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LONGEVITY MEME NEWSLETTER
January 07 2008
The Longevity Meme Newsletter is a weekly e-mail containing news, opinions
and happenings for people interested in healthy life extension: making use
of diet, lifestyle choices, technology and proven medical advances to live
healthy, longer lives. To subscribe or unsubscribe from the Longevity Meme
Newsletter, please visit http://www.longevity...org/newsletter/
______________________________
CONTENTS
- Another Swing Round the Sun
- Video FAQs on SENS and Other Longevity Science
- Creating Wealth or Persuading Wealth
- Discussion
- Latest Healthy Life Extension Headlines
ANOTHER SWING ROUND THE SUN
Here we are again, those of us who made it, a year older and a year more
experienced; another swing round the sun completed. We are somewhat more
damaged by the workings of our metabolisms and biochemical happenstance,
that much closer to catastrophic failure of one of the many intricate
biological systems we depend upon. I hope we've managed to use that time
well - it passes us at great cost, when considering what it will take to
create more of it:
http://www.fightagin...ives/001384.php
VIDEO FAQS ON SENS AND OTHER LONGEVITY SCIENCE
Five new sets of educational videos are up at the Methuselah Foundation
website. Each is a short explanation of a single important concept in
longevity science or the Strategies for Engineered Negligible Senescence
(SENS), presented by Foundation chair and biomedical gerontologist Aubrey
de Grey. Take a look:
http://www.mfoundati...ename=video_faq
http://www.mfoundati...ame=video_faq_2
http://www.mfoundati...ame=video_faq_3
http://www.mfoundati...ame=video_faq_4
http://www.mfoundati...ame=video_faq_5
If you find them useful, send the links to your friends or embed them on
your own websites or forum posts. They are hosted by VideoJug, so can be
embedded pretty much anywhere.
CREATING WEALTH OR PERSUADING WEALTH
We are fortunate to live in an era in which there is a chance to greatly
extend our healthy, active lives through pushing forward the frontiers of
medical science. But doing so will require significant resources - and
where are those resources going to come from?
http://www.fightagin...ives/001386.php
"Where do resources for research originate? From the wealth of those who
step up to make a difference. Those of us who strive to improve the lot of
longevity research are faced with a fairly simple economic choice whenever
we would like to pour more wealth into the pot, to help more hands make
progress arrive more rapidly. Do we work to create that needed wealth, or
do we work to persuade those with wealth to invest in research that will
benefit their future health and longevity? How long will each path take?
What is the likelihood of success in either case? I can assure you that
even if you don't think that you think about these things, you do. We are
all creatures of rational economic action, at every level of choice from
persuading a friend versus chipping in a dollar yourself up to making
investments to grow capital versus raising funds from investors and
philanthropists."
DISCUSSION
The highlights and headlines from the past week follow below. If you have
comments for us, please do send e-mail to newsletter@longevitymeme.org
Remember - if you like this newsletter, the chances are that your friends
will find it useful too. Forward it on, or post a copy to your favorite
online communities. Encourage the people you know to pitch in and make a
difference to the future of health and longevity!
Reason
reason@longevitymeme.org
______________________________
LATEST HEALTHY LIFE EXTENSION HEADLINES
To view commentary on the latest news headlines complete with links and
references, please visit the daily news section of the Longevity Meme:
http://www.longevitymeme.org/news/
Tissue Engineering Replacement Skin (January 04 2008)
http://www.scienceda...80104140344.htm
ScienceDaily looks at the work of a German group in the tissue engineering
field: "We pluck a few hairs off the back of the patient's head and extract
adult stem cells from their roots, which we then proliferate in a cell
culture for about two weeks. Then we reduce the nutrient solution until it
no longer covers the upper sides of the cells, exposing them to the
surrounding air. The increased pressure exerted by the oxygen on the
surfaces of the cells causes them to differentiate into skin cells ... In
this way, the researchers can grow numerous small pieces of skin, produced
individually for each patient, which add up to a surface area of 10 to 100
square centimeters when pieced together. ... The researchers expect to grow
skin grafts for 10 to 20 patients a month in 2008. ... At present, chronic
wounds are treated by grafting on the patients' own skin, which is normally
taken from the thigh. This leaves scars on both the thigh and the treated
wound ... we can achieve the same chances of recovery without hurting the
patient. Moreover, the artificial skin grows onto the wound without
scarring."
