Parkinson’s and Huntington’s
|
 Half of all
people who reach age 85 will likely be affected by Alzheimer’s
disease, with the onset age usually around 75. |
August 10, 2006 – For those who have wondered if
Alzheimer's disease is a consequence of aging or if it just takes a long
time for the toxic protein aggregates that cause it to form, researchers
have the answer. A collaboration between researchers at the Salk
Institute for Biological Studies and the Scripps Research Institute
shows that aging is the critical factor.
Harmful beta amyloid aggregates accumulate when
aging impedes two molecular clean-up crews from getting rid of these
toxic species.
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Closely Related Story |
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Cell Activities that
Protect against Alzheimer's Protein Buildup Found
Findings may lead to new therapies for
Neurodegenerative Diseases such as Alzheimer's and Parkinson's
 August 11, 2006 – Yesterday there was news of
research finding it is aging that actually causes the brain to stop
cleaning out the protein build-up that causes Alzheimer's. Today, it was
announced that those researchers have combined their work with another
group and have found new avenues to combat age-onset protein aggregation
diseases, such as AD, Parkinson's, Huntington's, and ALS.
Read more...
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More Related Stories |
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Genetics Used to Learn How People Reach 90 with Good
Mental Ability
August 10, 2006 - Scientists have identified genes
related to reaching age 90 with preserved cognition, according to a
study to be published in the September issue of the American Journal of
Geriatric Psychiatry. The study is among the first to identify genetic
links to mental longevity. The finding that genetics, lifestyle decision
making, and their interactions, may influence the ability to reach old
age with preserved cognition is described as "exciting."
Read more...
Drug Fully Reverses Age-Related Memory Loss by
Triggering Natural Mechanism
Study with rats shows ampakines boost brain’s
protein in government financed study
July 27, 2006 - A drug made to enhance memory
appears to trigger a natural mechanism in the brain that fully reverses
age-related memory loss, even after the drug itself has left the body,
according to researchers at UC Irvine. “This is a significant
discovery,” said Christine Gall, professor of anatomy and neurobiology.
“Our results indicate the exciting possibility that ampakines could be
used to treat learning and memory loss associated with normal aging.”
Read more...
Researchers find 'Probable Cause' for Parkinson's,
Alzheimer's, other Brain Disorders
June 28, 2006 - Parkinson's, Alzheimer's, Lou
Gehrig's disease and other brain disorders are among a growing list of
maladies attributed to oxidative stress, the cell damage caused during
metabolism when the oxygen in the body assumes ever more chemically
reactive forms.
Read more...
Read more
on
Alzheimer's, Dementia & Mental Health |
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This finding opens the door for development of
drugs preventing build-up of toxic protein aggregates in the brain. The
study appears in the Aug. 10 issue of Science Express, the advanced
online edition of the journal Science.
“Aging is the most important risk factor for
neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s
disease, and Huntington’s disease,” says senior author Andrew Dillin,
Ph.D., an assistant professor in the Salk Molecular and Cell Biology
Laboratory.
“Our study revealed that the age onset of these
diseases is not simply a matter of time but that the aging process plays
an active role in controlling the onset of toxicity,” he explains.
Beta amyloid production occurs in all brains, but
healthy cells clear away excess amounts. Brains of people with
Alzheimer’s disease, on the other hand, are unable to control beta
amyloid accumulation. For years, scientists have scrambled to find out
why.
To answer this vexing question, Dillin analyzed
protein aggregation in the roundworm, a streamlined organism that, like
mammals, uses the insulin/IGF-1 pathway to control lifespan but can be
rapidly manipulated genetically. Dillin used roundworms that produce
human beta amyloid peptide in body wall muscles. As the worms aged, the
protein formed toxic aggregates causing paralysis.
Then researchers experimentally decelerated aging
in engineered worms by lowering activity of the insulin/IGF-1 pathway
and asked whether it was simply the passage of time—not aging per
se—that favored protein aggregation. It wasn’t: chronologically “old”
worms crawled around happily, while counterparts whose insulin/IGF-1
pathway was normal could only helplessly wriggle their heads.
