Young mammals are capable of feats of regeneration: even in humans, it has been known for young children to regenerate lost fingertips. That capacity fades with age, however. Researchers are investigating the biochemistry of this behavior for much the same reasons as they look at regenerating species such as salamanders - if the capacity is there, perhaps it can be restored in adults. "Researchers, working with mice, found that a portion of the heart removed during the first week after birth grew back wholly and correctly - as if nothing had happened. ... This is an important step in our search for a cure for heart disease, the No. 1 killer in the developed world. We found that the heart of newborn mammals can fix itself; it just forgets how as it gets older. The challenge now is to find a way to remind the adult heart how to fix itself again. ... Previous research has demonstrated that the lower organisms, like some fish and amphibians, that can regrow fins and tails, can also regrow portions of their hearts after injury. ... In contrast, the hearts of adult mammals lack the ability to regrow lost or damaged tissue, and as a result, when the heart is injured, for example after a heart attack, it gets weaker, which eventually leads to heart failure. ... The researchers found that within three weeks of removing 15 percent of the newborn mouse heart, the heart was able to completely grow back the lost tissue, and as a result looked and functioned just like a normal heart. The researchers believe that uninjured beating heart cells, called cardiomyocytes, are a major source of the new cells. They stop beating long enough to divide and provide the heart with fresh cardiomyocytes."

Link: http://www.eurekalert.org/pub_releases/2011-02/usmc-nhm022311.php

A little while back, I was invited to preview an independent project under development at the behest of Alex Zhavoronkov, one of the trustees of the UK-based Biogerontology Research Foundation, a group with strong ties to the Methuselah Foundation and SENS Foundation communities. That project is now launched and open to the world: it is the International Aging Research Portfolio - "tracking international progress in aging research".

The site grants users access to research and funding information for over a million [projects]. The IARP is a fully searchable, flexible and highly scalable knowledge-management system developed to enable organizations to collaborate, track, analyze, structure, make decisions and set directions for future research efforts in aging. ... Aging research spans many areas of natural and social and behavioural sciences and requires a high degree of interdisciplinary and international cooperation. The goal of IARP is to provide a centralized decision support system for scientists, research institutes, funding organizations and policy makers involved in aging research.

If you are a statistics addict, this might keep you occupied for a while. The aggregated funding data and trends in research are particularly interesting, and could be more so if further sliced and diced. For example, funding by theory of aging:

Color me surprised that funding of work on telomeres in aging is so very far ahead - but there's the purpose of data mining, to learn. The hope here is that data mining tools that operate on this large data set will provide compelling benefits for the research community, such as by making it easier to match up research proposals to funding sources based on the sort of awards made in the past.

Public sources of funds are over-represented in this database by virtue of being public sources and thus producing records that are generally more accessible. One can imagine a slow extension of such a data aggregation operation into the private funding space based on the same provision of compelling benefits. If you make it worthwhile by streamlining the process of fundraising (on the research side) and the process of finding suitable projects to fund (on the funding source side), then people will use the system and in the process support its evolution and growth.

We expect to see good correlations between many aspects of our biology and aging: "Epigenetic variations have been widely described to occur during the aging process. To verify if these modifications are correlated with the inter-individual phenotypic variability of elderly people, we searched for a correlation between global DNA methylation levels and frailty. We found that the global DNA methylation levels were correlated to the frailty status in middle/advanced-aged subjects but not with age. A 7-year follow-up study also revealed that a worsening in the frailty status was associated to a significant decrease in the global DNA methylation levels. These results suggest that the relaxation of the epigenetic control in aging is specifically associated with the functional decline rather than with the chronological age of individuals. Thus, the modifications of DNA methylation, representing a drawbridge between the genetic and the environmental factors affecting the age-related decay of the organism, may play an important role in determining physiological changes over old age." Equally, it may go the other way - these changes could just as well be the symptoms of damaged systems flailing as they try to adapt to countless small breakages at the level of cells and molecular machinery. It is important in the development of therapies for aging to try to identify the root causes, as fixing those will also solve secondary issues.

Link: http://www.ncbi.nlm.nih.gov/pubmed/21336567

Decellularization is proving to be a versatile technology in tissue engineering: grow the tissue from stem cells or accept a donor organ, strip its cells to leave behind the extracellular matrix, and then repopulate it from the recipient's stem cells to make it ready for transplant. For example: "Heart bypass patients may soon be able to get new arteries without having to sacrifice vessels from other parts of their body, thanks to ready-made, off-the-shelf artificial blood vessels. Biomedical engineers have been trying to build replacement blood vessels, needed for coronary artery bypass surgery and kidney dialysis patients, for three decades. Researchers from Humacyte Inc., in Durham, N.C., discovered the trick: recruiting cells to build the vessel, then washing them away so the nonliving tissue is storable and works for anyone. ... The company has managed to make a "universal blood vessel. This is very practical and convenient for clinical applications. ... Other approaches, customized with a patient's own cells, take several months to prepare. ... Though Humacyte is starting to plan human clinical trials, it's too early to predict when the grafts would become available to the general public. ... [researchers] not yet know how much the grafts would cost, but anticipates it will be less than the $15,000-and-up for personalized grafts from patient's own cells. The company can use cells from multiple cadavers to generate hundreds of grafts at once, making production much cheaper."