On the Methuselah Mouse Prize (January 04 2008)
http://www.economist...ory_id=10423468
Thoughts on the Methuselah Mouse Prize for longevity research from the
Economist: "To encourage people to take his ideas seriously, Aubrey de
Grey, the originator of the strategies for engineered negligible
senescence, has organised a competition. He is offering a prize for the
development of what he calls a Methuselah mouse. There are actually two
prizes to be had. One is for longevity, the other for rejuvenation. The
prize for longevity can be won by a new strain of mouse - one bred or
genetically engineered to live a long time. That for rejuvenation requires
treatment to begin when the mice are already in middle age. ... The winner
establishes a record that others have to break. At the moment the records
for longevity and rejuvenation are five years and almost four in an animal
that normally lives for three. How translatable the lesson of a Methuselah
mouse will be to people is a matter of debate. ... The reason mice age
rapidly is that they have lots of predators and would get killed quickly
anyway. Humans have few predators and tend not to get killed - at least not
as easily as mice. It is therefore worthwhile for people to evolve better
repair mechanisms than mice, and thus to age more slowly." Nonetheless,
radical life extension in lesser mammals is an important step along the way
- not just as a proving ground for the science, but as a way of educating
the public as to the degree to which aging can potentially be reversed in
humans.
How Can Evolution Produce Ageless Animals? (January 03 2008)
http://dx.doi.org/10...al.pcbi.0030256
Many extremely long-lived animal species exist, and some may even be
ageless. How can evolution, biased to early reproductive success at all
reasonable cost, produce such a species? Some modelling in this paper:
"Senescent aging is an irreversible deterioration in physiological
condition with age, which many organisms express even when removed from
harmful environmental influences. The inevitability of senescence for
repeatedly reproducing organisms has well-developed theoretical
foundations. Since reproduction carries physiological costs, natural
selection in a hazardous environment favors reaping early benefits, and
delaying the cost in physiological decline until later in life when there
is a greater chance of being dead from exogenous factors. But some
organisms show negligible senescence, and a few, such as Hydra and the
Bristlecone Pine, appear to have indefinite lifespans. We ask how such
species could have evolved from ancestors with senescent life histories. In
large populations, juveniles attempting recruitment into the adult
population can be 'crowded out' by already established adults. We show how
this phenomenon can trigger a process of runaway selection on ever-reducing
senescence, which can even result in the evolution of intrinsic
immortality." There are good arguments for learning more about the biology
of longevity in species near and far from humans.
The Economist on Repairing Aging (January 03 2008)
http://www.economist...ory_id=10423439
The Economist looks at the Strategies for Engineered Negligible Senescence
(SENS) and other longevity research: "To think about the question, it is
important to understand why organisms - people included - age in the first
place. People are like machines: they wear out. That much is obvious.
However a machine can always be repaired. A good mechanic with a stock of
spare parts can keep it going indefinitely. Eventually, no part of the
original may remain, but it still carries on, like Lincoln's famous axe
that had had three new handles and two new blades. ... All organisms are
going to die of something eventually. That something may be an accident, a
fight, a disease or an encounter with a hungry predator. There is thus a
premium on reproducing early rather than conserving resources for a future
that may never come. The reason why repairs are not perfect is that they
are costly and resources invested in them might be used for reproduction
instead. Often, therefore, the body's mechanics prefer lash-ups to complete
rebuilds - or simply do not bother with the job at all. And if that is so,
the place to start looking for longer life is in the repair shop."
A Glance at Novel Cartilage Engineering (January 02 2008)
http://www.globes.co...c...85&fid=1724
Globes Online gives good insight into one of the more active areas at the
commercial end of tissue engineering research. Scaffold technology is
maturing in a number of directions, including this one: Regentis'
"replacement cartilage does not include live cells. In fact, it has
expunged the tissue itself from the underlying concept behind its
alternative tissue. Instead, it has formed a form of interim synthetic
bridge which when applied to the injured limb, allows natural tissue to
grow and regenerate. The company regulates the rate of the synthetic
product's disintegration, in tandem with the growth of natural tissue. ...
