[tt] Next Big Future - 2 new articles
Eugen Leitl
<eugen at leitl.org> on
Wed Aug 20 13:44:02 UTC 2008
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Date: Wed, 13 Aug 2008 03:20:07 -0400
To: eugen <eugen at leitl.org>
Subject: Next Big Future - 2 new articles
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"[2]Next Big Future" - 2 new articles
1. [3]Aging biomarkers
2. [4]One dose of RNAi reduces Cholesterol by 60% for three weeks
3. [5]More Recent Articles
4. [6]Search Next Big Future
[7]Aging biomarkers
Scientists have identified biomarkers that indicate telomere
shortening. CRAMP, stathmin, EF-1a, and chitinase are proteins that
they found to be secreted from telomere-dysfunctional bone-marrow
cells of late generation telomerase knockout mice. Their study, which
was published this week in PNAS, showed an increase in expression of
these markers in the blood of aging and geriatric people with
age-related disease; it also allowed them to discriminate between
young and old and between disease and healthy control groups. Protein
biomarkers are easier to track with inexpensive blood tests.
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[14]Proteins induced by telomere dysfunction and DNA damage represent
biomarkers of human aging and disease
Telomere dysfunction limits the proliferative capacity of human
cells by activation of DNA damage responses, inducing senescence or
apoptosis. In humans, telomere shortening occurs in the vast
majority of tissues during aging, and telomere shortening is
accelerated in chronic diseases that increase the rate of cell
turnover. Yet, the functional role of telomere dysfunction and DNA
damage in human aging and diseases remains under debate. Here, we
identified marker proteins (i.e., CRAMP, stathmin, EF-1a, and
chitinase) that are secreted from telomere-dysfunctional
bone-marrow cells of late generation telomerase knockout mice
(G4mTerc -/ -). The expression levels of these proteins increase in
blood and in various tissues of aging G4mTerc -/ - mice but not in
aging mice with long telomere reserves. Orthologs of these proteins
are up-regulated in late-passage presenescent human fibroblasts and
in early passage human cells in response to g-irradiation. The
study shows that the expression level of these marker proteins
increases in the blood plasma of aging humans and shows a further
increase in geriatric patients with aging-associated diseases.
Moreover, there was a significant increase in the expression of the
biomarkers in the blood plasma of patients with chronic diseases
that are associated with increased rates of cell turnover and
telomere shortening, such as cirrhosis and myelodysplastic
syndromes (MDS). Analysis of blinded test samples validated the
effectiveness of the biomarkers to discriminate between young and
old, and between disease groups (MDS, cirrhosis) and healthy
controls. These results support the concept that telomere
dysfunction and DNA damage are interconnected pathways that are
activated during human aging and disease.
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[32]One dose of RNAi reduces Cholesterol by 60% for three weeks
[33]Half of the people do not respond to current cholesterol drugs,
but one dose of a new RNAi treatment lowers LDL cholesterol by 60% in
mice and monkeys.
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The [40]Alnylam Pharmaceuticals drug might one day provide another
option for patients who are resistant to existing cholesterol-lowering
drugs due to genetic factors, or it might also be used in combination
with existing cholesterol-lowering drugs to increase their
effectiveness.
The drug employs an approach known as RNA interference, a principle
that is being studied to develop drugs for many diseases, including
cancer. With this technique, scientists create short RNA molecules
that bind to messenger RNA in the cell, causing it to self-destruct.
That interrupts the process of gene transcription, and thus the
synthesis of the proteins coded by the gene. Alnylam's new drug
targets an enzyme called PCSK9, previously shown to affect LDL
cholesterol levels and risk of heart disease.
PCSK9 is a hot drug target, says Kevin Fitzgerald, Alnylam's
director of research. But it's difficult to find small molecules
that block the enzyme directly because there's no obvious place for
those molecules to bind. The company's findings demonstrate that
blocking the production of PCSK9 with RNA interference works in
nonhuman primates, and that it's effective in a single dose, says
study coauthor Jay Horton, a professor of internal medicine at UT
Southwestern who focuses on digestive and liver diseases. The study
appears online in the Proceedings of the National Academy of
Sciences (PNAS).
The Alnylam researchers designed short, double-stranded RNA
molecules to silence the gene for PCSK9 in rodents, monkeys, and
humans. They packaged the molecules into lipid-based nanoparticles
developed by biomedical engineer Robert Langer and his group at
MIT. The nanoparticles protect the molecules in the bloodstream and
escort them to liver cells.
Injecting the drug into mice and rats lowered total cholesterol by
up to 60 percent, and in monkeys, a single dose cut LDL cholesterol
by 50 to 60 percent. The reduction lasted about three weeks.
Although PCSK9's importance was clear from genetic studies in
rodents and humans, "what was not known was, if you were to acutely
knock down the level of PCSK9, how long would it take for
cholesterol to go down," Fitzgerald says. "The answer was, if you
knock it down today, then your cholesterol is down tomorrow."
It's not yet clear how well an RNA-interference-based drug that
requires injections could compete with existing medicines for
lowering cholesterol. No such drugs have yet been approved by the
Food and Drug Administration, although several are in clinical
trials. While there have been some safety concerns with RNA-based
therapeutics, scientists at Alnylam say that they saw no
unacceptable side effects in animals given the cholesterol-lowering
treatment, and people who naturally lack PCSK9 seem healthy.
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----- End forwarded message -----
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Eugen* Leitl <a href="http://leitl.org">leitl</a> http://leitl.org
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ICBM: 48.07100, 11.36820 http://www.ativel.com http://postbiota.org
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