Link: http://www.latimes.com/health/la-he-blood-vessels-20110221,0,6930611.story

I am not complacent about the cancers that no doubt lie in my future - just as they lie in yours. But I am not terribly concerned either; I give more thought to the fate of my wallet than to the fate of my flesh when it comes to cancer. By the time I hit the stage of life at which cancers are most likely to manifest, then the state of the art in safe and robustly effective cancer therapies will be impressive indeed. That will be true even if all that happens in between now and then is that the present technology demonstrations carried out in laboratories are developed into commercially available therapies ... and I'd expect far more progress than that to happen over a twenty year span of time.

Here are two more reassuring examples of ongoing development in biotechnology for those of us fortunately enough to have the luxury of time when it comes to cancer - even if we certainly don't have the luxury of time when it comes to aging itself.

Nanotechnology may lead to new treatment of liver cancer:

Researchers evaluated the use of molecular-sized bubbles filled with C6-ceramide, called cerasomes, as an anti-cancer agent. Ceramide is a lipid molecule naturally present in the cell's plasma membrane and controls cell functions, including cell aging, or senescence. ... The beauty of ceramide is that it is non-toxic to normal cells, putting them to sleep, while selectively killing cancer cells

...

Cerasomes [can] target cancer cells very specifically and accurately, rather than affecting a larger area that includes healthy cells. The problem with ceramide is that as a lipid, it cannot be delivered effectively as a drug. To solve this limitation, the researchers use nanotechnology, creating the tiny cerasome, to turn the insoluble lipid into a soluble treatment.

...

Researchers [previously] observed that cerasome use led to complete remission in aggressive, large granular lymphocytic leukemia in rats. ... It is plausible that preventing liver tumor vascularization with cerasome treatment could induce widespread apoptosis, a genetically programmed series of events that leads to cell death in tumors

The Answer To Wiping Out Cancer Could Be World's First Chemical Guided Missile:

Current cancer treatments destroy the cells that form the bulk of the tumour, but are largely ineffective against the root of the cancer, the cancer stem cells. This suggests that in order to provide a cure for cancer we must accurately detect and eliminate the cancer stem cells.

...

researchers have [created a targeted] RNA aptamer, a chemical antibody that acts like a guided missile to seek out and bind only to cancer stem cells. The aptamer has the potential to deliver drugs directly to the stem cells (the root of cancer cells) and also to be used to develop a more effective cancer imaging system for early detection of the disease.

Many different research groups are developing many different competing methods of both targeting cancer cells and delivering existing chemotherapy compounds in a highly targeted way. The chemical compounds used in many existing cancer therapies could be the basis for very safe and very effective future therapies if only they could be delivered just to cancer cells, and in small doses that did not leak out into neighboring tissues. This is exactly the capability being demonstrated over the past few years in laboratories around the world.

Researchers demonstrate that exercise can counter some of the effects of an engineered acceleration of mitochondrial dysfunction: "researchers [found] that signs of premature aging were halted - and even reversed - in virtually every tissue and organ in the bodies of exercised mice. Mice genetically altered to age faster were forced to run on treadmills for 45 minutes, three times a week. Five months later, the mice looked as young, healthy and active as wild-type mice - mice that didn't have the genetic mutation - while their sedentary and same-aged siblings were balding, greying and shrinking. .. The mice were genetically manipulated to age twice as fast as normal because of a defect in the repair system of their mitochondria, the powerhouses or furnaces inside each cell that give our body energy. Evidence has been mounting for decades that the older we get, the more mutations we accumulate in mitochondrial DNA. The furnaces start to break down, resulting in a steady decline in tissue and organ function. ... In our study, we saw huge recovery in mitochondrial function [in] the exercised mice." We might expect this result, given that exercise is known to have an impact on longevity, as well as on many of the biological mechanisms that are associated with aging. Given the importance of mitochondria in aging, it is interesting to see more work on the links between exercise and their function - but we must always be careful when evaluating work based on engineered dysfunction or accelerated aging. It is often the case that the putative end result has little relevance to "normal" aging.

