Healthy Life Extension

Funding Aging Research

Critical Health/Longevity Technology

posted on January 17th, 2012

Dear Future Centenarian,

You would think three years doesn™t translate to extreme life extension, but let™s dig a little deeper.

First, we™re talking about three extra quality years. When people start down the declining slope from vigor to the all-too-common agonizing age-related deterioration that usually precedes death by many years, most would trade everything to reverse their agony. By then, it™s usually too late though. But you may be able to avoid it.

There™s much to be said for squaring the mortality curve. That means, instead of suffering for years before dropping out, we could not only live longer, but when we do die, we could do so with little or no suffering.

Second, increase that 15 minutes to 30 or 45 minutes, and add even more active years. Read on to see why.

Finally, for me, here™s the most important reason:

I™m totally convinced we will be able to control aging and enjoy open-ended youthfulness and vitality. But when? Nobody knows for sure. But I do know this:

The longer you live, the better chance you have to avoid being terminally sabotaged by aging before these life-enhancing technologies arrive.

Now back to those three years. Suppose you die two years or so before a breakthrough that could put you on the path to an open-ended future? Obviously, you™re out of luck unless you tacked on those extra years. Otherwise, you last remaining chance is to opt for cryonic suspension. Although that™s good life insurance, it™s not a sure thing. So why not hang around and enjoy life as long as possible?

Trading thirty minutes is even better and should buy you even more time. Look at this study data as reported in dpa Deutsche Presse-Agentur GmbH:

Taking a minimum of 15 minutes of exercise a day can extend life expectancy by up to three years, according to Germany’s Society of Neurologists and the Stroke Society.

A regular program of exercise can reduce the risk of stroke, cardiovascular illness, cancer and diabetes. The advice is based on a study of over 400,000 participants in Taiwan whose health status was checked regularly over eight years.

The study discovered that 15 minutes of exercise a day made a surprising contribution to improving overall health. The mortality rate for those who took the exercise was 14 per cent lower than the inactive participants.

Extrapolating the results over 30 years resulted in a projected extended life expectancy of three years as well as a reduced chance of developing cancer and diseases of the cardiovascular system. The conclusion was that the more a person exercises, the less chance they have of falling ill.

The recommended 15 minutes a day is half what the World Health Organization advises people to take.

So what are you waiting for Methuselah? Hit the gym now.

Long Life,
David Kekich


Via EurekAlert!: “For years, researchers seeking new therapies for traumatic brain injury have been tantalized by the results of animal experiments with stem cells. In numerous studies, stem cell implantation has substantially improved brain function in experimental animals with brain trauma. But just how these improvements occur has remained a mystery. Now, an important part of this puzzle has been pieced together by researchers. In experiments with both laboratory rats and an apparatus that enabled them to simulate the impact of trauma on human neurons, they identified key molecular mechanisms by which implanted human neural stem cells – stem cells that are in the process of developing into neurons but have not yet taken their final form – aid recovery from traumatic axonal injury.

A significant component of traumatic brain injury, traumatic axonal injury involves damage to axons and dendrites, the filaments that extend out from the bodies of the neurons. The damage continues after the initial trauma, since the axons and dendrites respond to injury by withdrawing back to the bodies of the neurons. Axons and dendrites are the basis of neuron-to-neuron communication, and when they are lost, neuron function is lost. In this study, we found that our stem cell transplantation both prevents further axonal injury and promotes axonal regrowth, through a number of previously unknown molecular mechanisms. We identified about 400 proteins that respond differently after injury and after grafting with neural stem cells. A group of cytoskeleton proteins was being changed, and in particular one called alpha-smooth muscle actin, which had never been reported in the neurons before.””

