A paper on the life span of neurons in relation to their host organism was published earlier in the year and has been doing the rounds in recent days:

Neurons in mammals do not undergo replicative aging, and, in absence of pathologic conditions, their lifespan is limited only by the maximum lifespan of the organism. Whether neuronal lifespan is determined by the strain-specific lifetime or can be extended beyond this limit is unknown. Here, we transplanted embryonic mouse cerebellar precursors into the developing brain of the longer-living Wistar rats. The donor cells integrated into the rat cerebellum developing into mature neurons while retaining mouse-specific morphometric traits.

In their new environment, the grafted mouse neurons did not die at or before the maximum lifespan of their strain of origin but survived as long as 36 mo, doubling the average lifespan of the donor mice. Thus, the lifespan of neurons is not limited by the maximum lifespan of the donor organism, but continues when transplanted in a longer-living host.

This is indeed the barnstorming age of biotechnology. As you might already know, we humans possess many nervous system cells that we were born with and which will last our entire lifetime. This is in contrast to much of the rest of our body where cells are replaced over various timescales, from years for some tissues to days for others. It is even that case that some individual macromolecules within brain cells last unchanged throughout life - not just the cell remaining on station for a lifetime, but some of its fundamental building blocks as well.

The fact that many neurons are never replaced is the source of a range of frailties and age-related conditions that result from increasing damage or buildup of unwanted metabolic byproducts in these long-lived cells. Nonetheless, it seems very reasonable to expect that our neurons are capable of outlasting the present limits of human life span, given the fact that it isn't neurodegeneration that kills supercentenarians - their brain cells are, by and large, still marching along even in the final years. No, death by aging is a systems failure, not a timed simultaneous failure of all the components that make up that system.

Is work on rodent neurons quoted above particularly relevant, or does it change anything? I is interesting, but I think that the answer is "no." We already know that developing the means to repair existing neurons in the brain is necessary. Boosting the rate at which new neurons are created will almost certainly be helpful, but a good portion of the brain stores the data that is the mind - those neurons and their encoded data have to be preserved and maintained, not replaced wholesale. So here it seems to me that knowing that neurons have a longer shelf-life doesn't change anything in the game plan.

Further, there's no guarantee that the longer neuron shelf-life in rodents has any great relevance to human cells. The analogous human study might be to pull long-lived neurons from a supercentenarian and culture them in a 3-D engineered environment that replicates their home tissue as closely as possible. Then you wait - for a fair number of decades. By the time that experiment comes to any interesting result, the whole issue will be moot. Either we will be dead, or SENS-like rejuvenation biotechnologies will be developed, and in either case researchers will already know so much more about cellular biology that they will be long past the point of answering all the questions that the study might help to resolve.

Source:
http://www.fightaging.org/archives/2013/03/neurons-can-outlast-their-host-in-at-least-one-species-but-is-that-at-all-relevant.php

Calorie restriction produces a general slowing of the progression of degenerative aging and creates sweeping changes at all levels of metabolism. Thus it should not be a surprise to find protective effects no matter how deep you dive into the biochemistry of calorie restricted laboratory animals. Here's one of the many more detailed examples, looking at the abundances of receptors known to be important in brain function:

The effects of aging and long-term caloric restriction, on the regulation of neuropeptide Y (NPY) Y(1), Y(2) and Y(5) receptors subtypes, was studied in 20-month-old male rats fed ad libitum (AL) or submitted to a 40% caloric restriction for 12 months.

In the brain of 3-month-old AL rats, the distribution and densities of Y(1), Y(2) and Y(5) receptors were in agreement with previous reports. In the brain of 20-month-old AL rats, a decrease of NPY receptor subtype densities in regions having important physiological functions such as the cingulate cortex, hippocampus and dentate gyrus, thalamus and hypothalamus was observed.

In contrast, caloric restriction had multiple effects. It induced specific decreases of Y(1)-receptor densities in the dentate gyrus, thalamic and hypothalamic nuclei and lateral hypothalamic area and Y(2)-receptor densities in the suprachiasmatic nucleus of hypothalamus. Moreover, it prevented the age-induced increase in Y(1)-receptor densities in the ventromedial hypothalamic nucleus and decrease in the mediodorsal thalamic nucleus, and increased Y(2)-receptor densities in the CA2 subfield of the hippocampus.