Link: http://www.vancouversun.com/health/health/4321105/story.html

An open access paper: "Nearly 50 years ago geneticist James Neel famously proposed that 'thrifty genes' were important contributors to the rising prevalence of diabetes. Such genes promote efficient use and conservation of food energy, he theorized, and thus were favored by natural selection to help our ancient ancestors cope with famines. Now widespread in various populations, they predispose to obesity and diabetes, abetting a tendency to prepare for famines that never come. ... Here I propose an extension of this reproduction-centered version of Neel's theory that bears on aging. One of my key premises is that many windows of opportunity for reproductive booms occurred during the Holocene as agricultural innovations spread, periodically increasing food availability between times of nutritional stress. The periods of plenty selected for genotypes capable of rapidly ramping up fecundity as food intake increased. ... I believe the boom times' selection of genotypes prone to nutrition-cued accelerated development is having an especially problematic effect today because of widespread childhood overnutrition. Accelerated development, which enhanced reproductive success in the past, now has a pro-aging effect with rapidly growing costs. Indeed, when viewed through the lens of the antagonistic pleiotropy theory of aging, this effect seems anything but thrifty: It predisposes toward what might be called the spendthrift phenotype, characterized by chronic activation of pro-growth pathways - notably those involving mTOR, insulin, and insulin-like growth factor-1 - that support rapid development and sexual maturation but that also underlie later senescence. The modern fallout encompasses a much broader array of age-associated ills than the diabetes that prompted Neel's original hypothesis. Indeed, the spendthrift phenotype may well increase the age-associated risks of most if not all diseases of aging, like the ruinous adult legacy of flush, fast-living youth."

Link: http://www.impactaging.com/papers/v3/n2/full/100286.html

Follow the links below for a little photography for an otherwise slow Tuesday:

My Visit to KrioRus - the First Cryonics Company in Europe and Asia

Yesterday I visited the facilities of the Russian cryonics company KrioRus, which are located just outside Moscow. That's the huge dewar flask where the cryopreserved bodies are stored. It's so big that one needs to climb up a ladder to peek through the steamy nitrogen. And in the picture below Alexei Turchin, a renowned futurologist and expert on global risks, and I are in front of the other dewar flask, now empty and waiting for the new cryo patients. Cryonics is an amazing opportunity to get a chance to find yourself in the future. I believe cryonics is the choice of truly smart people.

SENS Foundation 'Lab Warming'

One of the Foundation's achievements last year was our Research Center's moving to a larger laboratory space, in Mountain View, California. Earlier this month we held a small opening event. It gave us a chance to thank our Research Operations Manager, Tanya Jones, and her team, for all their work in yet-again increasing the capabilities of the Foundation to pursue its core research interests. Anyway ... I took some snapshots during the afternoon, and thought I'd share them.

KrioRus and the SENS Foundation are two amongst a wide range of modern ventures in longevity science - although very different in focus, both are just a few years old and spring from overlapping communities of supporters, most of whom have been involved in the space for a decade or two at most. The longevity advocacy and interest community has a much longer history, and has become generational in nature over time. The folk who were most active in the early 90s are largely not the folk who are most active now, and progress in the form of new initiatives and public interest tends to arrive in waves. This I see as a good thing: life is change, and all broad movements need the influx of new faces and new movers and shakers in order to progress.

A study conducted by a team of researchers from the University of Lausanne found that a diet rich in whey protein can reduce the amount of fat in the liver.

Researchers from the University of Lausanne found out that the supplementation of whey protein in a person’s diet can lower the risk of developing fatty liver disease in obese women by reducing the amount of fat in liver cells. The study was published in an issue of Clinical Nutrition. They also found that whey protein was able to improve the study participants’ blood lipid profile which is important in promoting a healthier heart. The participants were asked to take the whey protein supplements for a period of four weeks.

Lead researcher Murielle Bortolotti said that their study was uncontrolled and preliminary but it strongly suggests that whey protein supplementation helps reduce the risk of fatty liver disease and promotes cardiovascular health as a long-term benefit. The researchers gathered a group of obese patients with an average BMI of 37.6 and IHCL concentrations between 1.9 to 20.5 percent. The participants were also recorded to have noticeable resistance to insulin with an average insulin sensitivity score of 2.77. The researchers observed that, after four weeks of whey protein supplementation, the study participants’ average IHCL dropped by 21 percent while their plasma triglyceride levels also went down by 15 percent. Their overall plasma cholesterol concentration was down by more than 7 percent after about a month of taking whey protein supplements. Researchers said that the result of the study indicates that whey protein has the potential to improve triglyceride profiles and IHCL.

The Liver and Fatty Liver Disease

The liver is the largest and heaviest glandular organ in the human body with an average weight of 1.36 kilograms. It is divided into four lobes which are unequal in size and shape. It is located at the right part of the abdominal cavity and just below the diaphragm. The portal vein and hepatic artery are responsible for carrying nutrients from the small intestines and oxygen-rich blood to the liver, respectively.

