A look at ongoing work on nerve regeneration in one laboratory: "One technology used [by] neurosurgeons is the NeuraGen Nerve Guide, a hollow, absorbable collagen tube through which nerve fibers can grow and find each other. The technology is often used to repair nerve damage over short distances less than half an inch long. ... [Researchers] compared several methods to try to bridge a nerve gap of about half an inch in rats. The team transplanted nerve cells from a different type of rat into the wound site and compared results when the NeuraGen technology was was used alone or when it was paired with [dorsal root ganglion neurons, or DRG cells], or with other cells known as Schwann cells. After four months, the team found that the tubes equipped with either DRG or Schwann cells helped bring about healthier nerves. In addition, the DRG cells provoked less unwanted attention from the immune system than the Schwann cells, which attracted twice as many macrophages and more of the immune compound interferon gamma. While both Schwann and DRG cells are known players in nerve regeneration, Schwann cells have been considered more often as potential partners in the nerve transplantation process, even though they pose considerable challenges because of the immune system's response to them. ... In a related line of research, [scientists] are creating DRG cells in the laboratory by stretching them, which coaxes them to grow about one inch every three weeks. The idea is to grow nerves several inches long in the laboratory, then transplant them into the patient, instead of waiting months after surgery for the nerve endings to travel that distance within the patient to ultimately hook up."

Link: http://www.urmc.rochester.edu/news/story/index.cfm?id=3415

From the Methuselah Foundation blog: "A thin layer of human skeletal muscle is being printed by Chirag Khatiwala in a small, sterile room of San Diego-based startup Organovo. Each muscle cell from the company's signature 3-D printer is uniformly deposited in closely spaced lines on a petri dish. This allows the cells to grow and interconnect until they form working muscle tissue nearly indistinguishable from a human muscle biopsy. Unlike other experimental approaches that utilize ink-jet printers to deposit cells, Organovo's technology enables cells to interact with each other the way they do in the body. How? They are packed tightly together, sandwiched, if you will, and incubated. This prompts them to cleave to each other and interchange chemical signals. When printed, the cells are grouped together in a paste that helps them grow, migrate, and align themselves properly. In the case of muscle cells, the way they orient themselves in the same direction allow for contractions of the tissue. ... Methuselah Foundation honors the efforts of Organovo through early funding and support as well as through its new, highly anticipated New Organ Mprize. The true prize is elevated health and quality of life for those that have had to or will suffer the blows of a failing organ. Every $10 helps us work in tandem with today's stunningly advanced technology so that at some tomorrow, no one will have to suffer or die because of a diseased organ."

Link: http://blog.mfoundation.org/2012/02/_fantastical_scenes_from_the.html

The latest issue of the Cryonics magazine is available online in PDF format: "The January-February 2012 issue of Cryonics marks the return of Alcor's magazine as a bi-monthly professionally printed publication. This issue features two major articles on cryonics and brain-threatening disorders. The first article, by Cryonics editor Aschwin de Wolf, provides a framework for thinking about identity-destroying brain diseases and discusses what Alcor members can do to prevent them from threatening your cryopreservation. Alcor staff member Mike Perry returns to the topic of brain-threatening disorders and presents his updated findings on the options available to cryonicists who have been diagnosed with such a disease, (like Alzheimer's). After being CEO at Alcor for one year, Alcor CEO and President Max More reflects on his Alcor experience to date and we get a look into the interesting career of one of the pioneers of transhumanism. Another Alcor veteran, Russel Cheney, contributes an article about the importance of 'superfunding' your cryopreservation arrangements."

