Longevity Meme Newsletter, March 03 2008
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LONGEVITY MEME NEWSLETTER
March 03 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.

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CONTENTS

- A Longevity Research Conference in California
- From Last Year's Longevity Dividend Symposium
- Chemopreservation Versus Cryopreservation
- Discussion
- Latest Healthy Life Extension Headlines

A LONGEVITY RESEARCH CONFERENCE IN CALIFORNIA

The Methuselah Foundation is hosting a conference ("Understanding Aging: Biomedical and Bioengineering Approachs") and symposium ("Aging: the Disease, the Cure, the Implications") in California this coming June:

https://www.fightaging.org/archives/001423.php
http://blog.methuselahfoundation.org/2008/02/registration_opens_for_the_und_1.html

"The preliminary program already has over two dozen confirmed speakers, all of them world leaders in their field. As for previous conferences [organized by Aubrey de Grey], the emphasis of this meeting is on 'applied biogerontology' - the design and implementation of biomedical interventions that may, jointly, constitute a comprehensive panel of rejuvenation therapies, sufficient to restore middle-aged or older laboratory animals (and, in due course, humans) to a youthful degree of physiological robustness."

Mark your calendars, this promised to be much like the excellent SENS conference series of the past few years:

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

FROM LAST YEAR'S LONGEVITY DIVIDEND SYMPOSIUM

Transcripts of talks given by Ronald Bailey and Anders Sandberg at the "Securing the Longevity Dividend" event last year have been posted to Future Current. It's a fair sample of what the policy-focused people are thinking. Links and excerpts can be found in the following Fight Aging! post:

https://www.fightaging.org/archives/001426.php

"I would like to conclude that I think it is easily the case that these kinds of treatments are very likely to be affordable. The pro-mortalists fail to understand the effort to extend healthy human lifespan is a perfect flourishing of our uniquely human nature. The future generations will look back at the beginning of the 21st century with astonishment that some very well meaning and intelligent people actually wanted to stop biomedical research just to protect their cramped and limited vision of human nature. Those future generations will look back, I predict, and thank us for making their world of longer, healthier lives possible. To end, let me quote Sirtris Pharmaceuticals co-founder David Sinclair who said, 'I would be disappointed if we were all born one generation too early.' Me too."

CHEMOPRESERVATION VERSUS CRYOPRESERVATION

How much of an accident of history is it that we presently see a cryonics community instead of, say, something more like a plastination community? How did low temperature preservation of tissue and the fine structure of the brain come to dominate what is now the cryonics community rather than one or more of the alternative room-temperature technologies?

https://www.fightaging.org/archives/001427.php

"Part of the confusion around chemopreservation concerns the quality of preservation that is possible with this method. Chemical methods of preservation such as fixation are not only adequate, they have long been the gold standard for biologists studying the structure of cells and the brain. ... If personal identity is preserved in the brain in physical structures such as synaptic circuits, then we know that chemopreservation can preserve these structures just as well as cryopreservation."

It makes for interesting reading, as is true for most considerations of the paths left untaken.

DISCUSSION

The highlights and headlines from the past week follow below.

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


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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/

Targeting Cancer With Salmonella (February 29 2008)
http://www.sciencedaily.com/releases/2008/02/080229171124.htm
Researchers continue to expand the set of tools available to build therapies targeted to very specific types of cell. Via ScienceDaily: "Salmonella bacteria can be turned into tiny terminator robots that venture deep into cancerous tumors where conventional chemotherapy can't reach. Once in place, the bacteria manufacture drugs that destroy cancer cells. ... It sounds like science fiction, doesn't it? But Salmonella are little robots that can swim wherever they want. They have propellers in the form of flagella, they have sensors to tell them where they are going and they are also little chemical factories. What we do as engineers is to control where they go, what chemical we want them to make, and when they make it." The future of artificial or engineered cells and bacteria is a bright one - they will likely form the first generation of nanomedical robots, given how much easier it is to alter existing designs rather than build afresh.