The human liver serves numerous functions including the production of enzymes that break down fats and produce glycogen from glucose. It is also responsible for producing urea and certain amino acids, storing of vitamins like vitamins B12, K, D, A and some minerals. The liver also produces 80 percent of the cholesterol in the body. The common disorders of the liver are liver cirrhosis, liver cancer, hepatitis and Wilson’s disease. The most harmful habit that affects the proper function of the liver is the excessive drinking of alcohol which can potentially alter the metabolic processes in the organ.

The root cause of fatty liver disease remains to be unknown. But medical experts are looking at patients’ resistance to insulin as the primary cause of the condition. Insulin resistance is a metabolic disorder where the cells are no longer responding properly to insulin in order to metabolize glucose.  In other words, insulin is no longer capable of performing its natural task of regulating sugar levels in the body. Nonalcoholic fatty liver disease is characterized by the accumulation of fat in the liver without the presence of alcohol. It refers to a wide spectrum of liver diseases from steatosis or simple fatty liver, cirrhosis or the irreversible and advanced scarring of the liver, to nonalcoholic steatohepatitis. Fatty liver disease is common throughout any age group; children can start developing fatty liver disease at the age of 10.

Natural Ways to Promote Liver Health

The liver is a very important organ in the body. Though minor health conditions concerning the liver are often very treatable, it is still necessary to keep the liver functioning properly to promote overall health.

• Diet plays a very important role in keeping the liver in tiptop shape. Ignoring hunger pangs or sudden and unscheduled eating can literally surprise the liver. Every time this happens, the liver exerts effort to produce the necessary enzymes to digest and metabolize the food properly. Eating at different hours of the day will overwork the liver and cause it to become exhausted. When struck with a sudden desire to eat, choosing foods that are not too heavy to the stomach like salads and fruits is recommended. And it is also a good way of maintaining a healthy body weight.

• Drinking plenty of water helps in washing away impurities and toxins out of the kidneys and liver. But drinking too much water while eating can interrupt the normal digestive process. So remember to observe proper pacing.

• The body has a limited requirement for sugars. Eating too much sweet foods can be dangerous to the liver and the human body. Sweets, especially those made or composed of refined sugar, will result to the excessive accumulation of fats in certain body parts like the buttocks, abdomen, thighs and the liver. Too much refined sugar will also result to the production of more triglycerides in the blood which, in turn, can increase the risk of developing cardiovascular disease. Some artificial sweeteners had been found by different studies to be poisonous to the body and result to fatigue and hypoglycemia. Eating fruits or blackstrap molasses when you want to eat something sweet are excellent alternatives to artificial sweeteners, especially for individuals with diabetes.

• Foods rich in protein like eggs, chicken, whole grains and legumes can help promote better liver health by helping it maintain a normal protein level in the body since the liver is responsible for producing protein. Low levels of protein can be a strong indication of kidney and liver disease. Eating natural and organic foods that are free of artificial sweeteners, colors, flavors and preservatives can also help in keeping the liver healthy.

• Some disease-causing bacteria can breed in the intestines. These organisms can cause permanent damage to the liver. So it is important to keep the intestines clean by drinking enough liquids and foods rich in dietary fiber.

• Eating less to lose weight can result to an insufficiency of nutrients supplied to the body. This makes the liver weak and incapable of producing enzymes that are needed in the proper digestion of food. Stop worrying too much about gaining weight and instead direct your attention to the foods that you eat to keep your liver and body healthy. As a reward, your liver will be able to better digest food and contribute in managing your weight.

Sources
nutraingredients.com
gicare.com
medicinenet.com
fitness.ygoy.com

Discuss this post in Frank Mangano’s forum!

A study published in the February issue of the Chest revealed that vitamin D deficiency is linked to a higher risk of interstitial lung disease.

The Lungs

The principal function of the lungs is to transport the oxygen acquired through breathing to the blood streams and to release carbon dioxide back to the atmosphere. The whole process of respiration is accomplished by tiny specialized cells called alveoli or the air sacs. In the process of breathing, air passes through the nose then travels through the nasopharynx, larynx, trachea and through the branches of the bronchial tubes before finally reaching the aveoli. The diaphragm, on the other hand, is important in driving air to the lungs.

Pulmonary Health Risks

The increasingly deteriorating conditions of the environment make it even harder to keep the lungs healthy. Though the lungs are naturally capable of filtering the air that we breathe, they may not be able to filter toxic materials in the air that may affect our health. This results to lung problems that can be life threatening. Lung cancer, for example, has a high prevalence rate in the United States and other parts of the world.

The number one cause of lung damage is smoking. Numerous studies had found out that smoking can dramatically increase the risk of developing lung cancer and other pulmonary disorders. A single stick of cigarette can contain hundreds of toxins and harmful materials that can directly harm the lungs and other vital organs of the body. Indeed, smoking is bad for the health. Other factors and bad habits can also result to an increased risk of developing lung disease. Inhaling aerosols like paint and deodorants can result to serious damage of the lungs. Vehicles like trucks and cars release toxic fumes that can damage the lungs when inhaled. The lack of sufficient nutrition can also lead to certain lung problems.  A study published in the February issue of the Chest revealed that vitamin D deficiency can increase the risk of interstitial lung disease, a health condition associated with inflammation of the tissues surrounding the air sacs.