These results indicate that caloric restriction not only counteracts some of the deleterious effects of aging on NPY receptor subtype densities but exerts specific effects of its own. The overall impact of the regulation of NPY receptor subtypes in the brain of old calorie-restricted rats may protect the neural circuits involved in pain, emotions, feeding and memory functions.

Link: http://www.ncbi.nlm.nih.gov/pubmed/23410741

Source:
http://www.fightaging.org/archives/2013/03/calorie-restriction-protective-of-specific-brain-mechanisms.php

Studies suggest that longer life expectancy runs in families to some degree - though it is always the case that what you get in the genetic lottery can be squandered by poor lifestyle choices. Gene variants appear to be more important in determining remaining life expectancy at older ages than at younger ages, which is another way of saying much the same thing. Either way, the end result will be the same until we can build rejuvenation biotechnology.

According to the findings of some recent studies, the centenarians' offspring appear to represent a promising model for research on longevity and healthy aging. This study compares the health status and the functional status of three groups of subjects: 1. individuals with two long-lived parents (one of whom centenarian), 2. individuals with only one long-lived (centenarian) parent, and 3. individuals with no long-lived parents. The goal is to verify whether the centenarians' offspring display any advantage over the offspring of both non-long-lived parents and to evaluate whether the longevity of the non-centenarian parent provides a further advantage.

A total of 374 subjects (mean age approximately 70 years) was examined. A threshold for longevity was established for non-centenarian parents through demographic data available for Italy (males surviving to at least 81 years of age and females to 87 years). The participants were assessed for their health and functional status by means of a standardized questionnaire and tests of physical performance. Data were analyzed using multivariate regression models adjusted for socio-demographic characteristics and risk factors for age-related pathologies.

The results of the study show that centenarians' offspring have a better functional status, a reduced risk for several age-related pathologies and reduced drug consumption than the offspring of non-long-lived parents. In addition, the health status of centenarians' offspring does not appear to be influenced by the longevity of the second parent. It therefore seems possible to conclude that at ages around 70 years the genetic contribution to health status deriving from having one centenarian parent is not substantially improved if the other parent is also long-lived.

Link: http://www.ncbi.nlm.nih.gov/pubmed/23403041

Source:
http://www.fightaging.org/archives/2013/03/another-study-on-inheritance-of-human-longevity.php

Since it is possible to take a patient's cells and generate a very large number of immune cells, far more than the patient would ever have normally, and since it's possible to make some alterations to immune cells to make them more effective, why not do this? It's probably the case that even generally healthy older people would benefit from a regular infusion of large numbers of their own immune cells, or even donor cells, given the way in which the immune system declines with age, but under present medical regulation you'll only ever see it deployed as a treatment for late stage disease:

[Researchers] have successfully infused large numbers of donor T-cells specific for a key anti-leukemic antigen to prolong survival in high-risk and relapsed leukemia patients after stem cell transplantation. [T-cells were] taken from a donor, programmed in the lab to recognize the Wilm's Tumor Antigen 1 (WT1) and kill leukemia cells, grown in large numbers, and then infused into patients to promote anti-leukemic activity. The WT1 protein is overexpressed in leukemias and is in part responsible for why the cells have become leukemic.

All of the patients [received] adoptively transferred infusions of billions of enhanced CD8 cytotoxic T-cell clones. They were considered at high risk of death because they had already relapsed and/or had a poor prognosis due to unfavorable characteristics of their leukemia.

Four of the 11 patients in the trial received infusions of T-cells that targeted WT1 and were generated in the presence of IL-21. One had detectable relapsed disease and entered complete remission shortly after the T-cells were infused. All four survived after T-cell therapy without relapse for more than 30 months without suffering graft-vs.-host-disease and required no additional anti-leukemic treatment, according to the study.

Among the seven patients who received infused T-cells generated without the presence of IL-21, two showed direct evidence of anti-leukemic activity, including one patient with advanced progressive disease who had a temporary response.

Link: http://www.sciencedaily.com/releases/2013/02/130227151248.htm

Source:
http://www.fightaging.org/archives/2013/02/infusing-large-numbers-of-immune-cells-as-a-therapy.php