When body tissue has been damaged, a blood clot is usually formed which
also acts a bridge for the building of new tissue and sends a signal that
promotes tissue building. The problem occurs when the damage is too
extensive and the blood clot can't create the bridge. Once that happens it
disintegrates fairly quickly ... the implant can last for up to a year
without breaking down. It is very much like the process of coating drugs
with synthetic materials to enable a slow release."
More On Alpha-Synuclein and Parkinson's Disease (January 02 2008)
http://www.eurekaler...o-erd122107.php
Parkinson's disease researchers have been expanding their understanding of
- and interfering in - processes that involve alpha-synuclein. EurekAlert!
here looks at some of the important mechanisms of autophagy in this
context: "Alpha-synuclein molecules modified by dopamine bound tightly to
the lysosomal membrane, but they got stuck there and weren't effectively
transported into the lysosome ... As a result, the alpha-synuclein
molecules altered by dopamine were poorly degraded, and the presence of
these molecules on the lysosomal membranes interfered with autophagic
digestion of other compounds as well. ... We propose that inhibition of
autophagy caused by dopamine's alteration of alpha-synuclein could explain
the selective death of dopamine-producing nerve cells in Parkinson's
disease ... interference with autophagy has also been implicated in other
neurodegenerative diseases including Alzheimer's." One thread of the
Strategies for Engineered Negligible Senescence (SENS) is devoted to
repairing or preventing the failure of the lysosome under load - it is a
broad problem that contributes to many age-related conditions.
$100,000 More For SENS Research Donations In 2008 (January 01 2008)
http://blog.methusel...atching_ch.html
From the Methuselah Foundation, news of more support for research aimed
squarely at repairing the biological damage of aging: "I'm happy to report
that December 2007 year-end donations to fund the Methuselah Foundation's
Strategies for Engineered Negligible Senescence (SENS) research program
succeeded in matching two consecutive $25,000 matching grants from Michael
Cooper and Doug Arends. ... Looking to the year ahead, and plans for
expansion into new branches of SENS research, Foundation supporter Ryan
Scott has set up a $100,000 matching fund for all research donations made
in 2008. The same rules apply as for this past December: donations are
first matched 100% by Ryan's fund, and then that total is matched again at
50% by Peter Thiel's $3 million matching fund. That means that all your
SENS research donations will be tripled - a $100 donation becomes $300 for
new research into longevity medicine. Jump on in! These are the early years
in a steep growth curve - and it's up to all of us to help make that
statement true. Donations to help bring about a future of greater health
and longevity can be made at the Methuselah Foundation website, where you
can also learn more about how funds are spent and the results achieved to
date."
More On DNA Damage, Stem Cell Aging (January 01 2008)
http://nar.oxfordjou.../full/gkm1064v1
To what degree does accumulated DNA damage contribute to the aging of stem
cells? (Versus, say, changes in their niche or other potential causes).
From this freely available review paper: "Adult stem cells are extremely
important in the long-term maintenance of tissues throughout life. They
regenerate and renew tissues in response to damage and replace senescent
terminally differentiated cells that no longer function. Oxidative stress,
toxic byproducts, reduced mitochondrial function and external exposures all
damage DNA through base modification or mis-incorporation and result in DNA
damage. As in most cells, this damage may limit the survival of the stem
cell population affecting tissue regeneration and even longevity. ... a
number of human genetic abnormalities associated with aging, and those
replicated in the mouse, suggest that loss of DNA repair may contribute to
the aging process. This review will provide support for the argument that
maintenance of the adult stem cell genome through robust DNA repair is
fundamental in the prevention of aging and disease; furthermore, that
failure of genomic maintenance is a leading cause of cancer, as well as
senescence."
