Longevity Meme Newsletter, May 01 2006

May 01 2006

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.



- A Look at the Glenn Laboratories
- $75,000 More For the MPrize
- Anti-Aging, a Term Lost to the Junkyard?
- Discussion
- Latest Healthy Life Extension Headlines


You should take a look at the Paul F. Glenn Laboratories for the Biological Mechanisms of Aging. While the institution is just getting started, it represents the face of mainstream aging research a decade from now. No coyness, no beating about the bush, but right to the main goal: "The Paul F. Glenn Laboratory is dedicated to understanding the mechanisms of normal aging and the development of interventions to delay its onset and progression, thereby extending the healthy years of human life."


The Laboratories are playing host to a June 5th symposium on the biology of aging; a chance for the high-fliers in the mainstream of research to put forward their views:


You'll be seeing much more in the years ahead as researchers are recruited and the faculty grows. The Glenn Foundation For Medical Research has deep pockets and its founders have a strong interest in the long term - seeing this through and doing it right, step by step.


Larger donations are rolling into the Methuselah Foundation's MPrize for longevity research on a semi-regular basis nowadays:


Congratulations are due to the Foundation volunteers and all the generous donors of the past few years - working together, you have greatly advanced the cause of healthy life extension research.


Is it still worth trying to promote a wide-reaching cultural conversation on healthy life extension while using the term "anti-aging?" Or is it time to move on, admit defeat and cede that now-ugly field to the spam-mongers, potion vendors, marketeers, cosmeticians and other short-term profit seekers? See what you think:



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!


Founder, Longevity Meme



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/

Ever More Stem Cell Trials (April 30 2006)
(From the Times Online). At some point, folks really have to stop claiming their stem cell based heart therapy trial is the first of its kind. It's already a few years too late for that, especially given that some varieties of therapy are already commercially available. "These patients have had a heart attack and now have heart failure and diminished function. The hope is that stem cells from their own marrow, which have been grown in culture, can repair the damaged area, avoiding the need for replacement. ... In the trial these will be extracted from marrow in patients' pelvises and over three to six weeks hundreds of millions of cells will be grown in the laboratory from a base of 50,000. They will then be grafted into the patients' hearts."

That Barron's Article (April 30 2006)
The mixed Barron's article on healthy life extension from earlier this month is now available for non-subscribers at The Business Online: "A growing number of maverick scientists, doctors, researchers, biogeneticists and nano-technologists - many with impeccable academic credentials - insist that the war against ageing can be won. All believe significantly longer lifespans and, perhaps eventually, true biological immortality, are not only possible but also scientifically achievable. What's more, it could happen in time to aid those now living. ... Twenty years ago the idea of postponing aging, let alone reversing it, was weird and off-the-wall. Today there are good reasons for thinking it is fundamentally possible." Not mavericks, but rather next year's mainstream - the discussion has already moved on to timescales and methodologies.

Suppressing Amyloid Beta (April 29 2006)
The breadth of new approaches to developing the next generation of Alzheimer's therapies is a good thing; diversity and dynamism together indicate progress in medical science. Via the Globe and Mail: "TMP21 protein inhibits the production of a toxin in the brain called beta-amyloid, also known as Abeta, the main culprit in destroying brain cells in Alzheimer's patients. ... The protein appears to be very specific and only effects the toxin, but doesn't effect normal cell function." Attacking amyloid beta is one way forward, though scientists have shown that amyloid is not necessarily the real culprit. It's the most noteworthy late stage of a process best halted earlier, but at this point, too many people are suffering for lack of any port in the storm - a breadth of approaches is vital.

Attacking Inflammation (April 29 2006)
Via Genetic Engineering News, a sign that research into inflammation in age-related neurodegenerative diseases is starting to produce ways to interfere in its progression: "anti-[tumor necrosis factor (TNF)] treatment may reduce inflammation in the Alzheimer's patient's brain. An increasing body of research points to inflammation as a critical factor in the pathophysiology of Alzheimer's. ... So far this appears to be the most effective treatment for the reversal of some of the major symptoms of Alzheimer's disease. I have recommended that my patients continue on this treatment, as without it they continue to cognitively decline. ... Large scale clinical trials should begin immediately to define its most appropriate therapeutic use." Take with a grain of salt until controlled studies take place to confirm and quantify these results, but still promising news given the role inflammation plays in many age-related conditions.

