Monthly Archives: October 2010

Lengthened Telomeres Restore Immune System to a Younger State

A new study published in the Rejuvenation Research Journal shows that TA-65, a natural Telomerase Activator made and marketed by Telomerase Activation Sciences, Inc. (“T.A. Sciences“), reduces the percentage of short telomeres in immune cells and restores and remodels the aging human immune system to be more like that of a younger individual.

The year-long study of the first 100 clients of T.A. Sciences found that TA-65, a nutritional supplement marketed only through specialized doctors, had been successful in lengthening shortened telomeres.  Telomeres are sequences of DNA, located at the ends of all chromosomes, which serve as cellular clocks of aging. Every time a cell divides, telomeres shorten until they become critically short, and the cell either stops functioning properly or dies. By activating a gene that is normally turned off, TA-65 has been shown to activate the enzyme telomerase. Telomerase has the unique ability to restore telomere length and is so important that its discovery won the Nobel Prize for Medicine in 2009.

In addition to TA-65’s telomerase activating properties, the study observed a statistically significant decline in senescent cytotoxic (CD8+/CD28-) T cells. This resulted in the human subjects’ immune systems being restored to a more youthful state. A rejuvenated immune system holds great potential to help subjects whose immune systems have been weakened by a lifetime of various stresses and age related decline.

“Telomere science is relatively new and scientists are now beginning to understand the pervasive role telomeres play in the aging process and how much harm short telomeres cause,” said Noel Thomas Patton, Founder of T.A. Sciences. “Many studies have established that short telomeres are associated with the decline of the immune system and other major organ systems. Such effects of age-related decline are severe and the benefits of telomere rejuvenation can be profound. Rejuvenating shortened telomeres will change the nature of what healthy aging means.”

In addition to taking TA-65, which is a natural product derived from the Chinese herb Astragalus, subjects were given a comprehensive dietary supplement pack, and physician counseling. The study was led by Calvin Harley, Ph.D, and co-authored by Dr. Weimin Liu, Dr. Maria Blasco, Dr. Elsa Vera, Dr. William Andrews, Dr. Laura Briggs, and Dr. Joseph Raffaele.  Several hundred clients of T.A. Sciences have now received TA-65 without any reports of serious adverse events.

Read the full version of the study in the September 8th issue of Rejuvenation Research

Maria Konovalenko


Filed under Article, Life, Life Extension, Mechanisms of aging, Science

British Study Links Steroid Hormone to Higher Life Expectancy

A group of British researchers have linked an innate hormone found in the human body called ‘DHEAS’ (Dehydroepiandrosterone) with higher life expectancy.

DHEAS is a steroid hormone made by our adrenal glands. This hormone plays a role in improving memory and strengthening the immune system. It also aids in weight loss, helps maintain cardiovascular health and increases HDL levels, thus preventing obesity. The rate of production of the hormone is greatest in childhood and teenage years, before gradually declining through adult life.

Sir Michael Marmot and his colleagues from the University College London looked at hormone levels in the blood samples of more than 10,000 men aged over 50 years. The study subjects were being observed since year 2004. The research suggested that DHEAS levels were augmented in those who led an active life or those who have a better lifestyle, which typically comes with being wealthy.

“The findings could pave the way for new class of drugs, patches or injections which will help boost the DHEAS level. But, it’s too early to say higher level of DHEAS is a result of being rich,” said lead author, Sir Marmot.

“But, factors such as a better diet, greater control over life, less stress, more travel and involvement in the wider world through hobbies, sport or other interests, which all are benefits of wealth — seem to be encouraging the body to create DHEAS,” he said.

He said that popping up a pill to improve DHEAS levels was not a solution as “it is a much bigger issue and involves the package of choices that wealth opens up.”

The study also found that wealthier people had higher levels of another hormone – IGF-I (insulin-like growth factor I). DHEAS along with IGF-I helps regulate the body and control reactions to stress.

The English Longitudinal Study of Aging, or ELSA, is a comprehensive study into the economic, social, psychological and health elements of the aging process in Europe and it depicts a detailed picture of the lives of people in England aged 50 and over.

