33054641 story Posted by Soulskill on Tuesday May 15, @08:17PM from the boosterspice-before-i-get-old-please dept. Grond writes “ScienceDaily reports, ‘Researchers at the Spanish National Cancer Research Centre have demonstrated that the mouse lifespan can be extended by the application in adult life of a single treatment acting directly on the animal’s genes. Mice treated at the age of one lived longer by 24% on average (PDF), and those treated at the age of two, by 13%. The therapy, furthermore, produced an appreciable improvement in the animals’ health, delaying the onset of age-related diseases like osteoporosis and insulin resistance and achieving improved readings on aging indicators like neuromuscular coordination.’ Notably, the therapy did not cause an increase in the incidence of cancer.” You may like to read: Post

Life is the living you do, Death is the living you don’t do. — Joseph Pintauro

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Gene Therapy Extends Mouse Lifespan

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Gene therapy may extend life: Study

ScienceDaily (May 14, 2012) A new study consisting of inducing cells to express telomerase, the enzyme which — metaphorically — slows down the biological clock — was successful. The research provides a “proof-of-principle” that this “feasible and safe” approach can effectively “improve health span.”

A number of studies have shown that it is possible to lengthen the average life of individuals of many species, including mammals, by acting on specific genes. To date, however, this has meant altering the animals’ genes permanently from the embryonic stage — an approach impracticable in humans. Researchers at the Spanish National Cancer Research Centre (CNIO), led by its director Maria Blasco, have demonstrated that the mouse lifespan can be extended by the application in adult life of a single treatment acting directly on the animal’s genes. And they have done so using gene therapy, a strategy never before employed to combat aging. The therapy has been found to be safe and effective in mice.

The results were recently published in the journal EMBO Molecular Medicine. The CNIO team, in collaboration with Eduard Ayuso and Fatima Bosch of the Centre of Animal Biotechnology and Gene Therapy at the Universitat Autonoma de Barcelona (UAB), treated adult (one-year-old) and aged (two-year-old) mice, with the gene therapy delivering a “rejuvenating” effect in both cases, according to the authors.

Mice treated at the age of one lived longer by 24% on average, and those treated at the age of two, by 13%. The therapy, furthermore, produced an appreciable improvement in the animals’ health, delaying the onset of age-related diseases — like osteoporosis and insulin resistance — and achieving improved readings on aging indicators like neuromuscular coordination.

The gene therapy consisted of treating the animals with a DNA-modified virus, the viral genes having been replaced by those of the telomerase enzyme, with a key role in aging. Telomerase repairs the extreme ends or tips of chromosomes, known as telomeres, and in doing so slows the cell’s and therefore the body’s biological clock. When the animal is infected, the virus acts as a vehicle depositing the telomerase gene in the cells.

This study “shows that it is possible to develop a telomerase-based anti-aging gene therapy without increasing the incidence of cancer,” the authors affirm. “Aged organisms accumulate damage in their DNA due to telomere shortening, [this study] finds that a gene therapy based on telomerase production can repair or delay this kind of damage,” they add.

‘Resetting’ the biological clock

Telomeres are the caps that protect the end of chromosomes, but they cannot do so indefinitely: each time the cell divides the telomeres get shorter, until they are so short that they lose all functionality. The cell, as a result, stops dividing and ages or dies. Telomerase gets around this by preventing telomeres from shortening or even rebuilding them. What it does, in essence, is stop or reset the cell’s biological clock.

But in most cells the telomerase gene is only active before birth; the cells of an adult organism, with few exceptions, have no telomerase. The exceptions in question are adult stem cells and cancer cells, which divide limitlessly and are therefore immortal — in fact several studies have shown that telomerase expression is the key to the immortality of tumour cells.

It is precisely this risk of promoting tumour development that has set back the investigation of telomerase-based anti-aging therapies.

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First gene therapy successful against aging-associated decline: Mouse lifespan extended up to 24% with a single …

Gene therapy has been used to increase the lifespan of mice by up to 24 percent – and improve their health at the same time.

Telomerase helps to maintain the physical integrity of the ends of chromosomes. And mice that received a single treatment to deliver the enzyme to different cells in the body showed drastic improvements in health, fitness and longevity, says the team.