FROM THE PROGRAMMED AGING CAMP Thursday, January 12, 2012
Here is an open access paper from a researcher who focuses on mTOR and sees aging as almost entirely programmed, not the consequence of stochastic damage. His view as outlined in the paper is analogous to the view of nuclear DNA damage as not being significant over the present human life span. I think he has a very large hill of evidence for the damage-based view of aging to overcome in order to make a convincing point, however, and this should serve as a reminder that there are a great many diverse (but not necessarily well supported) views in the scientific community when it comes to the nuts and bolts of aging: “Aging is defined as a decline caused by accumulation of all sorts of damage, in particular, molecular damage. This statement seemed so obvious that it was not questioned. Yet several lines of evidence rule out molecular damage as a cause of aging. Yes, of course, molecular damage accumulates over time.

But this accumulation is not sufficient to cause organismal death. Eventually it would. But the organism does not live long enough, because another cause terminates life first. This cause is aging, a continuation of developmental growth. Definitely, developmental growth is not driven by accumulation of molecular damage, although molecular damage accumulates. Similarly, aging is not driven by damage. Growth is stimulated in part by mitogen- and nutrient-sensing (and other) signaling pathways such as mTOR. Aging, ‘an aimless continuation of developmental program’, is driven by the same signaling pathways including mTOR. Aging in turn causes damage: not molecular damage but non-random organ damage (stroke, infarction, renal failure and so on) and death. Seemingly, one objection to this concept is that cancer is caused by molecular damage. And cancer is often a cause of death in mammals. So how may one claim that damage does not drive aging, if it is involved in cancer. Let us discuss this.”

The latest in a series of articles on immunotherapies aimed at clearing out the build up of cellular aggregates involved in Alzheimer’s disease: “Immunotherapy targeting the age-related accumulation of extracellular aggregates, in the form of ß-amyloid, is the first rejuvenation biotechnology to reach Phase III human clinical trials. The promise of this therapy for the treatment and prevention of Alzheimer’s disease (and ultimately, of  so-called ‘normal’ brain aging) has sparked an interest in utilizing the same approach for other forms of aging damage, including the clearance of aggregated intracellular proteinaceous aging damage.

Notably, as we have reviewed in a series of four previous posts, recent years have seen the appearance of a rising number preclinical studies of therapeutic vaccines targeting pathological tau species accumulating in the brains and spinal cords of transgenic rodent models of tauopathic neurodegeneration. These studies have reported — somewhat surprisingly — the antibody-mediated clearance of these primarily intracellular aging lesions, accompanied by functional improvements in treated animals. These two forms of structural damage are major contributors to the age-related degeneration of the brain, whether it leads to frank dementia or to the diagnostic euphemism of ‘normal’ age-related cognitive decline, and novel therapeutics to effect the removal of both from aging neurons will be key elements of a comprehensive panel of rejuvenation biotechnologies.”

The decline of the brain is all the more reason to work harder on rejuvenation biotechnology and make better lifestyle choices: “researchers found a 3.6% decline in mental reasoning in women and men aged 45-49. They assessed the memory, vocabulary and comprehension skills of 7,000 men and women aged 45 to 70 over 10 years. Previous research had suggested that cognitive decline does not begin much before the age of 60. But the results of this study show that it could in fact begin in middle age. This is important, the researchers say, because dementia treatments are more likely to work at the time when individuals start to experience mental impairment. The results of the tests show that cognitive scores declined in all categories except vocabulary – and there was a faster decline in older people.

The study found a 9.6% decline in mental reasoning in men aged 65-70 and a 7.4% decline for women of the same age. We now need to look at who experiences cognitive decline more than the average and how we stop the decline. Some level of prevention is definitely possible. Rates of dementia are going to soar and health behaviors like smoking and physical activity are linked to levels of cognitive function. It’s important to identify the risk factors early. If the disease has started in an individual’s 50s but we only start looking at risk in their 60s, then how do you start separating cause and effect? Previous research suggests that our health in mid-life affects our risk of dementia as we age, and these findings give us all an extra reason to stick to our New Year’s resolutions. Although we don’t yet have a sure-fire way to prevent dementia, we do know that simple lifestyle changes – such as eating a healthy diet, not smoking, and keeping blood pressure and cholesterol in check – can all reduce the risk of dementia.”