Read more about DHEAS and increasing life expectancy

Maria Konovalenko

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Caloric Restriction: The defense against aging

Caloric Restriction: The defense against aging

Worried about getting old? It’s simple. Eat less and you could live longer. This is the view held by an increasing number of medical professionals, scientists and nutritionists around the world including experts at the Calorie Restriction Society. These beliefs are based on extensive research which suggests that caloric restriction (CR) can actually slow aging and reduce the incidence of disease, ultimately prolonging life!

CR has been investigated by gerontologists for more than 60 years and provides the only intervention tested to date in mammals (typically mice and rats) that repeatedly and strongly increases maximum life span while retarding the appearance of age-associated pathologic and biologic changes. Although the large majority of rodent studies have initiated CR early in life (1-3 mo of age), CR started in mid-adulthood (at 12 mo) also extended maximum life span in mice. There is evidence to suggest that age-associated increases in oxidative damage may represent a primary aging process that is weakened by CR. With regards to testing on primates, recent studies in monkeys subjected to CR support the notion of human translatability.

CR should not be confused with regular weight loss diets. In fact, weight loss is regarded as a side effect, not a goal. The main objective is to achieve a longer and healthier life by eating fewer calories, while maintaining a regular balance of vitamins, minerals and other essential nutrients. Following this diet brings about a reduction in the white adipose tissue mass and this has been proposed as a principal factor in longevity.

The pathways influenced by caloric restriction

The proteins altered by CR seem to be associated with several different cycles, including the glucose and lipid metabolic pathways which were consistent with increased lipid biosynthesis. The expression of proteins involved in the production of Oxalacetate and NADPH and in lipolysis and lipid biosynthesis was enhanced. In addition, certain insulin receptors were also increased by CR which was consistent with a higher response to lipogenic stimuli.

Other protein expression changes induced by CR gave improved protection against oxidative stress by halting the age-associated reduction in the levels of several antioxidant enzymes and decreasing the levels of stress-induced proteins.

Both CR and aging also changed the expression of proteins involved in the cytoskeleton, iron storage and energy metabolism as well as other proteins with currently unknown functions in adipose tissue.

The CR-induced changes are in line with reported microarray studies and will help to understand the molecular mechanisms behind the lifetime extension and the suppression of the effects of aging.

In the long term, the results could also lead to the identification of novel biomarkers of aging and possible targets for mimetics of CR that could provide the same outcome: an extended lifespan, without having to follow a rigorous and controlled diet.

Read more about calorie restriction and the molecular pathways that slow aging, improve health

Maria Konovalenko


Filed under Article, Life Extension, Science

New Study on the Somatic Mutations that Accumulate with Age

I would like to bring your attention to Dr. Jan Vijg who is leading several important research studies involving the role of non-cancerous mutations in aging.

Previous scientific reports of premature aging in mutant mice with greatly increased rates of mitochondrial DNA (mtDNA) appeared to confirm that accumulation of mtDNA mutations is a key mechanism of normal aging. Now, in a dramatic turnaround, a new study by Vijg and his team report that levels of mutations in tissues of aged normal mice are much lower than in the mutator mice, ruling out the causal role in normal aging!

Jan Vijg, Chair at the Department of Genetics at Albert Einstein College of Medicine and formerly the Director of the Buck Institute for Aging Research, has been focusing on genome instability and the mechanisms through which this may cause human disease and aging. Genome instability is generally considered as a cause of cancer and could play a general role in the overall etiology of human aging and disease.

The possible connection between damage to the genome and aging was supported in the discovery that heritable defects in genome maintenance are often associated with premature aging, as for example in Werner Syndrome and Hutchinson Gilford Progeria Syndrome. The DNA repair defects present in these conditions and other defects have been engineered in mice and shown to cause premature aging in these animals.

