Category Archives: Longevity Medicine

Low-level chronic inflammation is produced by the aging immune system and causes many further problems: "Osteoarthritis (OA) is the most common cause of chronic disability in older adults. Although classically considered a 'wear and tear' degenerative condition of articular joints, recent studies have demonstrated an inflammatory component to OA that includes increased activity of several cytokines and chemokines in joint tissues that drive production of matrix-degrading enzymes. Rather than directly causing OA, aging changes in the musculoskeletal system contribute to the development of OA by making the joint more susceptible to the effects of other OA risk factors that include abnormal biomechanics, joint injury, genetics, and obesity. Age-related sarcopenia and increased bone turnover may also contribute to the development of OA. Understanding the basic mechanisms by which aging affects joint tissues should provide new targets for slowing or preventing the development of OA."

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20699160

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The differences in a nutshell: "Calorie restriction (CR) is the only paradigm that has consistently increased lifespan in a wide variety of model organisms. Many hypotheses have been proposed as the underlying mechanism, including a reduction in body size and adiposity, which is commonly observed in calorie-restricted animals. This has led to investigations as to whether similar changes in body composition produced by increasing energy expenditure via exercise can replace or enhance the benefits of reducing energy intake. ... In rodents, the data clearly show that exercise, regardless of body weight changes, can improve health and survival, but unlike CR, fails to extend lifespan. In humans, short-term weight loss studies show that exercise and CR produce similar improvements in disease risk factors and biomarkers of aging, while some parameters clearly benefit more with exercise. Epidemiologic evidence in humans supports exercise as a strategy to reduce the risk of morbidity and mortality, but not to extend lifespan. It is unknown whether CR can extend human lifespan, but the metabolic profile of humans engaged in long-term CR shares many similarities with calorie restricted rodents and nonhuman primates. In conclusion, like CR, exercise can limit weight gain and adiposity, but only CR can extend lifespan. Therefore, in rodents, the ability of CR to slow aging is apparently more dependent on decreasing nutrient flux, rather than changes in energy balance and body composition."

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20703061

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While the FDA tries to block commercial application of stem cell therapies in the US, veterinary practices continue to demonstrate that the technology is ready and potentially useful: “A Golden Retriever, plagued with arthritis, recently underwent a stem cell extraction and implant to help with mobility. … From the sounds of things, you would never suspect McIntyre was a frail and feeble dog. And these days, he’s moving around pretty well, thanks to anti-inflammatory medicines, physical therapy and a new experimental surgery involving stem cells. … like family, she wanted McIntrye to feel better and have a better quality of life. Cells were taken from his belly fat and shipped to California. Stem cells were extracted and then implanted back into his joints by a vet in Alpharetta. … He’ll never be like a puppy as far as agility but it will just give him a quality of life where he doesn’t hurt and suffer.” Meanwhile, the actions of unaccountable, unelected bureaucrats at the FDA mean that US residents must travel overseas to find the same treatment offered to humans. More importantly, what might already be a wildly successful and growing field is slowed down to a comparative crawl. When you’re forbidden to sell a product, few organization will invest in development.

View the Article Under Discussion: http://www.walb.com/Global/story.asp?S=12964756

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Via EurekAlert! a reminder that we can think of most age-related conditions as resulting from one or more forms of damage that everyone suffers to some degree – but has progressed further in those who have the condition: “In many neurodegenerative diseases, such as Alzheimer’s and Huntington’s, clumps of proteins known as aggregates appear in the patients’ brains as the degeneration progresses. Those clumps contain some proteins that are unique to the specific disease (such as Abeta in Alzheimer’s), intertwined with many others that are common in healthy individuals. For years, those common proteins were thought to be accidental inclusions in the aggregates … In fact, they may not be innocent bystanders at all, but instead their presence may influence the course of neurodegenerative disease. … in the presence of proteins specific to Huntington’s disease, these aggregators actually sped up the course of the disease, indicating that they could be fundamental to its progression. These findings indicate that widespread protein insolubility and aggregation is an inherent part of aging and that it may influence both lifespan and neurodegenerative disease. The presence of insoluble protein aggregates has long been a hallmark of protein aggregation diseases such as Alzheimer’s, Huntington’s and amyotrophic lateral sclerosis (ALS) disease. The team [asked] a simple question that had never been asked before: do normal proteins form insoluble clumps when normal, healthy individuals age?” Those “normal, health individuals” are on their way to the same end destination of neurodegeneration, just not as fast.

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-08/plos-np080610.php

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From the Telegraph: “In as little as five years, researchers hope to be able to coax the heart into regenerating itself, repairing the damage caused by cardiac arrests and old age. … It works in a similar way to stem cells but instead of the new cells being grown outside the body and then injected back in, the technique simply makes the cells [transform] at the point where they are needed. … The main problem is that when beating muscles cells – known as cardiomyocytes – die during an attack there is no way to reactivate them and the surrounding connective tissue – known as fibroblasts – cannot take over their role.
Now [researchers] have discovered a way of reprogramming fibroblasts into cardiomyocytes. … We first have to test if the same factors can convert human fibroblasts to beating heart muscle and then find ways to safely introduce these factors, or small molecules that mimic these factors, into the coronary circulation so they can reprogram the existing fibroblasts in the heart. I envision such factors being loaded into a stent that is placed in the coronary artery and can elute (allow to emerge) the reprogramming factors over 1-2 weeks. … The team found that they needed a combination of just three substance – Gata4, Mef2c, and Tbx5 – to efficiently convert fibroblasts into cells that could beat like cardiomyocytes.”

View the Article Under Discussion: http://www.telegraph.co.uk/health/healthnews/7928426/Damaged-heart-could-be-coaxed-into-mending-itself-claim-scientists.html

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Via EurekAlert!: “Researchers for the first time have induced robust regeneration of nerve connections that control voluntary movement after spinal cord injury, showing the potential for new therapeutic approaches to paralysis and other motor function impairments. … They did this by deleting an enzyme called PTEN (a phosphatase and tensin homolog), which controls a molecular pathway called mTOR that is a key regulator of cell growth. PTEN activity is low early during development, allowing cell proliferation. PTEN then turns on when growth is completed, inhibiting mTOR and precluding any ability to regenerate. … Until now, such robust nerve regeneration has been impossible in the spinal cord. … An injury the size of a grape can lead to complete loss of function below the level of injury. For example, an injury to the neck can cause paralysis of arms and legs … These devastating consequences occur even though the spinal cord below the level of injury is intact. All these lost functions could be restored if we could find a way to regenerate the connections that were damaged. … are now studying whether the PTEN-deletion treatment leads to actual restoration of motor function in mice with spinal cord injury.”

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-08/uoc–ibn080510.php

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