Perhaps I'm just paying greater attention to the topic of late, but it seems like a fair number of large statistical studies that correlate exercise with increased life expectancy have shown up in the past couple of years - more than I recall prior to that. A few examples from the archives:

• Exercise, Longevity, and Long Term Medical Costs
• The Power of Moderate Exercise
• Another Study Suggests that Sedentary Behavior Adds Up

Here is a newly published study on this topic that pulls from a data set of around 95,000 people. It is presently open access, which is not usually the case for the journal in question, so take advantage of it while it lasts:

Years of Life Gained Due to Leisure-Time Physical Activity in the U.S.

Data from the National Health and Nutrition Examination Survey (2007-2010); National Health Interview Study mortality linkage (1990-2006); and U.S. Life Tables (2006) were used to estimate and compare life expectancy at each age of adult life for inactive (no moderate to vigorous physical activity); somewhat-active (some moderate to vigorous activity); and active ([more] moderate to vigorous activity) adults. Analyses were conducted in 2012.

Somewhat-active and active non-Hispanic white men had a life expectancy at age 20 years that was ?2.4 years longer than that for the inactive men; this life expectancy advantage was 1.2 years at age 80 years. Similar observations were made in non-Hispanic white women, with a higher life expectancy within the active category of 3.0 years at age 20 years and 1.6 years at age 80 years. In non-Hispanic black women, as many as 5.5 potential years of life were gained due to physical activity. Significant increases in longevity were also observed within somewhat-active and active non-Hispanic black men; however, among Hispanics the years-of-life-gained estimates were not significantly different from 0 years gained.

The estimates in the present study for non-Hispanic white men aged 20 years [suggest] that 2.6 hours [of overall life expectancy] are gained per hour of moderate activity and 5.2 hours were gained per hour of vigorous activity accrued in adulthood.

The effects of exercise on general health over the long term are possibly more striking. You can't exercise your way out of aging, but you can laze your way into a much more unpleasant and expensive later life. Exercise, calorie restriction, and the like are small stopgap measures, the poor and miserable best we can do right now in order to gain a better chance of being alive and in good health to great the arrival of rejuvenation biotechnologies - therapies that will repair and reverse the cellular and molecular damage that drives aging.

We need those biotechnologies to get out of this hole alive. They are the most important goal - don't lose sight of that behind the constant deluge of data on health, life expectancy, and how we can presently modestly adjust the pace at which we're aging to death.

Source:
http://www.fightaging.org/archives/2012/12/years-of-life-gained-due-to-leisure-time-physical-activity.php

The Eurosymposium on Healthy Aging took place in Brussels earlier this month, a gathering of researchers and advocates for longevity science. The presentations were recorded and videos have been posted to Youtube. I encourage you to browse. Here is a report on the event:

Theoretical questions of longevity were covered in the first day, including such themes as the general overviews of ageing theories, molecular damage in ageing, mitochondria and autophagy. The general panel on causes, mechanisms, and interventions in aging, featured Drs. Aubrey de Grey, David Gems, Kris Verburgh, and Diana Van Heemst, and was moderated by Sven Bulterijs of HEALES.

The second day featured an inspiring plethora of promising potential interventions for increasing healthy longevity: genetics of aging and centenarians research, nutritional and pharmacological interventions in aging, biomedical interventions such as repair of damaged mitochondria, destruction of senescent cells, use of telomerase to extend health span, remediation of the Alzheimer's disease, and regenerative medicine, including both cell material and computational aspects.

The main subject of the third day was the political and social promotion of research into the biology of aging and healthy longevity. Discussion groups were formed and tentative suggestions made for increasing funding for life extension research, improving public opinion of life extension, and scientific positioning of life-extension.

Link: http://hplusmagazine.com/2012/12/19/the-brussels-summit-of-longevity-activists/

Source:
http://www.fightaging.org/archives/2012/12/a-report-from-the-eurosymposium-on-healthy-aging.php

A successful demonstration of a novel form of immune therapy is noted in this article, and described in a recently published paper:

An experimental "Trojan-horse" cancer therapy has completely eliminated prostate cancer in experiments on mice. [The] team hid cancer killing viruses inside the immune system in order to sneak them into a tumour. [After] chemotherapy or radiotherapy is used to treat cancer, there is damage to the tissue. This causes a surge in white blood cells, which swamp the area to help repair the damage. "We're surfing that wave to get as many white blood cells to deliver tumour-busting viruses into the heart of a tumour."

[Researchers] blood samples and extract macrophages, a part of the immune system which normally attacks foreign invaders. These are mixed with a virus which, just like HIV, avoids being attacked and instead becomes a passenger in the white blood cell. In the study, the mice were injected with the white blood cells two days after a course of chemotherapy ended. At this stage each white blood cell contained just a couple of viruses. However, once the macrophages enter the tumour the virus can replicate. After about 12 hours the white blood cells burst and eject up to 10,000 viruses each - which go on to infect, and kill, the cancerous cells.

