LongeCity - Longevity Meme Newsletter

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.longevitymeme.org/newsletter/

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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.fightaging.org/archives/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.mfoundation.org/index.php?pagename=video_faq

http://www.mfoundation.org/index.php?pagename=video_faq_2

http://www.mfoundation.org/index.php?pagename=video_faq_3

http://www.mfoundation.org/index.php?pagename=video_faq_4

http://www.mfoundation.org/index.php?pagename=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.fightaging.org/archives/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

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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.sciencedaily.com/releases/2008/...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.com/science/displayst...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/10.1371/journal.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.com/science/displayst...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.il/serveen/globes/doc...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.eurekalert.org/pub_releases/200...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.methuselahfoundation.org/2008/...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.oxfordjournals.org/cgi/content/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.sciencentral.com/articles/view....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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If you have comments for us, please do send e-mail to

newsletter@longevitymeme.org.

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