Members of the Vijg lab generated transgenic mouse and fruit fly strains harboring plasmids containing the bacterial lacZ gene. These plasmids were recovered from genomic DNA and subsequently transferred into E. coli to positively select for colonies representing a mutant lacZ-plasmid. In this way it was demonstrated that as predicted, the frequency of mutations increases with age in most tissues and cell types. Both the rate of mutation accumulation and the mutation spectra were shown to be tissue-specific. Vijg also demonstrated in a mouse model for increased oxidative stress that mutation accumulation correlates with cancer in a tissue-specific manner. Similar studies in the fruit fly lacZ-plasmid model are currently underway.

The key types of mutation that are a focus at the Vijg labs are genome rearrangements. This type of mutation is caused by errors made during the repair of DNA double strand breaks, which are highly toxic. They accumulate during aging and in some tissues comprise a major fraction of the mutation spectrum. Genome rearrangements are currently emerging as a major causal factor in the non-cancer, degenerative component of the aging process.

Based on previous observations that genetic defects in genome maintenance are associated with multiple symptoms of premature aging, Vijg is also studying the mechanistic basis of the possible causal role of Genotoxic Stress in aging. This is caused by exposure to toxic agents, including the sun’s ultraviolet rays, background ionizing radiation, chemicals in food and the environment, and highly reactive molecules produced within cells during metabolism.

In his research, characterization at the phenotypic level showed that only mutations in select genome maintenance pathways, e.g., nucleotide excision repair, double-strand break repair, lead to premature aging. Other pathways, most notably DNA mismatch repair, are associated with cancer but do not elevate the frequency of non-cancer, degenerative symptoms in aging. It was found that both cellular responses to DNA damage, cellular senescence and increased levels of genome rearrangements were critical in the etiology of the observed premature aging phenotypes.

The overall main focus of these studies is to extend the concept of genome maintenance to healthy human aging. This research is important as it should lead to new intervention strategies aimed at improving late-life health and reducing mortality rates.

Read more about Dr. Vijg and his research on the role of non-cancer mutations in aging.

Maria Konovalenko

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Reverse Aging of Human Muscle Tissue

In this article, we re-examine a study by scientists from the University of California, Berkeley that had identified critical biochemical pathways linked to the aging of human muscle. By manipulating these pathways, the researchers were able to turn back the clock on old human muscle, restoring its ability to repair itself!

The study shows that the ability of old human muscle to be maintained and repaired by muscle stem cells can be restored to youthful vigor given the right mix of biochemical signals. Professor Irina Conboy, a faculty member in the graduate bioengineering program that is run jointly by UC Berkeley and UC San Francisco, is the head of the research team that conducted the study.

Previous research that Conboy had done in animals, revealed that the ability of adult stem cells to repair and replace damaged tissue is governed by the molecular signals they get from surrounding muscle tissue, and that those signals change with age in ways that preclude productive tissue repair. Those studies also demonstrated that the regenerative function in old stem cells can be revived given the appropriate biochemical signals!

What was not clear until this study was whether similar rules applied for humans.  Unlike humans, laboratory animals are bred to have identical genes and are raised in similar environments.  Moreover,  the typical human lifespan lasts seven to eight decades,  while lab mice are reaching the end of their lives by age 2.

Working in collaboration with Dr. Michael Kjaer and his research group at the Institute of Sports Medicine and Centre of Healthy Aging at the University of Copenhagen in Denmark, the UC Berkeley researchers compared samples of muscle tissue from nearly 30 healthy men who participated in an exercise physiology study. The young subjects ranged from age 21 to 24 and averaged 22.6 years of age, while the old study participants averaged 71.3 years, with a span of 68 to 74 years of age.

The researchers discovered that in the legs that remained immobile, mature stem cells used for repairing muscle tissue and restoration were present in quantities of roughly half as much in older muscle tissue as they were in the youthful samples. The variance was even more wide spread when the exercise period was factored in. The youthful tissue had approximately four times the amount of redevelopment cells that would vigorously mend damaged tissue when evaluated against the aged muscle tissue that contained vigorous stem cell activity.