Working to Prevent Dry AMD (February 29 2008)
http://www.sciencedaily.com/releases/2008/02/080220103541.htm
Researchers are making progress towards therapy and prevention of the dry form of age-related macular degeneration (AMD): "a deficiency of the CD36 receptor prevents the evacuation of oxidized lipids in the eye. Those oxidized lipids in turn accumulate and attack the layers beneath and over the retina - thereby causing vision loss. ... We found that a deficiency in CD36 receptors leads to significant and progressive age-related macular degeneration. CD36 deficiency leads to central vision loss -- a key feature of dry AMD ... Now that we have also developed the molecules that activate [the] CD 36 receptor, we are working on the validation of the efficacy of these molecules as potential therapeutic agents for dry AMD treatment with prospect at the horizon of 2015." A better approach would be to identify the source of those oxidized lipids and deal with that problem. They are likely a result of changes in the level of free radicals in the body, perhaps relating to the mitochondrial free radical theory of aging. But you won't know if you stop investigating as soon as you have a temporary patch for the symptoms.

Probing the Roots of Calorie Restriction (February 28 2008)
http://pmid.us/18302914
A clever experiment: "The ability of dietary restriction to increase animal life span is often thought to arise from differential allocation of resources between somatic investment and reproduction. In this theory, reproduction is repressed upon dietary restriction to make scarce nutrients available to somatic functions that increase survival. Here, we label nitrogen and carbon in the dietary yeast of Drosophila melanogaster with stable isotopes to determine whether resources are invested to somatic tissues at the expense of reproduction. We find that females on a full diet acquire and allocate more dietary carbon, nitrogen and essential amino acids (EAA) to eggs than females on a restricted diet. Full-diet females also invest more carbon, nitrogen and EAA into somatic tissue than those on a restricted diet. Thus, the longer lifespan of flies on a restricted diet relative to those on a full diet cannot be explained by greater absolute somatic investment, and high somatic investment does not ensure longevity." Alternative explanations: calorie restriction leads to changes in the efficiency with which resources are used, or in the efficiency with which cellular damage is repaired, either of which will reduce the rate at which damage accumulates - and thus tend to lengthen life.

Update on Targeting Specific Cell Types (February 28 2008)
http://www.forbes.com/claytonchristensen/2008/02/22/cancer-nanotechnology-therapies-lead-clayton-in_jw_0222claytonchristensen_inl.html
The next generation of cancer therapies will safely destroy cancer cells through targeting mechanisms that home in on specific cell characteristics. These technologies will be also be used to build therapies for any condition that can be treated by eliminating errant cells - and one of those conditions is aging itself. Removing the buildup of senescent cells - eliminate their detrimental effect on the cellular environment - will be a part of any successful attempt to repair the damage of aging. The technology base for targeted therapies being developed by the cancer research community is ideal for that task. Here, Forbes looks at the state of the art: "If you look at where we were five years ago, there was nothing mature enough that the FDA would even consider [it]. Today, there are 20 to 30 small companies in both diagnostics and therapeutics. A handful of those are in clinical trials, and we expect another three or four will file applications this year ... Cancer researchers believe that further engineering the shape or surface properties of nanoparticles can enable the particles to actively target tumors, and thereby maximize their diagnostic or therapeutic function at the cancer site, while minimizing collateral damage to healthy tissue."

Niches, the Future of Regenerative Medicine (February 27 2008)
http://pmid.us/18295578
It is becoming increasingly clear that many of the very powerful future applications of regenerative medicine - such as replacing age-damaged tissue with newly repaired, youthful tissue - depend upon understanding and control of stem cell niches in addition to control of stem cells: "Niches are local tissue microenvironments that maintain and regulate stem cells. Long-predicted from mammalian studies, these structures have recently been characterized within several invertebrate tissues using methods that reliably identify individual stem cells and their functional requirements. Although similar single-cell resolution has usually not been achieved in mammalian tissues, principles likely to govern the behavior of niches in diverse organisms are emerging. Considerable progress has been made in elucidating how the microenvironment promotes stem cell maintenance. Mechanisms of stem cell maintenance are key to the regulation of homeostasis and likely contribute to aging and tumorigenesis when altered during adulthood."

The Work of Engineering New Nerves (February 27 2008)
http://www.sciencedaily.com/releases/2008/02/080226135424.htm
ScienceDaily looks at progress in the tissue engineering of replacement nerves: researchers "induce tracts of nerve fibers called axons to grow in response to mechanical tension. They placed neurons from rat dorsal root ganglia (clusters of nerves just outside the spinal cord) on nutrient-filled plastic plates. Axons sprouted from the neurons on each plate and connected with neurons on the other plate. The plates were then slowly pulled apart over a series of days, aided by a precise computer-controlled motor system, creating long tracts of living axons. These cultures were then embedded in a collagen matrix, rolled into a form resembling a jelly roll, and then implanted into a rat model of spinal cord injury. ... the axons at the ends of the construct adjacent to the host tissue extended through the collagen barrier to connect with the host tissue as a sort of nervous tissue bridge." The researchers have also demonstrated essentially the same process with human nerve tissue.