Link: http://www.alcor.org/magazine/2012/02/17/cryonics-january-february-2012/

Via the Guardian: "Fasting for regular periods could help protect the brain against degenerative illnesses ... Researchers [had] found evidence which shows that periods of stopping virtually all food intake for one or two days a week could protect the brain against some of the worst effects of Alzheimer's, Parkinson's and other ailments. ... Reducing your calorie intake could help your brain, but doing so by cutting your intake of food is not likely to be the best method of triggering this protection. It is likely to be better to go on intermittent bouts of fasting, in which you eat hardly anything at all, and then have periods when you eat as much as you want. In other words, timing appears to be a crucial element to this process. ... have also worked out a specific mechanism by which the growth of neurons in the brain could be affected by reduced energy intakes. Amounts of two cellular messaging chemicals are boosted when calorie intake is sharply reduced. ... These chemical messengers play an important role in boosting the growth of neurons in the brain, a process that would counteract the impact of Alzheimer's and Parkinson's. ... The cells of the brain are put under mild stress that is analogous to the effects of exercise on muscle cells. The overall effect is beneficial. ... The link between reductions in energy intake and the boosting of cell growth in the brain might seem an unlikely one, but [there are] sound evolutionary reasons for believing it to be the case. ... When resources became scarce, our ancestors would have had to scrounge for food. Those whose brains responded best - who remembered where promising sources could be found or recalled how to avoid predators - would have been the ones who got the food. Thus a mechanism linking periods of starvation to neural growth would have evolved." You might recall that intermittent fasting and straight calorie restriction depend on different sets of genes in mice, suggesting that they are not working to enhance health in the same ways - this latest research tends to reinforce that view.

Link: http://www.guardian.co.uk/society/2012/feb/18/fasting-protect-brain-diseases-scientists

The present state of research in the accelerated aging condition progeria shows it to result from malformed proteins important to the structure of the cell nucleus - which is something that also occurs in normal aging, but to a much lesser degree. Here is a look at what some researchers are doing with this information - producing the tools needed to get to the next step in their investigations: "The premature aging disorder, Hutchinson-Gilford progeria syndrome (HGPS), is caused by mutant lamin A, which affects the nuclear scaffolding. The phenotypic hallmark of HGPS is nuclear blebbing. Interestingly, similar nuclear blebbing has also been observed in aged cells from healthy individuals. Recent work has shown that treatment with rapamycin, an inhibitor of the mTOR pathway, reduced nuclear blebbing in HGPS fibroblasts. However, the extent of blebbing varies considerably within each cell population, which makes manual blind counting challenging and subjective. Here, we show a novel, automated and high throughput nuclear shape analysis that quantitatively measures curvature, area, perimeter, eccentricity and additional metrics of nuclear morphology for large populations of cells. We examined HGPS fibroblast cells treated with rapamycin and RAD001 (an analog to rapamycin). Our analysis shows that treatment with RAD001 and rapamycin reduces nuclear blebbing, consistent with blind counting controls. In addition, we find that rapamycin treatment reduces the area of the nucleus, but leaves the eccentricity unchanged. Our nuclear shape analysis provides an unbiased, multidimensional 'fingerprint' for a population of cells, which can be used to quantify treatment efficacy and analyze cellular aging."

Link: http://impactaging.com/papers/v4/n2/full/100434.html

You may recall that levels of high-density lipoproteins (HDL) have been shown to correlate with human longevity, such as in centenarian studies. Here is another very long term study that also shows an association, using a "fifty-three-year prospective follow-up of Gofman's Livermore Cohort between 1954 and 2008. ... One thousand one hundred forty-four men who consented to the study, had analytic ultracentrifuge measurements of lipoprotein subfractions at baseline, and were old enough at baseline to have survived to age 85 during follow-up. ... Three hundred ninety men survived to 85 years old (34.1%). Survivors were less likely than nonsurvivors to be in the lowest HDL3 and HDL2 quartiles. Logistic regression analyses showed that the lowest HDL3 quartile significantly predicted shorter longevity. ... Men who were above the 25th HDL3 percentile had 70% greater odds of surviving until age 85 than those below this level, which persisted when adjusted for HDL2, very low-density lipoprotein (LDL), and standard risk factors. Proportional hazard analyses of survival before age 85 showed that being in the lowest HDL3 quartile increased age-adjusted cancer risk by 39% and noncancer risk by 23% when adjusted for other risk factors."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22329432

One of the ways in which major blood vessels decline in function with aging is that they lose their elasticity. The state of chronic inflammation that grows with aging contributes to this, as noted in this open access paper (in PDF format). This is probably connected to the fact that exercise helps improve the elasticity of arteries, given that exercise is shown to impact levels of inflammation: "Increased arterial stiffness is an independent predictor of cardiovascular disease independent from blood pressure. Recent studies have shed new light on the importance of inflammation on the pathogenesis of arterial stiffness. Arterial stiffness is associated with the increased activity of angiotensin II, which results in increased NADPH oxidase activity, reduced NO bioavailability and increased production of reactive oxygen species. Angiotensin II signaling activates matrix metalloproteinases (MMPs) which degrade TGFβ precursors to produce active TGFβ, which then results in increased arterial fibrosis. ... There is also ample clinical evidence that demonstrates the association of inflammation with increased arterial stiffness. Recent studies have shown that reductions in inflammation can reduce arterial stiffness. In patients with rheumatoid arthritis, increased aortic pulse wave velocity in patients was significantly reduced by anti tumor necrosis factor-α therapy. ... Thus, there is rationale for targeting specific inflammatory pathways involved in arterial stiffness in the development of future drugs. Understanding the role of inflammation in the pathogenesis of arterial stiffness is important to understanding the complex puzzle that is the pathophysiology of arterial stiffening and may be important for future development of novel treatments."