The researchers further examined the response of the human muscle to biochemical signals. They learned from previous studies that adult muscle stem cells have a receptor called Notch, which triggers growth when activated. Those stem cells also have a receptor for the protein TGF-beta that, when excessively activated, sets off a chain reaction that ultimately inhibits a cell’s ability to divide. The researchers said that aging in mice is associated in part with the progressive decline of Notch and increased levels of TGF-beta, ultimately blocking the stem cells’ capacity to effectively rebuild the body.
This study revealed that the same pathways are at play in human muscle, but also showed for the first time that mitogen-activated protein (MAP) kinase was an important positive regulator of Notch activity essential for human muscle repair, and that it was rendered inactive in old tissue.

MAP kinase [or MAPK] is commonly known to biologists in the developmental field due to it being an essential enzyme where organ growth is concerned in various species, some as atypical as nematodes, fruit flies and rodents. For aged muscle in humans, MAPK quantities are reduced so the Notch connection corridor remains un-stimulated and the stem cells don’t carry out the muscle restoration work as preprogrammed.

Conboy says: “Thanks to these discoveries, we now know that the MAPK pathway plays a key role in regulation and aging of human tissue regeneration. In practical terms, we know that to enhance regeneration of old human muscle and restore tissue health, we can either target the MAPK or the Notch pathways”

Read more about the Berkely study and the reverse aging of human muscle tissue.

Maria Konovalenko


Filed under Article, Science, Tissue rejuvenation

Life Extension through Nanotechnology

There are two ways in which nanotechnology may be able to extend our lives. One is by helping to eradicate life-threatening diseases such as cancer, and the other is by repairing damage to our bodies at the cellular level – in essence, a nano version of the fountain of youth!

Our average lifespan has been increased over the last 100 years by reducing the impact of life-threatening diseases. For example, vaccines have virtually eliminated smallpox. The application of nanotechnology in healthcare is likely to reduce the number of deaths from conditions such as cancer and heart disease over the next decade or so. There are many research programs working on these techniques;

Let’s look at the type of nano work that is currently being done in the way of eradicating cancer, one of the most serious of diseases on our planet:

An intriguing cancer treatment uses one nanoparticle to deliver a chemotherapy drug and a separate nanoparticle to guide the drug carrier to the cancer tumor. Nanorods circulating through the bloodstream exit where the blood vessels are leaking at the site of cancer tumors. Once the nanorods accumulate at the tumor they are used to concentrate the heat from infrared light, heating up the tumor. This heat increases the level of a stress related protein on the surface of the tumor. The drug carrying nanoparticle (a liposome) is attached to amino acids that bind to this protein, so the increased level of protein at the tumor speeds up the accumulation of the chemotherapy drug-carrying liposome at the tumor. Magnetic nanoparticles that attach to cancer cells in the blood stream may allow the cancer cells to be removed before they establish new tumors.

Read more about nanotechnology and its use in detecting and treating cancer

Another major killer in our time is heart disease. In this area, there are several efforts going on:

Researchers at the University of Santa Barbara have developed a nanoparticle that can deliver drugs to plaque on the wall of arteries. They attach a protein called a peptide to a nanoparticle which then binds with the surface of plaque. Studies have verified that the peptide attaches the nanoparticle to plaque. The researchers plan to use these nanoparticles to deliver imaging particles and drugs to both diagnosis and treat the condition.

Read more about this study of nanotechnology and heart disease

Perhaps the most exciting possibility exists in the potential for repairing our bodies at the cellular level. Techniques in Nanorobotics are being developed that should make the repair of our cells possible. For example, as we age, DNA in our cells is damaged by radiation or chemicals in our bodies. Nanorobots would be able to repair the damaged DNA and allow our cells to function correctly.

This ability to repair DNA and other defective components in our cells goes beyond keeping us healthy: it has the potential to restore our bodies to a more youthful condition. This concept is discussed by Eric Drexler, Ph.D., an established researcher and author whose work focuses on advanced nanotechnologies and directions for current research.