Interstitial Lung Disease

The air sacs found in the inner lining of the lungs plays a very important role in extracting oxygen from the air and are supported by a thin lining of tissue. When this tissue becomes inflamed, the function of the air sacs is affected. This health condition of the lungs is called interstitial lung disease. ILD is not limited to certain portions of the lungs but the inflammation can spread all throughout the lungs. Unlike pneumonia, the inflammation of the lungs in interstitial lung disease is not caused by infection but by other factors including the misdirected response of the immune system to infection and toxins like silica dusts and asbestos. Other cases of ILD are idiopathic or with no definite cause.

The first symptom of ILD is difficulty in breathing due to the reduced amounts of circulating oxygen in the body followed by frequent coughing. The condition can be mistakenly diagnosed as pneumonia. Health examinations to conclude ILD include blood tests to rule out infection, imaging studies like CT scans and chest x-rays, PFT or pulmonary function tests and biopsy. Though all these tests are not required in order to determine ILD, some cases may need more examinations that others.

Vitamin D Deficiency and Lung Health

In a study conducted by a team of researchers from the University of Cincinnati College of Medicine, results revealed that vitamin D deficiency can affect the proper function of the lungs. The researchers observed that patients with interstitial lung disease or ILD are mostly deficient in vitamin D especially in patients with connective tissue disease or CTD. They gathered a group of 67 patients with CTD-ILD and 51 patients with other types of ILD and found that the prevalence of vitamin D insufficiency and deficiency is 69 percent and 38 percent, respectively.  Vitamin D plays an important role in maintaining healthy lung function. And aside from keeping the respiratory system in tip-top shape, vitamin D also plays an essential role in other body functions.

Health Benefits of Vitamin D

United States laws require the fortification of all milk brands with vitamin D. So drinking one to two glasses of milk a day can supply the body with its needed dosage of vitamin D to maintain and promote better health. Other rich sources of vitamin D are cream, butter, and other dairy products. Some oysters and fish are also rich sources of vitamin D.

The efficient absorption of calcium in the bones need the assistance of vitamin D. Vitamin D deficiency is commonly associated with rickets in children and osteoporosis in older adults. Too much vitamin D can also have adverse effects to the body since it results to the excessive absorption of calcium which can accumulate in vital organs like the heart and lungs. Muscle weakness, vomiting and the appearance of kidney stones are also linked to too much vitamin D.

Infants and children aged 0 to 13 years need 5 micrograms of vitamin D a day; this recommended daily intake of vitamin D is relatively consistent up to the age of 50 with an increase to 10 micrograms for people 51 years and older.

Natural Ways to Promote Lung Health

Frequent exercise, proper nutrition and avoiding harmful habits are keys to keeping the lungs healthy. Even if the person exercise frequently and is receiving sufficient nutrition, smoking can keep his risk of developing lung disease high compared to sedentary and malnourished non-smokers. It has been well established that smoking can lead to numerous health conditions like lung cancer and other types of cancer. Smoking can also weaken the immune system and make the person more susceptible to infection.

Medical experts advise regular check-ups for the early diagnosis of a lung disorder. Taking the stairs instead of using the lift will also give the lungs a healthy workout if there’s no time to go to the gym. Second hand smoke can damage the lungs more than cigarette does to the actual smoker. So try to stay away from smoky areas and always make it a point to take the non-smokers area in bars and restaurants. Certain household products may also release toxic fumes when used. Make it a habit to always check the labels of household cleaning products before buying or using them.

Sources
medicinenet.com
eurekalert.org
medicinenet.com
nlm.nih.gov
ods.od.nih.gov
rd.com

Discuss this post in Frank Mangano’s forum!

Around these parts Aubrey de Grey and the SENS Foundation should require no introduction. His advocacy and the Foundation's work on the science of repairing aging is well known, and has been mentioned here at Fight Aging! too many times to count. In my eyes, the Strategies for Engineered Negligible Senescence (SENS) continue to be the best extant plan for extending human life span as rapidly as possible - and within our lifetimes. The more funding that is devoted to realizing that plan, the better all of our futures will be.

I noticed that a podcast interview with de Grey is up at the Singularity Weblog:

Last time I had Dr. Aubrey de Grey on Singularity 1 on 1 the interview turned out to be a hit. In fact it is still by far the most popular podcast that I have done and the audio file has been listened to or downloaded over 30,000 times. Given Aubrey's popular appeal and the importance of his work, it is no surprise that I am very happy to have him back for a second interview. ... During this conversation I ask Dr. de Grey to discuss issues such as: the term natural death and its impact; the publicity and importance of two long-awaited documentaries about Ray Kurzweil - Transcendent Man and The Singularity is Near; traditional metabolic and more recent DNA tests such as the ones done by 23andMe and others; the slow developmental process of new drugs and therapies, and the problems of taking them from testing in lab rats to humans; the Thomas Malthus argument of overpopulation and Aubrey's reply to it.

