Exercise Makes You Better & Smarter

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Funding Aging Research

Exercise Makes You Better & Smarter


posted on February 7th, 2012

Dear Future Centenarian,

I™ve been encouraging you to exercise since I started this newsletter over five years ago. Since then, we have been bombarded with new evidence supporting this position. We now know, beyond a shadow of a doubt, that exercise is good for your long term health. And researchers from the Department of Molecular and Biomedical Pharmacology at the University of Kentucky College of Medicine, can increasingly tell you exactly why this is the case:

http://www.fightaging.org/archives/2011/11/quantifying-the-beneficial-effects-of-exercise-on-the-brain.php

Armed with newer, cheaper, and better biotechnologies, researchers can measure ever more of the detailed effects of good health practices such as regular exercise, calorie restriction, and the like.

It is possible now to examine the workings of metabolism in any specific part of the body in very great detail, all the way down to the molecular machinery in our cells, see how it changes with age, and see how those changes differ with different lifestyle choices.

Healthy brain aging and cognitive function are promoted by exercise. The benefits of exercise are attributed to several mechanisms, many which highlight its neuroprotective role via actions that enhance the formation of nerve tissue, neuronal form and structure and/or the family of proteins that induce the survival, development, and function of neurons.

However, the brain is also composed of glial and vascular elements, and comparatively less is known regarding the effects of exercise on these components in the aging brain. Nearly 90 percent of the brain is composed of glial cells, not neurons. Glial cells are nerve cells that don't carry nerve impulses. The various glial (meaning "glue") cells perform many important functions, including: digestion of parts of dead neurons, manufacturing myelin (protective sheaths) for neurons, providing physical and nutritional support for neurons, controlling blood flow to regions of brain activity and sending information to neurons.

Here, we show that aerobic exercise at mid-age [also] counters several well-established glial markers of brain aging. Similarly, we show that age-related changes in neurovascular structure and function were reduced with exercise.

So results show that exercise can potentially reduce progressive age-related changes in several key non-neuronal elements of the brain. Further, it shows that these brain processes are still highly responsive to exercise in the midlife age range, consistent with studies showing that cognitive function can benefit from exercise even if initiated at later ages.

It™s not to late to make your œNew Year™s Resolution to move more buckaroo.

Long Life,
David Kekich
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LATEST HEADLINES FROM FIGHT AGING!

RAPID REPAIR OF SEVERED NERVES DEMONSTRATED IN RATS Friday, February  3, 2012 http://www.fightaging.org/archives/2012/02/rapid-repair-of-severed-nerves-demonstrated-in-rats.php
An advance in the methodologies of nerve repair: "scientists believe a new procedure to repair severed nerves could result in patients recovering in days or weeks, rather than months or years. The team used a cellular mechanism similar to that used by many invertebrates to repair damage to nerve axons. We have developed a procedure which can repair severed nerves within minutes so that the behavior they control can be partially restored within days and often largely restored within two to four weeks. If further developed in clinical trials this approach would be a great advance on current procedures that usually imperfectly restore lost function within months at best.
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Nerve axons of invertebrates which have been severed from their cell body do not degenerate within days, as happens with mammals, but can survive for months, or even years. The severed proximal nerve axon in invertebrates can also reconnect with its surviving distal nerve axon to produce much quicker and much better restoration of behaviour than occurs in mammals. Severed invertebrate nerve axons can reconnect proximal and distal ends of severed nerve axons within seven days, allowing a rate of behavioural recovery that is far superior to mammals. In mammals the severed distal axonal stump degenerates within three days and it can take nerve growths from proximal axonal stumps months or years to regenerate and restore use of muscles or sensory areas, often with less accuracy and with much less function being restored. The team described their success in applying this process to rats. The team were able to repair severed sciatic nerves in the upper thigh, with results showing the rats were able to use their limb within a week and had much function restored within 2 to 4 weeks."

A STUDY OF DNA ALTERATIONS IN THE OLD Friday, February  3, 2012 http://www.fightaging.org/archives/2012/02/a-study-of-dna-alterations-in-the-old.php
To what degree does nuclear DNA damage contribute to aging? That remains a debated question. Here, researchers show that, at least in immune cells, there are perhaps more forms of large DNA damage than thought in the old: "researchers compared the DNA of identical (monozygotic) twins of different age. They could show that structural modifications of the DNA, where large or small DNA segments change direction, are duplicated or completely lost are more common in older people. The results may in part explain why the immune system is impaired with age. During a person's life, continuous alterations in the cells' DNA occur. The alterations can be changes to the individual building blocks of the DNA but more common are rearrangements where large DNA segments change place or direction, or are duplicated or completely lost. The results showed that large rearrangements were only present in the group older than 60 years. The most common rearrangement was that a DNA region, for instance a part of a chromosome, had been lost in some of the blood cells.

Rearrangements were also found in the younger age group. The changes were smaller and less complex but the researchers could also in this case show that the number of rearrangements correlated with age. We were surprised to find that as many as 3.5 percent of healthy individuals older than 60 years carry such large genetic alterations. We believe that what we see today is only the tip of the iceberg and that this type of acquired genetic variation might be much more common. The researchers believe that the increased number of cells with DNA alterations among elderly can have a role in the senescence of the immune system. If the genetic alterations lead to an increased growth of the cells that have acquired them, these cells will increase in number in relation to other white blood cells. The consequence might be a reduced diversity among the white blood cells and thereby an impaired immune system." Compare that with the other explanations for reduced diversity that involve persistent and pervasive viruses like CMV.