Drexler states: “Aging is fundamentally no different from any other physical disorder; it is no magical effect of calendar dates on a mysterious life-force. Brittle bones, wrinkled skin, low enzyme activities, slow wound healing, poor memory, and the rest all result from damaged molecular machinery, chemical imbalances, and mis-arranged structures. By restoring all the cells and tissues of the body to a youthful structure, repair machines will restore youthful health. ”

Read more about the advances of Nanotechnology from Eric Drexler’s book: Engines of Creation, The Coming Era of Nanotechnology

Maria Konovalenko



Filed under Life Extension

First Clinical Trial of Human Embryonic Stem Cell Therapy in the World Begins

Human embryonic stem cell therapy is being tried on a human for the first time in a new clinical trial. This is the first clinical trial of its kind in the world. The trial is designed to test the safety of the treatment, not how well it works. Nonetheless, this is a huge step for regenerative medicine, embryonic stem cell research and science in general!

Working in a handful of medical centers around the country, the biotech firm Geron is treating eight to 10 recent paraplegics. The patients will receive an injection of neurons to the site of the damage, followed by a short treatment of anti-rejection drugs. The first patient is reported as a patient in an Atlanta spinal cord and brain injury rehabilitation hospital. To take part in the study, the patient had to have suffered a spinal or brain injury that resulted in paralysis from the chest down. This patient was injected with cells derived from human embryonic stem cells obtained from a fertility clinic. Researchers are optimistic that this human embryonic stem cell therapy will not only help alleviate the symptoms of the injury, but permanently repair the damage that caused the paralysis from the spinal cord injury.

Embryonic stem cell-derived neural cells have been used by researchers to treat nervous system disorders in animal models. In the case of spinal cord injuries, neural cells derived from animal embryonic stem cells and injected into the spinal cord injury site produced significant recovery of the animal’s ability to move and bear weight.

To apply those observations to humans, Geron had derived oligodendrocyte progenitor cells (GRNOPC1) from Human Embryonic Stem Cells (HESCs). “Initiating the GRNOPC1 clinical trial is a milestone for the field of human embryonic stem cell-based therapies,” said Thomas B. Okarma , Geron’s president and CEO. “When we started our work back in 1999, many predicted that it would be a number of decades before a cell therapy would be approved for human clinical trials. This accomplishment results from extensive research and development and a succession of inventive steps to enable production of cGMP master cell banks, scalable manufacture of differentiated cell product, and preclinical studies in vitro and in animal models of spinal cord injury, leading to concurrence by the FDA to initiate the clinical trial.”

Stem cells have attracted huge scientific and public interest, not only because they bear the promise of miracle cures for age-related diseases, but also because their medical use is so appealing: stem-cell therapies like those that have recently begun could augment the human body’s own regenerative capacity, which declines as we grow older. The appropriate source of cells for these applications is hotly debated, but the technical feasibility of generating replacement tissues and organs is now within realistic projections.

Read more about the human embryonic stem cell therapy clinical trials

Maria Konovalenko


Filed under Regenerative medicine

Bioprinting: Laboratory Grown Body Parts Now a Reality

Your liver is failing critically. A transplant would save your life, but there’s a long waiting list and the odds are stacked against you. So instead, doctors extract some of your bone marrow, liver and muscle cells, go back to their laboratory and return in a few weeks with … a freshly grown liver! Does this sound like material from a Hollywood sci-fi movie? Well Not anymore. Australian researchers in Melbourne are now hard at work growing spare parts, proving their stuff in animal – and even human trials!

“It’s a remarkable field, with enormous potential,” says Wayne Morrison, director of the O’Brien Institute at St Vincent’s Hospital in Melbourne and professorial fellow in the department of surgery at the University of Melbourne.

“There is a sense of steady advance,” Morrison says, noting that a key reason for progress is the multidisciplinary nature of tissue generation and regeneration.

“Historically, there has not been much interaction between surgeons, cell biologists, as well as chemical engineers and designers. I’m pleased to say that is changing with both the practical people and the theory experts learning a great deal from each other.”