Link: http://dx.doi.org/10.3349/ymj.2012.53.2.258

From Maria Konovalenko: "I am proud to announce that Science for Life Extension Foundation is one of the organizers of the 2nd international Genetics of Aging and Longevity conference. It is going to be an amazing and actually unprecedented conference focused on genetic mechanisms of aging and longevity. Check out the list of our invited speakers. I can't wait to hear the prominent researchers sharing their experience in making model animals live longer. By the way, we are proud to have all the longevity-record braking researchers, who extended the lifespan of yeast, nematodes, fruit flies and mice. You can't miss this meeting. I encourage you to go ahead and register. It's the end of April, beautiful spring in Moscow. For those who have never been here before, here's your chance to kill two birds with one stone - learn a lot about aging and discover one of the most beautiful and dynamic cities in the world."

Link: http://aging-genes2012.ru/en/

I would take this as an indicator that simple, ongoing maintenance of fitness and avoidance of a sedentary lifestyle pays off: "Simple tests such as walking speed and hand grip strength may help doctors determine how likely it is a middle-aged person will develop dementia or stroke. ... More than 2,400 men and women with an average age of 62 underwent tests for walking speed, hand grip strength and cognitive function. Brain scans were also performed. During the follow-up period of up to 11 years, 34 people developed dementia and 70 people had a stroke. The study found people with a slower walking speed in middle age were one-and-a-half times more likely to develop dementia compared to people with faster walking speed. Stronger hand grip strength was associated with a 42 percent lower risk of stroke or transient ischemic attack (TIA) in people over age 65 compared to those with weaker hand grip strength. This was not the case, however, for people in the study under age 65. ... Researchers also found that slower walking speed was associated with lower total cerebral brain volume and poorer performance on memory, language and decision-making tests. Stronger hand grip strength was associated with larger total cerebral brain volume as well as better performance on cognitive tests asking people to identify similarities among objects." We might theorize that this is related to exercise and blood flow in the brain, and related effects on the heath of blood vessels in the brain.

Link: http://www.sciencedaily.com/releases/2012/02/120215185850.htm

Average telomere length in at least some tissues makes a good marker for general health, but the progressive shortening of telomeres may or may not be a root cause of aging. Telomere length results from a dynamic system of lengthening and shortening processes, which seems more likely to be a reflection of underlying function and dysfunction: "In an ongoing study of almost 20,000 Danes, a team of researchers [have] isolated each individual's DNA to analyse their specific telomere length - a measurement of cellular aging. ... The risk of heart attack or early death is present whether your telomeres are shortened due to lifestyle or due to high age ... The recent Copenhagen General Population Study involved almost 20,000 people, some of which were followed during almost 19 years, and the conclusion was clear: If the telomere length was short, the risk of heart attack and early death was increased by 50 and 25 per cent, respectively. ... That smoking and obesity increases the risk of heart disease has been known for a while. We have now shown, as has been speculated, that the increased risk is directly related to the shortening of the protective telomeres - so you can say that smoking and obesity ages the body on a cellular level, just as surely as the passing of time. ... one in four Danes has telomeres with such short length that not only will they statistically die before their time, but their risk of heart attack is also increased by almost 50 per cent. Future studies will have to reveal the actual molecular mechanism by which the short telomere length causes heart attacks. Does one cause the other or is the telomere length and the coronary event both indicative of a third - yet unknown - mechanism?" I lean towards the latter hypothesis, that both risk of catastrophic failure in bodily systems and telomere length reflect levels of accumulated damage at the level of cells and macromolecules in the body.

Link: http://news.ku.dk/all_news/2012/2012.2/cellular-aging-increases-risk-of-heart-attack/