Health Agency

Our immune systems can destroy cancer - but the immune system grows less effective with age, and sometimes it fails in this task. That "sometimes" is enough to kill a quarter of humanity, the fraction of us who die from cancer. Researchers are closing in on the mechanisms that separate success from failure, however, and in the years ahead will be able to tune our immune systems to destroy cancer nearly 100% of the time: "A specific type of T helper cell awakens the immune system to the stealthy threat of cancer and triggers an attack of killer T cells custom-made to destroy the tumors ... The role of Th17, one of only four known types of T helper cell, opens a possible avenue for overcoming cancer's ability to suppress or hide from the body's immune system ... While there is much work to be done, these preclinical findings imply the possibility of taking a patient's Th17 cells, expanding them in the lab, and then re-infusing them as treatment ... Development of a vaccine to stimulate Th17 cells would be another possible application."

View the Article Under Discussion: http://www.sciencedaily.com/releases/2009/10/091029125534.htm
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

The Baltimore Longitudinal Study on Aging has been running since 1958, but this Canadian study is just getting started - a much larger project planned to run for decades: "Canadians are living longer, and older persons are making up a larger share of the population (14% in 2006, projected to rise to 20% by 2021). The Canadian Longitudinal Study on Aging (CLSA) is a national longitudinal study of adult development and aging that will recruit 50,000 Canadians aged 45 to 85 years of age and follow them for at least 20 years. All participants will provide a common set of information concerning many aspects of health and aging, and 30,000 will undergo an additional in-depth examination coupled with the donation of biological specimens (blood and urine). The CLSA will become a rich data source for the study of the complex interrelationship among the biological, physical, psychosocial, and societal factors that affect healthy aging." I suspect that the most important role for these studies in the future will be to more rapidly evaluate the effectiveness of specific longevity therapies as they arrive in the clinic.

View the Article Under Discussion: http://www.clsa-elcv.ca
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Will it be possible to use patient-derived cell transplants to heal the brain in much the same way as can be done with other organs? From EurekAlert!: researchers have "found that using an animal's own brain cells (autologous transplant) to replace degenerated neurons in select brain areas of donor primates with simulated but asymptomatic Parkinson's disease and previously in a motor cortex lesion model, provides a degree of brain protection and may be useful in repairing brain lesions and restoring function. ... We aimed at determining whether autografted cells derived from cortical gray matter, cultured for one month and re-implanted in the caudate nucleus of dopamine depleted primates, effectively survived and migrated. The autologous, re-implanted cells survived at an impressively high rate of 50 percent for four months post-implantation ... Researchers found that the cultured cells migrated, re-implanted into the right caudate nucleus, and migrated through the corpus callosum to the contralateral striatum. Most of the cells were found in the most dopamine depleted region of the caudate nucleus. This study replicated in primates the success the research team had previously reported using laboratory mice."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2009-10/ctco-rfb102809.php
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

The trend in human longevity is upward, but how much of that is due to unintended slowing of the aging process via general advances in medicine and better treatment of the diseases of aging? A paper: "The distinction between senescent and non-senescent mortality proves to be very valuable for describing and analysing age patterns of death rates. Unfortunately, standard methods for estimating these mortality components are lacking. The first part of this paper discusses alternative methods for estimating background and senescent mortality among adults and proposes a simple approach based on death rates by causes of death. The second part examines trends in senescent life expectancy (i.e., the life expectancy implied by senescent mortality) and compares them with trends in conventional longevity indicators between 1960 and 2000 in a group of 17 developed countries with low mortality. Senescent life expectancy for females rises at an average rate of 1.54 years per decade between 1960 and 2000 in these countries. The shape of the distribution of senescent deaths by age remains relatively invariant while the entire distribution shifts over time to higher ages as longevity rises."

View the Article Under Discussion: http://pmid.us/19851933
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

This seems potentially important: "Despite a 30-year lifespan that gives ample time for cells to grow cancerous, a small rodent species called a naked mole rat has never been found with tumors of any kind - and now [biologists] think they know why. ... the mole rat's cells express a gene called p16 that makes the cells 'claustrophobic,' stopping the cells' proliferation when too many of them crowd together, cutting off runaway growth before it can start. The effect of p16 is so pronounced that when researchers mutated the cells to induce a tumor, the cells' growth barely changed ... Like many animals, including humans, the mole rats have a gene called p27 that prevents cellular overcrowding, but the mole rats use another, earlier defense in gene p16. Cancer cells tend to find ways around p27, but mole rats have a double barrier that a cell must overcome before it can grow uncontrollably. ... It's very early to speculate about the implications, but if the effect of p16 can be simulated in humans we might have a way to halt cancer before it starts. ... We haven't come across this anticancer mechanism before because it doesn't exist in the two species most often used for cancer research: mice and humans. Mice are short-lived and humans are large-bodied. But this mechanism appears to exist only in small, long-lived animals."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2009-10/uor-sdg102609.php
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/