p66(Shc) and Mechanisms of Mouse Longevity (December 31 2007)
http://pmid.us/18162611
As noted back in the Fight Aging! archives, scientists have been picking
away at the knot that is p66(Shc) for a while now, tying the activity of
this protein to many of the other mechanisms of metabolism considered
important to longevity and resistance to common age-related damage and
disease. Here's more on the topic: "The notion that mice carrying a
targeted mutation of the p66(Shc) gene display prolonged lifespan, reduced
production of intracellular oxidants, and increased resistance to oxidative
stress-induced apoptosis prompted a series of studies aimed at defining the
biochemical function of p66(Shc) and its possible implication in
cardiovascular diseases. Indeed, p66(Shc-/-) mice are protected against
vascular, cardiac, and renal impairment attributable to
hypercholesterolemia, aging, diabetes, and ischemia/reperfusion. ... On the
whole, the evidence so far reported and here discussed supports the concept
that pharmacological modulation of p66(Shc) expression and activity may be
a novel and effective target for the treatment of atherosclerotic vascular
disease as well as myocardial adaptation to hypertrophic, inflammatory and
neuro-hormonal stimuli in the overloaded heart."
More Gene Therapy For Parkinson's Disease (December 31 2007)
http://www.sciencent...le_id=218393043
ScienCentral on trials of one particular gene therapy aimed at ameliorating
the symptoms of Parkinson's disease: "The gene therapy study was to look at
an area of the brain called the subthalamic nucleus. The area is overactive
when you have Parkinson's disease. ... treatment relaxed brain activity in
the motor network, making a patient with severe over-activity look like a
person with moderate or mild Parkinson's disease. And because patients only
received the therapy on one side of their brains, the researchers used the
untreated side as a control. ... The network activity in the treated side
went down while the other network in fact got worse over the period of
time. It was as if the disease had progressed on one side of the brain, but
not the other. But just as important was to determine whether the gene
therapy affected the thinking network - and results show it did not. ...
[researchers] plan to start their next [phase II] clinical trial in early
2008." While this is more patch than regeneration of causative damage in
Parkinson's, we should welcome advances in safely manipulating the brain.
However the future of healthy life extension progresses, we are going to
have to become very proficient at repairing brain biochemistry in situ.
______________________________
If you have comments for us, please do send e-mail to
newsletter@longevitymeme.org.
January 07 2008
The Longevity Meme Newsletter is a weekly e-mail containing news, opinions
and happenings for people interested in healthy life extension: making use
of diet, lifestyle choices, technology and proven medical advances to live
healthy, longer lives. To subscribe or unsubscribe from the Longevity Meme
Newsletter, please visit http://www.longevity...org/newsletter/
______________________________
CONTENTS
- Another Swing Round the Sun
- Video FAQs on SENS and Other Longevity Science
- Creating Wealth or Persuading Wealth
- Discussion
- Latest Healthy Life Extension Headlines
ANOTHER SWING ROUND THE SUN
Here we are again, those of us who made it, a year older and a year more
experienced; another swing round the sun completed. We are somewhat more
damaged by the workings of our metabolisms and biochemical happenstance,
that much closer to catastrophic failure of one of the many intricate
biological systems we depend upon. I hope we've managed to use that time
well - it passes us at great cost, when considering what it will take to
create more of it:
http://www.fightagin...ives/001384.php
VIDEO FAQS ON SENS AND OTHER LONGEVITY SCIENCE
Five new sets of educational videos are up at the Methuselah Foundation
website. Each is a short explanation of a single important concept in
longevity science or the Strategies for Engineered Negligible Senescence
(SENS), presented by Foundation chair and biomedical gerontologist Aubrey
de Grey. Take a look:
http://www.mfoundati...ename=video_faq
http://www.mfoundati...ame=video_faq_2
http://www.mfoundati...ame=video_faq_3
http://www.mfoundati...ame=video_faq_4
http://www.mfoundati...ame=video_faq_5
If you find them useful, send the links to your friends or embed them on
your own websites or forum posts. They are hosted by VideoJug, so can be
embedded pretty much anywhere.