Secrets of Telomerase (April 28 2006)
A little Friday science; telomerase - or rather its sub-unit, Telomerase Reverse Transcriptase (hTERT) - appears to influence the way and degree to which oxidative stress damages mitochondrial DNA (mtDNA), causing cells to die via apoptosis. If you remove the capability for hTERT to interact with mitochondria via a suitable mutation, you find this: "Cells carrying this mutated hTERT not only have significantly reduced levels of mtDNA damage following [induction of oxidative stress], but strikingly also do not shown any loss of viability or cell growth. ... nuclear-targeted hTERT, in the absence of mitochondrial localization, is associated with diminished mtDNA damage, increased cell survival and protection against cellular senescence." A number of groups are working on the technologies required to manipulate telomeres and telomerase - these tools will be most useful.

What We Learned From Progeria (April 28 2006)
Malformed lamin A proteins lie at the root of the accelerated aging condition progeria. Via Nature, efforts to apply this new knowledge to "normal" aging: "In cells taken from the elderly, the nuclei tend to be wrinkled up, the DNA accumulates damage, and the levels of some proteins that package up DNA go askew ... This mirrors the same changes that they previously observed in cells from [Hutchinson-Gilford progeria syndrome (HGPS)] children. ... The team suggests that healthy cells always make a trace amount of an aberrant form of lamin A protein, but that young cells can sense and eliminate it. Elderly cells, it seems, cannot. Critically, blocking production of this deviant protein corrected all the problems with the nucleus. ... You can take these old cells and make them young again."

Checking In On ACT (April 28 2006)
Advanced Cell Technology (ACT) is on the product development track, aiming at regenerative medicine for skin by the look of this press release over at Genetic Engineering News: ACT "will provide the human embryonic stem cell-derived skin cells, and Xgene will provide its technology for reconstituting skin from cultured cells, to achieve the mutually beneficial development of advanced in vitro human skin models. The goal of the collaboration is to test the functionality of embryonic skin cells in regenerating skin for numerous applications in medicine. ... The potential of progenitor cells for healing wounds, and restoring lost functionality to patient skin, while minimizing scarring, could be important for the future practice of dermatology."

Oxidative Stress and Parkinson's (April 27 2006)
EurekAlert reports on research on the link between oxidative stress and Parkinson's disease: "the protein DJ-1 is oxidatively damaged in non-hereditary (sporadic) Parkinson's disease. While scientists do not know the function of DJ-1, they have previously identified abnormalities in DJ-1 that directly cause hereditary (familial) Parkinson's disease. ... Aware of the connection between DJ-1 mutations and familial Parkinson's disease, Dr. Li and her collaborators examined the oxidation levels of the protein in sporadic cases. Their hypothesis that DJ-1 was the missing link proved to be correct: DJ-1 in patients who had Parkinson's disease showed signs of oxidative damage. ... The protein unfolds and cannot function normally. Not recognizing the unfamiliar shape, the protein is broken down by the cell. The end result is the same: you lose your protein. Any mutation or modification causing this protein to lose its function will then lead to neurodegeneration in Parkinson's disease."

Reviewing CR Mimetics (April 26 2006)
A number of groups, including venture-funded startups, are engaged in the search for viable calorie restriction (CR) mimetics: "When considering all [presently] possible aging interventions evaluated to date, it is clear that calorie restriction (CR) remains the most robust. ... Evidence emerging from studies in rhesus monkeys suggests that their response to CR parallels that observed in rodents. To assess CR effects in humans, clinical trials have been initiated. However, even if results from these studies could eventually substantiate CR as an effective pro-longevity strategy for humans, the utility of this intervention would be hampered because of the degree and length of restriction required. As an alternative strategy, new research has focused on the development of 'CR mimetics'. The objective of this strategy is to identify compounds that mimic CR effects by targeting metabolic and stress response pathways affected by CR, but without actually restricting caloric intake."