However, close inspection of the data revealed a
surprise: “Worms with reduced insulin signaling seemed perfectly fine
although they had high molecular weight aggregates, while worms with an
accelerated aging program were extremely sensitive to the toxic effects
of beta amyloid but we couldn’t detect any large fibrils,” explains
postdoctoral researcher and co-lead author Ehud Cohen, Ph.D.
Intrigued, Dillin turned to an expert on beta
amyloid biochemistry, Jeffery Kelly, Ph.D., a professor of chemistry at
Scripps and a member of its Skaggs Institute of Chemical Biology.
Together they found that cells use an unexpected
two-pronged strategy to rid themselves of harmful aggregates. Kelly
explains, “One pathway disaggregated beta amyloid fibrils, while the
other actively packed them into high molecular weight aggregates. But
the latter only kicks in when the cell is left with no other options.”
The surprise was that very high molecular weight
species were actually less toxic than smaller aggregates. “For a long
time large protein aggregates were considered the toxic species,”
explains Cohen. “The fact that cells protect themselves by temporarily
storing small fibrils as high molecular weight aggregates marks a clear
paradigm shift.”
Two proteins controlled by insulin/IGF-1 signaling
orchestrate detoxification—HSF-1, which takes care of aggregate
break-down, and DAF-16, which mediates formation of safer, super-sized
aggregates as debris accumulates. “We assumed that DAF-16 and HSF-1
would do the same job, but they don’t. This is extremely exciting
because it gives us two unique opportunities to attenuate beta amyloid-mediated
toxicity by manipulating the activity of these factors,” says Dillin.
New model for neurodegenerative diseases
Half of all people who reach age 85 will likely be
affected by Alzheimer’s disease, and the onset age – usually around 75 –
is almost the same for all sporadic neurodegenerative aggregation
diseases. Thus, Salk researchers have developed a model that explains
why these disorders occur late in life.
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The
tiny worms used in the Alzheimer's research in this story are
also playing a leading role in the fight against cancer. See
story below. |
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Tiny Worm is Newest Weapon to Discover
Cancer-Causing Compounds in Household Products
Helps detect virtually any potential cancer-causing
chemical
June 21, 2006 – A little worm has enabled scientist
to detect action that blocks "cell suicide," and causes chemical
compounds in household products, like mothballs and air fresheners, to
become possible cancer-causing agents.
Read
more...
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Throughout life, brain cells produce
aggregation-prone beta-amyloid fragments that must be cleared. “This
process is very efficient when we are young but as we get older it gets
progressively less efficient,” says Cohen. As the affected individual
reaches the seventh decade of life the clearance machineries fail to
degrade the continually forming toxic aggregates and the disease
emerges.
In individuals who carry early onset Alzheimer’s-linked
mutation, an increased “aggregation challenge” leads to clearance
failure and the emergence of Alzheimer’s much earlier – usually during
their fifth decade.
“It was very satisfying when the biochemical data
from Jeffery’s lab and genetic results from our lab came together,”
recalls Dillin. Both scientists are continuing the collaboration by
searching for small molecules that delay the aging program and boost
protective mechanisms.
Other contributing authors were co-lead author Jan
Bieschke, Ph.D., formerly at Scripps and now at Max Delbrueck Center in
Berlin, and research assistant Rhonda M. Perciavalle.
The Salk Institute for Biological Studies in La
Jolla, California, is an independent nonprofit organization dedicated to
fundamental discoveries in the life sciences, the improvement of human
health and the training of future generations of researchers. Jonas
Salk, M.D., whose polio vaccine all but eradicated the crippling disease
poliomyelitis in 1955, opened the Institute in 1965 with a gift of land
from the City of San Diego and the financial support of the March of
Dimes.
>> Read the Associated Press story on this research
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