“Gene therapy is typically thought of as a way to deliver genes into cells to correct genetic defects or diseases. However, if we consider that ageing is, at least in part, the consequence of defective gene function, gene therapy is also a valid strategy to delay ageing or to increase lifespan,” says Maria Blasco, director of the Spanish National Cancer Research Centre.

“Our results show that telomerase gene therapy is not only a viable anti-ageing intervention but it also has remarkably beneficial effects on health and fitness without increasing the incidence of cancer.”

Telomeres are the caps of repetitive DNA nucleotide sequences that sit at the ends of chromosomes, and are known to play a part in ageing. As they are gradually worn down, cell stop dividing and eventuially die.

The scientists used an adeno-associated virus vector to introduce the telomerase gene into the cells of adult mice, where it added DNA back to the ends of chromosomes.

The mice that were used in the experiments typically live for approximately 150 weeks. However, one-year-old mice that received the gene therapy lived on average 24 percent longer, and the average lifespan of two-year-old mice increased by 13 percent.

“In addition to living longer, engineered mice had stronger bones, improved metabolic functions, better motor coordination and balance, as well as improved performance in object-recognition tests,” says Bruno Bernardes de Jesus, a researcher at the Spanish National Cancer Research Centre.

The findings are the first proof-of-principle that telomerase gene therapy is both feasible and potentially safe. The team now plans to investigate whether the therapy could work for animals with longer lifespans.

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Gene therapy dramatically extends mouse lifespan

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Gene therapy extends mouse lifespan by 24 pc

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The study involved painstaking molecular analysis of blood samples taken annually from the patients, who participated in separate studies begun in 2000, 2002, and 2004.

“We were astonished that we could detect the modified cells for so long. It’s a relatively small number of patients, but more than 500 years of patient data,” said University of Pennsylvania pathologist Bruce Levine, a leader of the research. “But it’s difficult to separate with certainty the effectiveness of this treatment from the antiretrovirals.”

Gene therapy harnesses the insidious ability of viruses to slip their DNA into the cells they infect. By neutralizing a virus and then using it as a “vector” to insert DNA that is helpful rather than harmful, gene therapy can theoretically treat ailments ranging from arthritis to infections and cancer.

Levine, his Penn colleague Carl June, and their team have tested a variety of ways to outwit HIV with gene therapy. Their approach has focused on T cells, which are the big guns of the immune system but also the cells that HIV infects. The researchers took some of the patients’ T cells and inserted a gene that makes them better at recognizing and killing HIV-infected cells. Then these super-T cells were multiplied using growth-stimulation technology and put back into the patient.

Over the years, many other research groups have tried using modified T cells, but the patient’s immune system perceived them as invaders and wiped them out, sometimes within hours.

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Penn researchers report a gene-therapy success

Public release date: 11-May-2012 [ | E-mail | Share ]

Contact: Quinn Eastman qeastma@emory.edu 404-727-3990 Emory University

Regenerating sensory hair cells, which produce electrical signals in response to vibrations within the inner ear, could form the basis for treating age- or trauma-related hearing loss. One way to do this could be with gene therapy that drives new sensory hair cells to grow.

Researchers at Emory University School of Medicine have shown that introducing a gene called Atoh1 into the cochleae of young mice can induce the formation of extra sensory hair cells.

Their results show the potential of a gene therapy approach, but also demonstrate its current limitations. The extra hair cells produce electrical signals like normal hair cells and connect with neurons. However, after the mice are two weeks old, which is before puberty, inducing Atoh1 has little effect. This suggests that an analogous treatment in adult humans would also not be effective by itself.

The findings were published May 9 in the Journal of Neuroscience.

“We’ve shown that hair cell regeneration is possible in principle,” says Ping Chen, PhD, associate professor of cell biology at Emory University School of Medicine. “In this paper, we have identified which cells are capable of becoming hair cells under the influence of Atoh1, and we show that there are strong age-dependent limitations on the effects of Atoh1 by itself.”

The first author of the paper, Michael Kelly, now a postdoctoral fellow at the National Institute on Deafness and Other Communication Disorders, was a graduate student in Emory’s Neuroscience program.