Chronogen, Oxidative Stress (April 26 2006)
Chronogen is moving forward with development of a drug to suppress oxidative stress, a cause of cellular damage and death in numerous age-related diseases (but not the root cause of the conditions, it must be noted). "CHGN111 is an inhibitor of the mitochondrial enzyme CLK-1 ... Numerous parameters of mitochondrial function are altered when the activity of CLK-1 is reduced, which results in a decrease of [reactive oxygen species] at critical cellular sites, as well as in a decrease of systemic oxidative stress. ... Compared to free radical scavengers or other detoxifying agents they directly modulate reactive oxygen species production and detoxification at an early stage to prevent damage and stop disease initiation as well as progression." This is fairly slow, standard old school drug development - and the press release is for an early stage of that inch by inch process. To me, the most interesting part of it all is that Chronogen feels the need to clearly disclaim any interest in preventing aging on their home page.

Cancer Suppresses Anti-Cancer Genes (April 25 2006)
A potentially important insight into how cancer gets started from EurekAlert; at least some types of cancer suppress anti-cancer mechanisms in nearby tissues. "Large regions of DNA are 'switched off' in colon cancer. ... These large regions - referred to as suburbs - contain genes that normally function to prevent the development of tumours. ... In cancer, the DNA methylation pattern of many genes changes. However, until now, it was believed that only individual single genes were silenced by methylation. But this is not necessarily the case. ... What we've found is that non-methylated genes that reside in a particular suburb near methylated genes are also silenced. Their physical proximity to the methylated genes affects their ability to function. ... The team also hope that new cancer therapies, which can reverse DNA methylation, will restore the cell's normal regulation and treat and prevent cancer."

General Health and Longevity (April 25 2006)
The BBC reports on a study quantifying the longevity you can expect to lose, on average, if you don't take care of the healthy basics: "stopping smoking, exercising more and eating better could give you the life expectancy of a person 11 to 12 years younger." Or rather, smoking, lack of exercise and poor diet (and the accompanying excess fat in your body, leading to more chronic inflammation amongst other line items) will cut more than a decade from your life - and make your later years much more expensive and unpleasant to boot. If you want to live to take advantage of the coming era of longevity-enhancing medical technology, best to take care of the health basics today. Why set yourself up to miss out on the chance of a far longer, healthier life?

New Alzheimer's Research (April 24 2006)
Nice work by the Buck Institute researchers, reported in Newswise: "There are approximately 200 mice at the Buck Institute that should have the symptoms of Alzheimer's disease (AD). But these mice, despite the fact that their brains are loaded with the sticky deposits commonly associated with the neurodegenerative disease, have normal memories, and show no signs of the brain shrinkage and neuron damage commonly associated with AD. ... Buck scientists saved the mice from their prescribed fate by a blocking a newly discovered molecular pathway ... AD may be a more subtle disease, which develops when the normal process of nerve signaling goes out of balance. The alteration we produced allowed normal neuron connections to occur, even in the presence of the senile plaques."

Revealing the Secrets of WRN (April 24 2006)
Rare acelerated aging syndromes have a great deal to teach us about the biochemistry of aging and cancer. Great progress has been made in deciphering progeria, and now Werner's syndrome research is catching up : "One reason we are particularly interested in WRN is because Werner's syndrome is unusual among premature-aging diseases, in that children are born normal and show no signs of disease until early adulthood. This gives us a better chance of clearly separating defects in development from aging. ... Among other things, WRN is involved in repairing double-strand breaks, single-strand breaks, replication forks and junctions, even DNA-RNA duplexes. How does one protein know how to interact in so many different processes? If we can understand how this unique protein works, we'll have a key to how all these pathways work in human beings." Understanding DNA repair is the first step towards greatly improving DNA repair.



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