Morrison is a plastic and reconstructive surgeon. Part of his work involves transplanting blood vessels from a healthy part of a patient’s body to a diseased or injured part to aid recovery. He noticed the new blood vessel would start to promote tissue growth, although the process wasn’t easy to observe.

“We came up with the idea of enclosing the [growing tissue] in a plastic chamber that was surgically inserted into the patient’s body,” he says, explaining that the idea was to see what was happening.

“We were surprised that the chamber quickly filled up with healthy tissue around the vessel. The chamber was acting like a scaffold, a magnet for cells. So in trying to do one thing we found something that was even more important.”

Further experiments revealed that the location of a chamber determined the types of tissue that were generated. Morrison says it’s not clear how this happens but he suggests it may be linked to the proximity of other types of cells, which cue the formation of the new tissue.

When it comes to growing new tissues for transplants, the truly sci-fi advance is the bio-printer a device that “prints” three-dimensional tissue on to a template. A Melbourne company Invetech developed the technology for Organovo, a biotech firm based in San Diego, California.

“It was a matter of applying Invetech’s expertise in engineering and automation with Organovo’s background in regenerative medicine,” says Invetech’s managing director Fred Davis. “This collaboration was important not only on the robotics side, but also in areas like the software that controls the living cell printing process, where Organovo biologists worked with Invetech software engineers to provide easy-to-use shape programming.”

The bio-printer works by dispensing cells taken from the patient’s body, layer by layer, to create a 3-D tissue or organ. A gel is used to fill in gaps and provide physical support while the cells organize themselves into patterns and bind together. The gel is removed in the lab during a maturation process and the fully formed tissue or organ is then ready for the surgeon to transplant into the patient.

Invetech delivered the first bio-printer to Organovo late last year and Davis predicts production models will roll out soon.

It would seem as though science is really making head way into the future. While creating living tissue is important, the larger aim for science and medicine is creation of functioning human organs. Scientists have very high hopes that one day on the horizon not only organs can be grown in a lab but also nerves and tendons lost in such cases as spinal cord injuries and paralysis. Organ replacement will eventually enable humans to have indefinite lifespans through complete rejuvenation to a youthful condition.

Read more about tissue regeneration and organ growth research

Here’s a fascinating video on the 3D Bio-Printer

Maria Konovalenko


Filed under Regenerative medicine

Expert on Cellular and Organ Aging: “The Body’s Ability to Dispose of Cell Debris Could Extend Life.”

One of the main goals of my blog is to keep readers aware of important research and discoveries in the field of life extension, longevity and anti-aging. To that end, we have been following the work of Dr. Ana Maria Cuervo (, a molecular biology professor at the Albert Einstein College of Medicine and would like to provide some details into her important research and recent findings.
According to Cuervo, “the current challenges in the field of aging are two-fold: To continue and complete the molecular dissection of the factors that contribute to aging and to promote the translation of these novel findings into interventions to improve the health-span of the aging human population”.

Dr. Cuervo identified certain defects that lead to decreased activity of Chaperone-Mediated Autophagy (CMA) ( with age and how to correct and improve cellular function. Dr. Cuervo theorized that the decrease of Autophagy could be a determining factor in why some older organisms are unable to fight off cell abnormalities. Her research looked at the breakdown of the various autophagic pathways as the body ages and if restoring these pathways would jumpstart normal cellular activity. CMA is involved in at least 30% of the body’s cell degradation processes and upon studying this pathway, Cuervo determined that the LAMP-2A protein acts as a vital receptor in the pathway.

In recent experiments, livers in genetically modified mice 22 to 26 months old (the equivalent of octogenarians in human years), that were injected with the LAMP-2A protein, cleaned blood as efficiently as those in animals a quarter their age! By contrast, the livers of normal mice in a control group began to fail. While her paper didn’t show increased survival rates among the mice, Dr. David le Couteur (, a leading Australian ageing researcher and Professor of Geriatric Medicine at the University of Sydney, says the paper was a major breakthrough and that Cuervo’s data definitely demonstrated improved survival rates. “She has single-handedly shown that lysosome function is a crucial part of the ageing process,” he says. Cuervo has also shown, he says, the critical role the lysosomal receptor molecules play in keeping the liver clean of damaged proteins.