Kelly and his coworkers engineered mice to turn on the Atoh1 gene in the inner ear in response to the antibiotic doxycycline. Previous experimenters had used a virus to introduce Atoh1 into the cochleae of animals. This approach resembles gene therapy, but has the disadvantage of being slightly different each time, Chen says. In contrast, the mice have the Atoh1 gene turned on in specific cells along the lining of the inner ear, called the cochlear epithelium, but only when fed doxycycline.

Young mice given doxycycline for two days had extra sensory hair cells, in parts of the cochlea where developing hair cells usually appear, and also additional locations (see accompanying image).

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Gene therapy for hearing loss: Potential and limitations

Todays post is a repost from October 2010. Ive got some major stuff cooking in the lab right now and I need all of my brain power for it. Enjoy the repost and I shall return!

Reader David sent me this paper the other day, and asked if I could blog about it. I said ok, maybe, and then I read

Gene therapy

oooooh

Sounds very cool, doesnt it? Sounds like the FUTURE! Wheres my JETPACK!!!?!?!

But of course gene therapy is kind of a buzzword. A lot of people throw it around, but it seems like a lot of people dont know what it really MEANS, and what it can be used for.

But it turns out, it can be used for quite a lot! And it may not be quite so far in the future. After all, theyre marketing jetpacks.

Alexander et al. Reversal of Depressed Behaviors in Mice by p11 Gene Therapy in the Nucleus Accumbens Science Translational Medicine, 2010.

So lets start with gene therapy and what it is, and then well go into why they used it in this particular paper. Gene therapy is based on the idea of inserting a gene into someones genome, either in the whole body or in specific parts, to change the gene expression of that cell or group of cells, and to use this technology to treat disease. In this case, what were talking about is viral-mediated gene expression. This is where we use a virus (for our own nefarious purposes mwah-ha-ha-ha!!), take out the nasty bits of the viral DNA, and load the virus with the gene you want to express. You then inject the virus into your area of interest (normally this is really site specific), and the virus, using its own virusy ways, will insert your gene of interest into your area of interest. The gene will get incorporated into the genome, and get expressed by your cells!

Original post:
Repost: Depressed mice, gene therapy, and p11

Lorena Ramos, 14, struggles to lose weight.

The show opens with the 14-minute story Childhood Obesity: Kids Fight Back. One in six kids in the United States is obese, a condition that doubles their risk of heart disease. Castro Valley teenager Lorena Ramos, 14, has been overweight since she was a small child. Now, with the help of her mother and the Healthy Hearts clinic at Children’s Hospital Oakland, she’s fighting to exercise, eat healthily and drop weight. Will she succeed?

A heart patient is treated at John Muir Medical Center in Concord.

Rushing to Save Heart Attack Patients tells the story of Arlene Skuba, who survived a heart attack at 72, after doctors at the John Muir Medical Center in Concord rapidly unclogged her arteries. Just 30 years ago, doctors could only watch patients as they suffered their heart attacks. As many as 20 percent of them ended up dying. Now, by opening their blocked arteries while their heart attacks are underway, they save all but 5 percent of those who make it to a hospital.

After being injected with three genes, the hearts of mice who had suffered a heart attack pumped blood normally. All photos by Gabriela Quirós.

The special report’s final 4-minute story, New Hope for Heart Repair, takes us into the future, to a time when a single injection of three genes might be able to repair damaged hearts and give heart attack survivors their quality of life back. We visit the Gladstone Institutes, in San Francisco, and watch as researchers repair tiny mice hearts using the next generation of cell reprogramming.

You can watch each of the three stories individually, as well, by following the links below:

Tags: cell reprogramming, childhood obesity, Children's Hospital Oakland, featured, gene therapy, gladstone institutes, heart, heart attack, heart disease, John Muir Medical Center Concord, obesity, overweight
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Cancer Gene Therapy advance online publication, May 4, 2012.
doi:10.1038/cgt.2012.19

Authors: M S Villaverde, M L Gil-Cardeza, G C Glikin
& L M E Finocchiaro (Source: Cancer Gene Therapy)Source:
http://www.medworm.com/rss/medicalfeeds/therapies/Gene-Therapy.xml