CREATING WEALTH OR PERSUADING WEALTH
We are fortunate to live in an era in which there is a chance to greatly
extend our healthy, active lives through pushing forward the frontiers of
medical science. But doing so will require significant resources - and
where are those resources going to come from?
http://www.fightagin...ives/001386.php
"Where do resources for research originate? From the wealth of those who
step up to make a difference. Those of us who strive to improve the lot of
longevity research are faced with a fairly simple economic choice whenever
we would like to pour more wealth into the pot, to help more hands make
progress arrive more rapidly. Do we work to create that needed wealth, or
do we work to persuade those with wealth to invest in research that will
benefit their future health and longevity? How long will each path take?
What is the likelihood of success in either case? I can assure you that
even if you don't think that you think about these things, you do. We are
all creatures of rational economic action, at every level of choice from
persuading a friend versus chipping in a dollar yourself up to making
investments to grow capital versus raising funds from investors and
philanthropists."
DISCUSSION
The highlights and headlines from the past week follow below. If you have
comments for us, please do send e-mail to newsletter@longevitymeme.org
Remember - if you like this newsletter, the chances are that your friends
will find it useful too. Forward it on, or post a copy to your favorite
online communities. Encourage the people you know to pitch in and make a
difference to the future of health and longevity!
Reason
reason@longevitymeme.org
______________________________
LATEST HEALTHY LIFE EXTENSION HEADLINES
To view commentary on the latest news headlines complete with links and
references, please visit the daily news section of the Longevity Meme:
http://www.longevitymeme.org/news/
Tissue Engineering Replacement Skin (January 04 2008)
http://www.scienceda...80104140344.htm
ScienceDaily looks at the work of a German group in the tissue engineering
field: "We pluck a few hairs off the back of the patient's head and extract
adult stem cells from their roots, which we then proliferate in a cell
culture for about two weeks. Then we reduce the nutrient solution until it
no longer covers the upper sides of the cells, exposing them to the
surrounding air. The increased pressure exerted by the oxygen on the
surfaces of the cells causes them to differentiate into skin cells ... In
this way, the researchers can grow numerous small pieces of skin, produced
individually for each patient, which add up to a surface area of 10 to 100
square centimeters when pieced together. ... The researchers expect to grow
skin grafts for 10 to 20 patients a month in 2008. ... At present, chronic
wounds are treated by grafting on the patients' own skin, which is normally
taken from the thigh. This leaves scars on both the thigh and the treated
wound ... we can achieve the same chances of recovery without hurting the
patient. Moreover, the artificial skin grows onto the wound without
scarring."
On the Methuselah Mouse Prize (January 04 2008)
http://www.economist...ory_id=10423468
Thoughts on the Methuselah Mouse Prize for longevity research from the
Economist: "To encourage people to take his ideas seriously, Aubrey de
Grey, the originator of the strategies for engineered negligible
senescence, has organised a competition. He is offering a prize for the
development of what he calls a Methuselah mouse. There are actually two
prizes to be had. One is for longevity, the other for rejuvenation. The
prize for longevity can be won by a new strain of mouse - one bred or
genetically engineered to live a long time. That for rejuvenation requires
treatment to begin when the mice are already in middle age. ... The winner
establishes a record that others have to break. At the moment the records
for longevity and rejuvenation are five years and almost four in an animal
that normally lives for three. How translatable the lesson of a Methuselah
mouse will be to people is a matter of debate. ... The reason mice age
rapidly is that they have lots of predators and would get killed quickly
anyway. Humans have few predators and tend not to get killed - at least not
as easily as mice. It is therefore worthwhile for people to evolve better
repair mechanisms than mice, and thus to age more slowly." Nonetheless,
radical life extension in lesser mammals is an important step along the way
- not just as a proving ground for the science, but as a way of educating
the public as to the degree to which aging can potentially be reversed in
humans.