Cuervo’s findings suggest that therapies for boosting protein clearance might help stave off some of the declines in function that accompany old age. This is especially positive news for those suffering from Alzheimer’s, Parkinson’s and Huntington’s disease as Dr. Cuervo has linked these diseases to a toxic buildup from mutated proteins possibly due to a breakdown in autophagy.

Dr. Cuervo is also working with pharmaceutical companies to identify drugs that will turn receptors on, or make them more active. Cuervo believes maintaining efficient protein clearance may improve longevity and function in all the body’s tissues. “The benefits of restoring the cleaning mechanisms found inside all cells could extend far beyond a single organ”, says Cuervo. “If the body’s ability to dispose of cell debris within the cell were enhanced across a wider range of tissues, she says, it could extend life as well”.

Read more about chaperone-mediated autophagy and the published research findings of Dr. Ana Maria Cuervo:

Maria Konovalenko


Filed under Life, Life Extension

Scientists Discover New Way to Detect and Fix DNA Damage

Researchers at Vanderbilt University, Pennsylvania State University and the University of Pittsburgh have discovered a new mechanism that detects and repairs a more common form of DNA damage called alkylation.
In a typical day, about one million bases in the DNA of a human cell are damaged. These lesions are caused by a combination of normal chemical activity within the cell and exposure to radiation and toxins coming from environmental sources including cigarette smoke, grilled foods, UV rays and industrial waste. These lesions cause structural damage to the DNA molecule, and can dramatically alter the cell’s way of reading the information encoded in its genes. Luckily, repairing damage and maintaining the integrity of its DNA is one of the cell’s highest priorities. 

As cells age however, the DNA repair process can no longer keep up with ongoing DNA damage. The cell then suffers one of three possible outcomes:
* An irreversible state of dormancy, known as senescence (
* Cell suicide, also known as apoptosis ( or programmed cell death
* Cancer
When cells become senescent, alterations in their gene regulation cause them to function less efficiently, which inevitably causes disease. The DNA repair ability of a cell is vital to its normal functioning and to the health and longevity of the organism. Many genes that are shown to influence lifespan are associated with DNA damage repair and protection.

“There is a general belief that DNA is ‘rock solid’ – extremely stable,” said Brandt Eichman (, associate professor of biological sciences at Vanderbilt, who directed the project. “Actually DNA is highly reactive,” he was quoted as saying.
According to the Vanderbilt study, when a DNA base becomes alkylated, it forms a lesion that distorts the shape of the molecule enough to prevent successful replication. Human cells contain a single glycosylase (, named AAG that repairs alkylated bases. It’s specialized to detect and delete “ethenoadenine” bases, which have been deformed by combining with highly reactive, oxidized lipids in the body.

“It’s hard to figure out how glycosylases recognize different types of alkylation damage from studying AAG since it recognizes so many. So we have been studying bacterial glycosylases to get additional insights into the detection and repair process,” said Eichman.
That is how they discovered the bacterial glycosylase AlkD with its unique detection and deletion scheme. “All the known glycosylases work in basically the same fashion: hey flip out the deformed base and hold it in a special pocket while they excise it. AlkD, by contrast, forces both the deformed base and the base it is paired with to flip to the outside of the double helix.”

“Understanding protein-DNA interactions at the atomic level is important because it provides a clear starting point for designing drugs that enhance or disrupt these interactions in very specific ways,” says Eichman. “So it could lead to improved treatments for a variety of diseases, including cancer.”

So there is a vast body of evidence that correlates DNA damage to death and disease. As indicated by the findings of the Vanderbilt study, increasing the activity of some DNA repair enzymes could cause a decrease in the rate of cell damage which would result in adding many healthy and disease-free years to our aging population.
Read about the DNA Repair study: (

Maria Konovalenko 

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