May 16
errofsemqopatience cancer research centre, health span
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 Mari?a 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 Fa?tima Bosch of the Centre of Animal Biotechnology and Gene Therapy at the Universitat Auto?noma 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The gene therapy consisted of treating the animals with a DNA-?modified virus, the viral genes having been replaced by those of the telomerase enzyme, with a key role in aging.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.
In 2007, Blasco’s group demonstrated that it was feasible to prolong the lives of transgenic mice, whose genome had been permanently altered at the embryonic stage, by causing their cells to express telomerase and, also, extra copies of cancer-??resistant genes. These animals live 40% longer than is normal and do not develop cancer.
The mice subjected to the gene therapy now under test are likewise free of cancer. Researchers believe this is because the therapy begins when the animals are adult so do not have time to accumulate sufficient number of aberrant divisions for tumours to appear.
Also important is the kind of virus employed to carry the telomerase gene to the cells. The authors selected demonstrably safe viruses that have been successfully used in gene therapy treatment of hemophilia and eye disease. Specifically, they are non-??replicating viruses derived from others that are non-??pathogenic in humans.
This study is viewed primarily as “a proof-??of-??principle that telomerase gene therapy is a feasible and generally safe approach to improve healthspan and treat disorders associated with short telomeres,” state Virginia Boccardi (Second University of Naples) and Utz Herbig (New Jersey Medical School-??University Hospital Cancer Centre) in a commentary published in the same journal.
Although this therapy may not find application as an anti-??aging treatment in humans, in the short term at least, it could open up a new treatment option for ailments linked with the presence in tissue of abnormally short telomeres, as in some cases of human pulmonary fibrosis.
More healthy years
As Blasco says, “aging is not currently regarded as a disease, but researchers tend increasingly to view it as the common origin of conditions like insulin resistance or cardiovascular disease, whose incidence rises with age. In treating cell aging, we could prevent these diseases.”
With regard to the therapy under testing, Bosch explains: “Because the vector we use expresses the target gene (telomerase) over a long period, we were able to apply a single treatment. This might be the only practical solution for an anti-??aging therapy, since other strategies would require the drug to be administered over the patient’s lifetime, multiplying the risk of adverse effects.”
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The above story is reprinted from materials provided by Centro Nacional de Investigaciones Oncologicas (CNIO).
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Bruno Bernardes de Jesus, Elsa Vera, Kerstin Schneeberger, Agueda M Tejera, Eduard Ayuso, Fatima Bosch, Maria A. Blasco. Telomerase gene therapy in adult and old mice delays ageing and increases longevity without increasing cancer. EMBO Molecular Medicine, 2012 (in press) DOI: 10.1002/emmm.201200245
Note: If no author is given, the source is cited instead.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
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May 15
errofsemqopatience 9to5mac, ivy bridge, MacBook
Yup, Apples are bound to flow beneath the Ivy Bridge at some point, but how much of a performance boost will they deliver? If you’re happy to hold onto a little skepticism, then two unexpected appearances on the Geekbench site could offer some early answers. The first purports to be an unknown ‘MacBookPro9,1′ laptop powered by an Ivy Bridge Core i7-3820QM running at 2.7GHz, which achieved a benchmark of 12252 — that’s around 17 percent better than a current equivalent Core i7 15-inch or 17-inch MacBook Pro. The second benchmark comes from an ‘iMac13,2′ running off Intel’s next-gen Core i7-3770 desktop chip clocked at 3.4GHz, which only merits a score of 12183 because it’s hobbled by 4GB of RAM. If you exclude memory and compare only the CPU integer and floating point scores, then you’re looking at a roughly nine percent gain over a current 27-inch iMac with a 3.4Ghz Core i7-2600 processor. Now, these benchmarks could be faked, or represent non-final hardware, but the motherboard codes look valid (see the source links) and they generally tally with what we’ve come to expect from Ivy Bridge: a healthy oar-stroke forwards, but nothing that would frighten the fish.
Update: 9to5Mac has done some digging and come up with a few more interesting tidbits about the upcoming MacBook Pro refresh. For one, code pulled from the Mountain Lion beta appears to indicate that the Ivy Bridge machines will boast USB 3.0 and a new GPU in the NVIDIA GeForce GT 650M. The site also claims that the laptops will be slimmer than the current gen, a rumor that we’ve been hearing for quite some time now.
MacBook Pro and iMac with next-gen Ivy Bridge processors crop up on benchmarks (update) originally appeared on Engadget on Mon, 14 May 2012 08:49:00 EDT. Please see our terms for use of feeds.
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Some people just love Google+ and others just hate the company’s efforts to create a social network and a social layer across all of its services. Google itself seems to be pretty happy with the results it is getting from Google+ so far – or at least that’s what the company is saying publicly. No matter your overall feelings about Google+, though, Google’s