The important portion of a targeted therapy for killing cells – cancer cells in this case – is not the part that destroys the cell itself. Any old chemotherapy drug can be used to that end. The point of the targeting mechanism is that the drug can be delivered in tiny, precise doses to minimize side-effects and any harm to surrounding tissues.These technologies are well worth watching because they will have far broader applications than just cancer. There are many areas in the aging body where targeted cell destruction will do a great deal of good, such as senescent cells and portions of the immune system. Here is an example from the cancer research community: “The process involved is akin to building and equipping a car with the finest features, adding a passenger (in this case the cancer drug), and sending it off to its destination (in this case the cancer cell).

To design the ‘vehicle,’ researchers used a selection strategy developed by Farokhzad’s team that allowed them to essentially select for ligands (molecules that bind to the cell surface) that could specifically target prostate cancer cells. The researchers then attached nanoparticles containing chemotherapy, in this case docetaxel, to these hand-picked ligands. To understand Farokhzad’s selection strategy, one must understand ligand behavior. While most ligands mainly have the ability to bind to cells, the strategy of Farokhzad and his colleagues allowed them to select specific ligands that were not only able to bind to prostate cancer cells, but also possessed two other important features: 1) they were smart enough to distinguish between cancer and non-cancer cells and 2) they were designed to be swallowed by cancer cells. Most ligands are engulfed by cells, but not efficiently. We designed one that is intended to be engulfed.”

The processes that keep cells clear of debris and otherwise well maintained are important in aging – what we know of autophagy should make that clear. Here, researchers are taking a brute force approach to enumerating the controlling mechanisms of cellular homeostasis: “To do its job properly within the cell, a protein first must fold itself into the proper shape. If it doesn’t, trouble can result. More than 300 diseases have at their root proteins that misfold, aggregate and eventually cause cellular dysfunction and death. [The] research identifies new genes and pathways that prevent protein misfolding and toxic aggregation, keeping cells healthy, and also identifies small molecules with therapeutic potential that restore health to damaged cells, providing new targets for drug development.

These discoveries are exciting because we have identified genes that keep us healthy and small molecules that keep us healthy. Future research should explain how these two important areas interact. [Researchers] tested all of the approximately 19,000 genes in C. elegans. They reduced expression of each gene one at a time and looked to see if the gene suppressed protein aggregation in the cell. Did the gene increase aggregation or lessen it or have no effect at all? The researchers found 150 genes that did have an effect. They then conducted a series of tests and zeroed in on nine genes that made all proteins in the cell healthier. These nine genes define a core homeostastis network that protects the animal’s proteome (the entire set of proteins expressed by the organism) from protein damage. These are the most important genes. Figuring out how nine genes – as opposed to 150 – work is a manageable task.”

Via EurekAlert!: researchers “have found that the age-related impairment of the body’s ability to replace protective myelin sheaths, which normally surround nerve fibers and allow them to send signals properly, may be reversible, offering new hope that therapeutic strategies aimed at restoring efficient regeneration can be effective in the central nervous system throughout life. Using a surgical technique, the researchers introduced an experimental demyelinating injury in the spinal cord of an old mouse, creating small areas of myelin loss, and then exposed those areas to cells found the blood of a young mouse. By doing so, they found that the influx of certain immune cells, called macrophages, from the young mouse helped resident stem cells restore effective remyelination in the old mouse’s spinal cord.

This ‘rejuvenating’ effect of young immune cells was mediated in part by the greater efficiency of the young cells in clearing away myelin debris created by the demyelinating injury. Prior studies have shown that this debris impedes the regeneration of myelin. Aging impairs regenerative potential in the central nervous system. This impairment can be reversed, however, suggesting that the eventual development of cell-based or drug-based interventions that mimic the rejuvenation signals found in our study could be used therapeutically.”

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