Head on over there to watch or listen.

The investigation of the mechanisms of calorie restriction continues apace. Here, researchers "report for the first time that deactivation of a protein called CRTC1 in roundworms increases their lifespan, most likely mediating the effects of calorie restriction. Previously, researchers knew hunger promoted longevity by activating an enzyme called AMPK, which senses that food is scarce and pushes cells into a low energy state. ... We knew AMPK was a major energy sensor but didn't know what it was talking to. Our goal was to understand the genetic circuitry that registered that response. ... It was clear that one pathway that coordinated metabolism with growth in response to nutrients was AMPK signaling. Studies had also suggested that AMPK might regulate lifespan in worms. What was not known was what factors downstream of AMPK mediated those effects. ... they searched the genome of Caenorhabditis elegans for likely AMPK targets, and identified one suspect encoding a protein called CRTC1, which was expressed at the same time and place as AMPK. To determine if CRTC1 played any role in lifespan, the team fed worms an inhibitory RNA engineered to deplete them of CRTC1 protein. When they measured the worms' lifespan-normally about 3 weeks-they found that worms fed the anti-CRTC1 RNA lived a whopping 40% longer, suggesting that AMPK retards aging by antagonizing CRTC1 activity. ... AMPK deactivated CRTC1 by adding phosphates to a specific region of the CRTC1 protein, an effect equivalent to eliminating CRTC1 altogether. Likewise, when the worms were fed an inhibitory RNA depleting them of an enzyme that lops off the CRTC1 phosphates, they lived longer, showing that AMPK and the lopper - known to scientists as calcineurin - determine lifespan by controlling the extent to which CRTC1 is phosphorylated."

Link: http://www.newswise.com/articles/hungering-for-longevity-salk-scientists-identify-the-confluence-of-aging-signals

From ScienceDaily: "It has been long known that stress plays a part not just in the graying of hair but in hair loss as well. ... Now, a team [that] was investigating how stress affects gastrointestinal function may have found a chemical compound that induces hair growth by blocking a stress-related hormone associated with hair loss - entirely by accident. ... Our findings show that a short-duration treatment with this compound causes an astounding long-term hair regrowth in chronically stressed mutant mice. This could open new venues to treat hair loss in humans through the modulation of the stress hormone receptors, particularly hair loss related to chronic stress and aging. ... the researchers had been using mice that were genetically altered to overproduce a stress hormone called corticotrophin-releasing factor, or CRF. As these mice age, they lose hair and eventually become bald on their backs, making them visually distinct from their unaltered counterparts. The [researchers] had developed the chemical compound, a peptide called astressin-B, and described its ability to block the action of CRF. ... researchers injected the astressin-B into the bald mice to observe how its CRF-blocking ability affected gastrointestinal tract function. .... About three months later, the investigators returned to these mice to conduct further gastrointestinal studies and found they couldn't distinguish them from their unaltered brethren. They had regrown hair on their previously bald backs."

Link: http://www.sciencedaily.com/releases/2011/02/110216185406.htm

The latest issue of Rejuvenation Research is available online, and it opens with what is perhaps one of the best of points to make in a world in which people are dying all around us:

I welcome Dr. Paula Moreira as a new member of our editorial board, but for the worst possible reason. Moreira has been appointed as a replacement for Mark Smith, a fellow professor at Case Western Reserve University, who tragically died in a car accident late last year. What is even worse is that Smith is not the only loss that the field of biogerontology has suffered in 2010. In fact, I am aware of fully five other researchers who died during 2010. Amir Abramovich (whose Ph.D. advisor has penned a brief obituary that appears later in this issue) and Estela Medrano also succumbed to road accidents. James Joseph died from complications following heart surgery. Chris Heward was the victim of a particularly aggressive esophageal cancer. And Bob Butler died very suddenly of leukemia.

...

I have chosen to highlight these sombre events in this space not only to commemorate lost friends and colleagues. My main reason for doing so is to draw attention to the questionable validity of our tendency to grieve especially intensely for those who die when still highly active. Though I share this tendency, I think it deserves scrutiny, because it is founded on an assumption that profoundly contradicts the motivation for the work to which we, as did the colleagues I have just listed, dedicate our lives.

Aging kills people, just as cars do. There are only two things that distinguish aging from other killers: it kills people very slowly, only after gradually and progressively debilitating them over many years, and it only kills people who were born quite a long time ago. The combination of these features seems to be the only available explanation for why we so meekly and calmly accept the deaths of so vast a number of people from aging, while feeling much more intense anger and despair at the comparatively rare deaths that occur in the industrialized world at younger ages.