How Can Evolution Produce Ageless Animals? (January 03 2008)
http://dx.doi.org/10...al.pcbi.0030256
Many extremely long-lived animal species exist, and some may even be
ageless. How can evolution, biased to early reproductive success at all
reasonable cost, produce such a species? Some modelling in this paper:
"Senescent aging is an irreversible deterioration in physiological
condition with age, which many organisms express even when removed from
harmful environmental influences. The inevitability of senescence for
repeatedly reproducing organisms has well-developed theoretical
foundations. Since reproduction carries physiological costs, natural
selection in a hazardous environment favors reaping early benefits, and
delaying the cost in physiological decline until later in life when there
is a greater chance of being dead from exogenous factors. But some
organisms show negligible senescence, and a few, such as Hydra and the
Bristlecone Pine, appear to have indefinite lifespans. We ask how such
species could have evolved from ancestors with senescent life histories. In
large populations, juveniles attempting recruitment into the adult
population can be 'crowded out' by already established adults. We show how
this phenomenon can trigger a process of runaway selection on ever-reducing
senescence, which can even result in the evolution of intrinsic
immortality." There are good arguments for learning more about the biology
of longevity in species near and far from humans.
The Economist on Repairing Aging (January 03 2008)
http://www.economist...ory_id=10423439
The Economist looks at the Strategies for Engineered Negligible Senescence
(SENS) and other longevity research: "To think about the question, it is
important to understand why organisms - people included - age in the first
place. People are like machines: they wear out. That much is obvious.
However a machine can always be repaired. A good mechanic with a stock of
spare parts can keep it going indefinitely. Eventually, no part of the
original may remain, but it still carries on, like Lincoln's famous axe
that had had three new handles and two new blades. ... All organisms are
going to die of something eventually. That something may be an accident, a
fight, a disease or an encounter with a hungry predator. There is thus a
premium on reproducing early rather than conserving resources for a future
that may never come. The reason why repairs are not perfect is that they
are costly and resources invested in them might be used for reproduction
instead. Often, therefore, the body's mechanics prefer lash-ups to complete
rebuilds - or simply do not bother with the job at all. And if that is so,
the place to start looking for longer life is in the repair shop."
A Glance at Novel Cartilage Engineering (January 02 2008)
http://www.globes.co...c...85&fid=1724
Globes Online gives good insight into one of the more active areas at the
commercial end of tissue engineering research. Scaffold technology is
maturing in a number of directions, including this one: Regentis'
"replacement cartilage does not include live cells. In fact, it has
expunged the tissue itself from the underlying concept behind its
alternative tissue. Instead, it has formed a form of interim synthetic
bridge which when applied to the injured limb, allows natural tissue to
grow and regenerate. The company regulates the rate of the synthetic
product's disintegration, in tandem with the growth of natural tissue. ...
When body tissue has been damaged, a blood clot is usually formed which
also acts a bridge for the building of new tissue and sends a signal that
promotes tissue building. The problem occurs when the damage is too
extensive and the blood clot can't create the bridge. Once that happens it
disintegrates fairly quickly ... the implant can last for up to a year
without breaking down. It is very much like the process of coating drugs
with synthetic materials to enable a slow release."
More On Alpha-Synuclein and Parkinson's Disease (January 02 2008)
http://www.eurekaler...o-erd122107.php
Parkinson's disease researchers have been expanding their understanding of
- and interfering in - processes that involve alpha-synuclein. EurekAlert!
here looks at some of the important mechanisms of autophagy in this
context: "Alpha-synuclein molecules modified by dopamine bound tightly to
the lysosomal membrane, but they got stuck there and weren't effectively
transported into the lysosome ... As a result, the alpha-synuclein
molecules altered by dopamine were poorly degraded, and the presence of
these molecules on the lysosomal membranes interfered with autophagic
digestion of other compounds as well. ... We propose that inhibition of
autophagy caused by dopamine's alteration of alpha-synuclein could explain
the selective death of dopamine-producing nerve cells in Parkinson's
disease ... interference with autophagy has also been implicated in other
neurodegenerative diseases including Alzheimer's." One thread of the
Strategies for Engineered Negligible Senescence (SENS) is devoted to
repairing or preventing the failure of the lysosome under load - it is a
broad problem that contributes to many age-related conditions.