At the end of the 40-day study, all the mice who were given the Trojan treatment were still alive and had no signs of tumours. By comparison, mice given other treatments died and their cancer had spread.

Link: http://www.bbc.co.uk/news/health-20795977

Source:
http://www.fightaging.org/archives/2012/12/using-immune-cells-to-deliver-cancer-killing-viruses.php

I noticed a good, comprehensible open access paper today: a review that summarizes what is known of the biology of the most common type of long-lived genetically engineered mouse species, those with disrupted or suppressed growth hormone (GH) activity. These include Ames dwarf mice, Snell dwarf mice, and growth hormone receptor knockout (GHRKO) mice. The present record for mouse longevity is held by the results of a GHRKO study, some of the mice involved living more than 60% longer than peers.

If you'd like to better understand how this all fits together under the hood and how it relates to other areas of study where metabolism, genetic engineering, and aging overlap - such as calorie restriction - then take a look:

Metabolic characteristics of long-lived mice

The remarkable extension of longevity in mice lacking GH or GH receptors appears to be due to multiple interacting mechanisms including reduced activation of growth-promoting pathways, greater stress resistance, reduced inflammation, increased reservoir of pluripotent stem cells, and improved genome maintenance.

Data summarized in this article indicate that alterations in energy metabolism and improved insulin control of carbohydrate homeostasis have to be added to this list. In fact, these metabolic adaptations may represent key features of the "longevous" phenotype of these animals and important mechanisms of the extension of both healthspan and lifespan in GH-related mutants.

Importantly, many of the metabolic features of long-lived mutant mice described in this article have been associated with extended human longevity. Comparisons between centenarians and elderly individuals from the same population and between the offspring of exceptionally long-lived people and their partners indicate that reduced insulin, improved insulin sensitivity, increased adiponectin, and reduced pro-inflammatory markers consistently correlate with improved life expectancy.

Source:
http://www.fightaging.org/archives/2012/12/an-introduction-to-whats-going-on-inside-long-lived-mice.php

I noticed a good, comprehensible open access paper today: a review that summarizes what is known of the biology of the most common type of long-lived genetically engineered mouse species, those with disrupted or suppressed growth hormone (GH) activity. These include Ames dwarf mice, Snell dwarf mice, and growth hormone receptor knockout (GHRKO) mice. The present record for mouse longevity is held by the results of a GHRKO study, some of the mice involved living more than 60% longer than peers.

If you'd like to better understand how this all fits together under the hood and how it relates to other areas of study where metabolism, genetic engineering, and aging overlap - such as calorie restriction - then take a look:

Metabolic characteristics of long-lived mice

The remarkable extension of longevity in mice lacking GH or GH receptors appears to be due to multiple interacting mechanisms including reduced activation of growth-promoting pathways, greater stress resistance, reduced inflammation, increased reservoir of pluripotent stem cells, and improved genome maintenance.

Data summarized in this article indicate that alterations in energy metabolism and improved insulin control of carbohydrate homeostasis have to be added to this list. In fact, these metabolic adaptations may represent key features of the "longevous" phenotype of these animals and important mechanisms of the extension of both healthspan and lifespan in GH-related mutants.

Importantly, many of the metabolic features of long-lived mutant mice described in this article have been associated with extended human longevity. Comparisons between centenarians and elderly individuals from the same population and between the offspring of exceptionally long-lived people and their partners indicate that reduced insulin, improved insulin sensitivity, increased adiponectin, and reduced pro-inflammatory markers consistently correlate with improved life expectancy.

Source:
http://www.fightaging.org/archives/2012/12/an-introduction-to-whats-going-on-inside-long-lived-mice.php

Many of the early forms of stem cell therapy involve cell transplants, and seem to produce benefits without those transplanted cells creating replacements for lost native cells. Instead the newcomers are improving the local environment and issuing signals that allow greater survival and repair among the native cell populations. Here is an example of the type:

Promising new research provides evidence that amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, may be treatable using neural stem cells. A consortium of researchers at multiple institutions [have] shown that neural stem cells, when transplanted into the spinal cord of a mouse model with familial ALS, slow disease onset and progression while improving motor function, breathing and survival time compared to untreated mice.

Neural stem cells are the precursors of all brain cells. They can self-renew, making more neural stem cells, and differentiate, becoming nerve cells or other brain cells. These cells can also rescue malfunctioning nerve cells and help preserve and regenerate brain tissue. But they've never before been studied extensively in a good model of adult ALS.

In 11 independent studies [researchers] transplanted neural stem cells into the spinal cord of a mouse model of ALS. The transplanted neural stem cells benefited the mice with ALS by preserving the health and function of the remaining nerve cells. Specifically, the neural stem cells promoted the production of protective molecules that spared remaining nerve cells from destruction. They also reduced inflammation and suppressed the number of toxin-producing and disease-causing cells in the host's spinal cord.

Link: http://www.eurekalert.org/pub_releases/2012-12/uomm-tns121912.php

Source:
http://www.fightaging.org/archives/2012/12/treating-als-with-neural-stem-cell-transplants.php