Investigating the Damage Done By AGEs (February 26 2008)
http://pmid.us/18297408
A buildup of AGEs, advanced glycation endproducts, is responsible for a portion of the damage of aging. As biotechnology advances, researchers can investigate how this happens in more detail: "The Maillard reaction and its end products, AGE-s (Advanced Glycation End products) are rightly considered as one of the important mechanisms of post-translational tissue modifications with aging. We studied the effect of two AGE-products [on] the expression profile of a large number of genes potentially involved in the above mentioned effects of AGE-s. The two AGE-products were added to human skin fibroblasts and gene expression profiles investigated using microarrays. ... Most of the gene-expression modifications are in agreement with biological effects of Maillard products, especially interference with normal tissue structure and increased tissue destruction." This sort of investigation should be able to confirm present thinking on the most important forms of AGE - such as the emphasis on glucosepane - and therefore focus efforts on ways to safely remove those forms first of all.

Pondering IGF-1 Signaling (February 26 2008)
http://ouroboros.wordpress.com/2008/02/25/mechanisms-of-lifespan-regulation-by-igf-i/
Ouroboros looks at the unknowns of IGF-1 signaling. It is clearly important to aging and longevity, but we are still left with many unanswered questions: "it has become apparent that single gene mutations in the insulin and insulin-like growth-factor signalling pathways can lengthen lifespan in worms, flies and mice, implying evolutionary conservation of mechanisms. Importantly, this research has also shown that these mutations can keep the animals healthy and disease-free for longer and can alleviate specific ageing-related pathologies. These findings are striking in view of the negative effects that disruption of these signalling pathways can also produce. ... The underscored passage brings up an issue that we've discussed here previously: Why is it that IGF-I pathway mutations can confer long healthy lives on organisms, even though supplementation with IGF-I is often quite beneficial, and depletion of IGF-I is often bad for individual organ systems? Indeed, according to another recent study, low doses of IGF-I appear to protect the mitochondria in aging rodents - why then do completely IGF-I-deficient animals enjoy extended and healthy lives?"

Pointing the Finger at Mitochondria Again (February 25 2008)
http://pmid.us/18284913
You may be familiar with the mitochondrial free radical theory of aging - that accumulated damage to mitochondrial DNA provides a strong contribution to age-related degeneration. A little more contributory evidence here: "we have used a systems biology approach to study the molecular basis of aging of the mouse heart. We have identified eight protein spots whose expression is up-regulated due to aging and 36 protein spots whose expression is down-regulated due to aging ... Among the up-regulated proteins, we have characterized five protein spots and two of them, containing three different enzymes, are mitochondrial proteins. Among the down-regulated proteins, we have characterized 27 protein spots and 16 of them are mitochondrial proteins. Mitochondrial damage is believed to be a key factor in the aging process. Our current study provides molecular evidence at the level of the proteome for the alteration of structural and functional parameters of the mitochondria that contribute to impaired activity of the mouse heart due to aging." Aging is the chain of events resulting from important changes in biochemistry - the more we know about those changes, the better placed we are to reverse them.

The Spreading Search For Longevity Genes (February 25 2008)
http://www.thehindubusinessline.com/2008/02/24/stories/2008022451030100.htm
Via the Hindu Business Line, news of a longevity study in India: "The Avestagenome project, that seeks to plot the genetic and medical database of the Parsi community, expects to start its Mumbai-leg of the study this April. The project would open a base in Mumbai, the centre with the largest Parsi population, for voluntary collection of blood samples from the community ... With Parsis showing high levels of longevity, the project seeks to undertake genetic studies to examine the basis of the longevity, besides identifying genes that may be linked to age-related neurological conditions such as Alzheimer's and Parkinson's. The study will also focus on two cancers, including breast cancer." The article compares the work to that of deCODE in Iceland, though it seems closer in nature to longevity studies of the Ashkenazi Jewish population - a small, distinct population in which it is easier to uncover meaningful genetic differences.

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