...

Is it somehow OK, or at least only a little bit sad, when someone dies of "natural causes" after "a good innings"? I would suggest that it is not OK.

Ageism permeates our societies, and our descendants will look back in disgust and horror at the way in which we allowed our historical legacy of prejudice to suppress and slow down progress towards the biotechnologies of rejuvenation. We younger folk write off the old in so many ways, and in doing so each of us is only sticking the knife into the person we'll be a few decades down the line - and teaching our children to do exactly the same. Every death is a tragedy, but so many people work so hard to pretend otherwise.

Old people suffer from a terrible debilitating medical condition: aging. Why view them any differently than the victims of any other deadly disease? If not weighed down by the degenerations of aging and the knowledge of suffering a certainly terminal condition, elderly folk could contribute greatly to all fields of human endeavor, applying the experience and knowledge of a lifetime - or adeptly applying the savings of a lifetime to fund the work of others. We would all be far wealthier if the ongoing ability to create value offered by human beings was not destroyed after a bare few decades of productivity.

Even if it wasn't the case that it is in our immediate economic self-interest to build rejuvenation biotechnologies, working to cure aging would still be the greatest of charitable causes. No other aspect of human biology or the human condition causes as much pain and death.

Aging is a horror, and it twists our society into further horrors - such as the often shameful ways in which the young treat the old. The sooner that aging can be repaired and removed as a threat to human existence, the better the human condition will become.

From the Monterey Herald: " Within a Northeast Ohio lab, a hairless mouse is growing an ear from the cells of a Wadsworth, Ohio, preschooler. Dr. William Landis, the G. Stafford Whitby Chair of Polymer Science at the University of Akron, is leading groundbreaking, tissue-engineering research to grow human cartilage - first in the lab, now in animals and, eventually, in patients. His work is part of a fast-developing field that could help millions of patients repair injuries, replace worn body parts or fix birth defects with tissue grown from their own cells in the not-so-distant future. ... Kyle Figuray's parents agreed to be the first area participants and donors of his otherwise useless cartilage. The healthy, friendly 5-year-old was born with a congenital defect that caused the exterior ear and ear canal on his right side to develop improperly. Typically, the malformed ear cartilage is discarded as medical waste after it's removed during the first of three procedures to craft a new ear out of rib. Instead, the tissue removed [was] placed inside a vial and shared with Landis' research team, who carefully cleansed the cells and fed them special nutrients to coax them to proliferate in the lab. A few weeks later, enough cells were available for researchers to 'seed' them onto a biodegradable, biocompatible polymer scaffold. A few days later, the seeded ear scaffold was implanted under the skin of a hairless mouse ... The mouse will be studied over the next year to determine how the cells are behaving and progressing toward normal cartilage. If all goes well, the biodegradable polymer scaffold should disappear, leaving behind only Kyle's cartilage cells in the shape of an ear. The hope is that an affected person's cells someday can be harvested, seeded onto similar polymer scaffolds and implanted under the patient's own skin in the abdomen or back until they grow into replacement tissue. At that point, the new tissue could be removed and used to replace the patient's injured or defective tissue."

Link: http://www.montereyherald.com/science/ci_17411698

Research into Laron dwarfism in a population in Ecuador has been taking place for a few years now: "People living in remote villages in Ecuador have a mutation that some biologists say may throw light on human longevity and ways to increase it. The villagers are very small, generally less than three and a half feet tall, and have a rare condition known as Laron syndrome or Laron-type dwarfism. ... though cancer was frequent among people who did not have the Laron mutation, those who did have it almost never got cancer. And they never developed diabetes, even though many were obese, which often brings on the condition. ... [this is] an opportunity to explore in people the genetic mutations that researchers [found] could make laboratory animals live much longer than usual. ... The Laron patients' mutation means that their growth hormone receptor lacks the last eight units of its exterior region, so it cannot react to growth hormone. In normal children, growth hormone makes the cells of the liver churn out another hormone, called insulinlike growth factor, or IGF-1, and this hormone makes the children grow. If the Laron patients are given doses of IGF-1 before puberty, they can grow to fairly normal height. This is where the physiology of the Laron patients links up with the longevity studies that researchers have been pursuing with laboratory animals. IGF-1 is part of an ancient signaling pathway that exists in the laboratory roundworm as well as in people. The gene that makes the receptor for IGF-1 in the roundworm is called DAF-2. And worms in which this gene is knocked out live twice as long as normal."

Link: http://www.nytimes.com/2011/02/17/science/17longevity.html

There is clearly a point in Alzheimer's, and other neurodegenerative diseases, beyond which the damage caused by the condition is irreversible. Neurons die, and in large enough numbers to destroy vast swathes of information held in the brain - the very foundation of who you are, and the vital components of systems needed to live a normal life. All is not gloom, however. Studies in past years have suggested that up to that point, much of the loss of function that accompanies Alzheimers is in principle reversible:

Some evidence suggests that the worst effects of Alzheimer's disease can be repaired - that memories are not destroyed, but rather become inaccessible.