AGE CHANGES THE EXTRACELLULAR MATRIX Wednesday, February  1, 2012 http://www.fightaging.org/archives/2012/02/age-changes-the-extracellular-matrix.php
The extracellular matrix (ECM) surrounds and supports cells, both structurally and in a range of other ways, such as by mediating cell signalling. With age, however, the ECM changes for a variety of reasons - it is damaged by the actions of senescent cells, for example. This has consequences, such as on the capacity of stem cells to maintain tissue. Here is a review paper: "Aging is characterized by reduced tissue and organ function, regenerative capacity, and accompanied by a decrease in tissue resident stem cell numbers and a loss of potency. The impact of aging on stem cell populations differs between tissues and depends on a number of non cell-intrinsic factors, including systemic changes associated with immune system alterations, as well as senescence related changes of the local cytoarchitecture.

The latter has been studied in the context of environmental niche properties required for stem cell maintenance. Here, we will discuss the impact of the extracellular matrix (ECM) on stem cell maintenance, its changes during aging and its significance for stem cell therapy. It is concluded that a remodeled ECM due to age related inflammation, fibrosis or oxidative stress provides an inadequate environment for endogenous regeneration or stem cell therapies." The question of whether an old body can fully benefit from stem cell therapies continues to arise - eventually the stem cell research community will have to start addressing the damage of aging in order to assure the performance of their therapies when treating the old.

CONTRIBUTION OF TRADITIONAL DRUG DEVELOPMENT TO LONGEVITY Tuesday, January 31, 2012 http://www.fightaging.org/archives/2012/01/contribution-of-traditional-drug-development-to-longevity.php
To what degree does the slow, expensive, and over-regulated institution of drug development - Big Pharma - contribute to the gentle upward trend in human life expectancy that has held over the past few decades? "This paper investigates the contribution of pharmaceutical innovation to recent longevity growth in Germany and France. The effect of the vintage of prescription drugs (and other variables) on the life expectancy and age-adjusted mortality rates of residents of Germany is examined, using longitudinal, annual, state-level data during the period 2001-7.

The estimates imply that about one-third of the 1.4-year increase in German life expectancy during the period 2001-7 was due to the replacement of older drugs by newer drugs. The effect of the vintage of chemotherapy treatments on age-adjusted cancer mortality rates of residents of France is also investigated, using longitudinal, annual, cancer-site-level data during the period 2002-6. The estimates imply that chemotherapy innovation accounted for at least one-sixth of the decline in French cancer mortality rates, and may have accounted for as much as half of the decline."

INCREASED DISC DEGENERATION IS ANOTHER CONSEQUENCE OF TOO MUCH FAT Tuesday, January 31, 2012 http://www.fightaging.org/archives/2012/01/increased-disc-degeneration-is-another-consequence-of-too-much-fat.php
Here is another good reason not to get fat and not to stay fat: "One of the largest studies to investigate lumbar spine disc degeneration found that adults who are overweight or obese were significantly more likely to have disc degeneration than those with a normal body mass index (BMI). Assessments using magnetic resonance imaging (MRI) show elevated BMI is associated with an increased number of levels of degenerated disks and greater severity of disc degeneration, including narrowing of the disc space. Previous research has linked higher BMI to low back pain, which is often debilitating and can limit function, impact psychological well being, diminish overall quality of life, and is associated with substantial socioeconomic and health-care costs.

The team recruited 2,599 participants aged 21 and older from Southern China between 2001 and 2009. Participants were from diverse social and economic backgrounds and were recruited regardless of whether they had lower back pain or not. The study group included 1,040 men and 1,559 women who had a mean age of 42 years. Researchers conducted radiographic and clinical assessments, and MRIs of the lumbar spine were obtained for all subjects. Study findings reveal that 73% of participants displayed disc degeneration, with men (76%) having a significantly higher prevalence of degeneration than women (71%). Not surprisingly, increasing age was found to increase the prevalence of disc degeneration. The authors suggest that with weight gain, physical loading on the disc and/or a chronic low-grade inflammation from the fat cells may play a role in disc degeneration."

ANOTHER MOUSE LONGEVITY MUTATION Monday, January 30, 2012 http://www.fightaging.org/archives/2012/01/another-mouse-longevity-mutation.php
An open access paper: "The amount of fat mass of an organism is emerging as key determinant in longevity. Too little or too much fat is associated with early mortality in rodents and humans, whereas leanness, intermediate with respect to these two extremes is associated with relative longevity, possibly reflecting an optimal amount of fat. Calorie restriction results in leanness, which is linked to metabolic conditions that favor longevity.

We show here that deficiency of the triglyceride synthesis enzyme acyl CoA:diacylglycerol acyltransferase 1 (DGAT1), which promotes leanness, also extends longevity without limiting food intake. Female DGAT1-deficient mice were protected from age-related increases in body fat, tissue triglycerides, and inflammation in white adipose tissue. This protection was accompanied by increased mean and maximal life spans of ~25% and ~10%, respectively. Middle-aged Dgat1-/- mice exhibited several features associated with longevity, including decreased levels of circulating insulin growth factor 1 (IGF1) and reduced fecundity. Thus, deletion of DGAT1 in mice provides a model of leanness and extended lifespan that is independent of calorie restriction."

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