$100,000 More For SENS Research Donations In 2008 (January 01 2008)
http://blog.methusel...atching_ch.html
From the Methuselah Foundation, news of more support for research aimed
squarely at repairing the biological damage of aging: "I'm happy to report
that December 2007 year-end donations to fund the Methuselah Foundation's
Strategies for Engineered Negligible Senescence (SENS) research program
succeeded in matching two consecutive $25,000 matching grants from Michael
Cooper and Doug Arends. ... Looking to the year ahead, and plans for
expansion into new branches of SENS research, Foundation supporter Ryan
Scott has set up a $100,000 matching fund for all research donations made
in 2008. The same rules apply as for this past December: donations are
first matched 100% by Ryan's fund, and then that total is matched again at
50% by Peter Thiel's $3 million matching fund. That means that all your
SENS research donations will be tripled - a $100 donation becomes $300 for
new research into longevity medicine. Jump on in! These are the early years
in a steep growth curve - and it's up to all of us to help make that
statement true. Donations to help bring about a future of greater health
and longevity can be made at the Methuselah Foundation website, where you
can also learn more about how funds are spent and the results achieved to
date."
More On DNA Damage, Stem Cell Aging (January 01 2008)
http://nar.oxfordjou.../full/gkm1064v1
To what degree does accumulated DNA damage contribute to the aging of stem
cells? (Versus, say, changes in their niche or other potential causes).
From this freely available review paper: "Adult stem cells are extremely
important in the long-term maintenance of tissues throughout life. They
regenerate and renew tissues in response to damage and replace senescent
terminally differentiated cells that no longer function. Oxidative stress,
toxic byproducts, reduced mitochondrial function and external exposures all
damage DNA through base modification or mis-incorporation and result in DNA
damage. As in most cells, this damage may limit the survival of the stem
cell population affecting tissue regeneration and even longevity. ... a
number of human genetic abnormalities associated with aging, and those
replicated in the mouse, suggest that loss of DNA repair may contribute to
the aging process. This review will provide support for the argument that
maintenance of the adult stem cell genome through robust DNA repair is
fundamental in the prevention of aging and disease; furthermore, that
failure of genomic maintenance is a leading cause of cancer, as well as
senescence."
p66(Shc) and Mechanisms of Mouse Longevity (December 31 2007)
http://pmid.us/18162611
As noted back in the Fight Aging! archives, scientists have been picking
away at the knot that is p66(Shc) for a while now, tying the activity of
this protein to many of the other mechanisms of metabolism considered
important to longevity and resistance to common age-related damage and
disease. Here's more on the topic: "The notion that mice carrying a
targeted mutation of the p66(Shc) gene display prolonged lifespan, reduced
production of intracellular oxidants, and increased resistance to oxidative
stress-induced apoptosis prompted a series of studies aimed at defining the
biochemical function of p66(Shc) and its possible implication in
cardiovascular diseases. Indeed, p66(Shc-/-) mice are protected against
vascular, cardiac, and renal impairment attributable to
hypercholesterolemia, aging, diabetes, and ischemia/reperfusion. ... On the
whole, the evidence so far reported and here discussed supports the concept
that pharmacological modulation of p66(Shc) expression and activity may be
a novel and effective target for the treatment of atherosclerotic vascular
disease as well as myocardial adaptation to hypertrophic, inflammatory and
neuro-hormonal stimuli in the overloaded heart."
More Gene Therapy For Parkinson's Disease (December 31 2007)
http://www.sciencent...le_id=218393043
ScienCentral on trials of one particular gene therapy aimed at ameliorating
the symptoms of Parkinson's disease: "The gene therapy study was to look at
an area of the brain called the subthalamic nucleus. The area is overactive
when you have Parkinson's disease. ... treatment relaxed brain activity in
the motor network, making a patient with severe over-activity look like a
person with moderate or mild Parkinson's disease. And because patients only
received the therapy on one side of their brains, the researchers used the
untreated side as a control. ... The network activity in the treated side
went down while the other network in fact got worse over the period of
time. It was as if the disease had progressed on one side of the brain, but
not the other. But just as important was to determine whether the gene
therapy affected the thinking network - and results show it did not. ...
[researchers] plan to start their next [phase II] clinical trial in early
2008." While this is more patch than regeneration of causative damage in
Parkinson's, we should welcome advances in safely manipulating the brain.
However the future of healthy life extension progresses, we are going to
have to become very proficient at repairing brain biochemistry in situ.
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