Another recent study adds to this picture:

Amyloid-beta and tau protein deposits in the brain are characteristic features of Alzheimer disease. The effect on the hippocampus, the area of the brain that plays a central role in learning and memory, is particularly severe. However, it appears that the toxic effect of tau protein is largely eliminated when the corresponding tau gene is switched off.

Researchers from the Max Planck Research Unit for Structural Molecular Biology at DESY in Hamburg have succeeded in demonstrating that once the gene is deactivated, mice with a human tau gene, which previously presented symptoms of dementia, regain their ability to learn and remember, and that the synapses of the mice also reappear in part. The scientists are now testing active substances to prevent the formation of tau deposits in mice. This may help to reverse memory loss in the early stages of Alzheimer disease - in part, at least.

For yet another consideration of early to mid-stage Alzheimer's as a form of dynamic blockage of memory access, you might also look at the effects of some newer anti-inflammatory treatments:

The [study from 2008] documents a dramatic and unprecedented therapeutic effect in an Alzheimer's patient: improvement within minutes following delivery of perispinal etanercept, which is etanercept given by injection in the spine.

Putting aside a discussion of the mechanisms by which this happens, the very fact that it can happen demonstrates the possibility of reversing the worst aspects of Alzheimer's. Thus memories and the working structures of the brain must remain largely intact until fairly late in the progression of the disease.

There is clearly a point in Alzheimer's, and other neurodegenerative diseases, beyond which the damage caused by the condition is irreversible. Neurons die, and in large enough numbers to destroy vast swathes of information held in the brain - the very foundation of who you are, and the vital components of systems needed to live a normal life. All is not gloom, however. Studies in past years have suggested that up to that point, much of the loss of function that accompanies Alzheimers is in principle reversible:

Some evidence suggests that the worst effects of Alzheimer's disease can be repaired - that memories are not destroyed, but rather become inaccessible.

Another recent study adds to this picture:

Amyloid-beta and tau protein deposits in the brain are characteristic features of Alzheimer disease. The effect on the hippocampus, the area of the brain that plays a central role in learning and memory, is particularly severe. However, it appears that the toxic effect of tau protein is largely eliminated when the corresponding tau gene is switched off.

Researchers from the Max Planck Research Unit for Structural Molecular Biology at DESY in Hamburg have succeeded in demonstrating that once the gene is deactivated, mice with a human tau gene, which previously presented symptoms of dementia, regain their ability to learn and remember, and that the synapses of the mice also reappear in part. The scientists are now testing active substances to prevent the formation of tau deposits in mice. This may help to reverse memory loss in the early stages of Alzheimer disease - in part, at least.

For yet another consideration of early to mid-stage Alzheimer's as a form of dynamic blockage of memory access, you might also look at the effects of some newer anti-inflammatory treatments:

The [study from 2008] documents a dramatic and unprecedented therapeutic effect in an Alzheimer's patient: improvement within minutes following delivery of perispinal etanercept, which is etanercept given by injection in the spine.

Putting aside a discussion of the mechanisms by which this happens, the very fact that it can happen demonstrates the possibility of reversing the worst aspects of Alzheimer's. Thus memories and the working structures of the brain must remain largely intact until fairly late in the progression of the disease.

A promising open access study: "Transplanting autologous renal progenitor cells (RPCs), (kidney stem cells derived from self-donors), into rat models with kidney damage from pyelonephritis - a type of urinary infection that has reached the kidney - has been found to improve kidney structure and function. ... Advancements in stem cell therapies and tissue engineering hold great promise for regenerative nephrology. Our RPC transplant study demonstrated benefits for pyelonephritis, a disease characterized by severe inflammation, renal function impairment and eventual scarring, and which remains a major cause of end-stage-renal disease worldwide. ... The researchers divided 27 rats into three groups, two of which were modeled with an induced pyelonephritis in their right kidneys, while the third group did not have induced disease. RPCs were obtained from the diseased animals' left kidneys and injected into the right kidney six weeks later. Two weeks after injection, tubular atrophy was reduced. After four weeks, fibrosis was reduced and after sixty days, right renal tissue integrity was 'significantly improved.' ... We propose that kidney augmentation was mainly due to functional tissue regeneration following cellular transplantation. Kidney-specific stem/progenitor cells might be the most appropriate candidates for transplantation because of their inherent organ-specific differentiation and their capacity to modulate tissue remodeling in chronic nephropathies. ... The researchers concluded that because renal fibrosis is a common and ultimate pathway leading to end-stage renal disease, amelioration of fibrosis might be of major clinical relevance."

Link: http://www.eurekalert.org/pub_releases/2011-02/ctco-sct021411.php