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  • A new anti age drug

    If this works it will be brilliant for the kids who suffer the awful disease ,,and rusty as well



    Scientists have found a drug which may slow down the ageing process while conducting research into a disease which causes children to age at an accelerated rate.
    The drug could potentially be used to treat children with a rare genetic condition called Progeria which causes them to age up to eight times faster than normal. The average life expectancy for someone with the condition is around 13 years.
    Durham University scientists, who led the study, said the treatment may also help to slow down some of the damaging effects of ageing in older people.
    Professor Chris Hutchison, from the Biophysical Institute at the university, said: "Our findings could be an important step to helping children with Progeria and older people live lives that are less debilitating in terms of health problems.
    "It would be great to find a way to help relieve some of the effects of Progeria and help increasingly ageing populations.
    "The findings are at a very early stage but they show potential for helping people live more comfortable lives when they reach 70, 80 and beyond."
    The study, published in the journal Human Molecular Genetics, found that a drug called N-acetyl cysteine (NAC) was able to reduce the levels of reactive oxygen species (ROS), molecules which cause damage to cells and to cellular DNA.
    The same molecules are partly responsible for premature ageing as well as normal ageing.
    Although the drug did not affect some types of cellular damage, the researchers said that these can be controlled by drugs currently in use.
    The findings suggest that the combination of existing drugs and NAC could improve the health of children with progeria, the researchers said.
    They added that the findings were at an early stage and further studies and human clinical trials would be needed to develop effective drug treatments.
    Dr Leslie Gordon, medical director for The Progeria Research Foundation, said: "Dr. Hutchison's study has not only confirmed basic cellular defects in Progeria, but has also identified potential ways to improve those defects.
    "This type of biological science is how progress towards treatments and a cure for children with Progeria will advance."

  • #2
    Another interesting anti-aging finding this week. This study below is extremely interesting, in that killing the senescent cells in real animals lead to slowing of the signs of aging. Note however, that the drug only works on the genetically engineered mice used in this study, whose senescent cells are designed to produce a special reactive marker molecule. A true drug will have to find a way to recognize senescent cells in humans without the benefit of genetic engineering.

    Ridding body of old "zombie" cells slows aging process, study shows - HealthPop - CBS News
    Ridding body of old "zombie" cells slows aging process, study shows

    By
    David W Freeman


    Two 9-month-old mice used in the study. The mouse on the right received the drug to eliminate senescent cells.
    (Credit: Jan van Deursen)
    (CBS) It's not quite the fountain of youth, but Mayo Clinic scientists may have hit upon a way to slow the aging process. The key, they report in a tantalizing new study, is purging the body of senescent cells - old "zombie" cells that no longer work as they should.

    PICTURES: 9 big lies about longevity

    "By attacking these cells and what they produce, one day we may be able to break the link between aging mechanisms and predisposition to diseases like heart disease, stroke, cancers and dementia," the clinic's Dr. James Kirkland, a co-author of the study, said in a written statement. "There is potential for a fundamental change in the way we provide treatment for chronic diseases in older people."

    And maybe not just chronic diseases. The researchers say that eliminating senescent cells could also delay the onset of cataracts and the gradual loss of muscle tissue that often comes with aging.

    How about slowing the progression of aging-related problems that have already shown up? The purging process may be able to do that too.

    "Therapeutic interventions to get rid of senescent cells or block their effects may represent an avenue to make us feel more vital, healthier, and allow us to stay independent for a much longer time," the Mayo Clinic's Dr. Jan van Deursen, a study co-author, said in the statement.

    The research - published in the journal Nature - grew out of the long-ago discovery that cells in the body don't keep dividing forever. Instead, they reach a state of limbo scientists call cellular senescence, in which they no longer divide but release substances that damage adjacent cells and cause inflammation. The immune system is supposed to sweep away these zombie cells but gradually loses its ability to do so.

    But where nature has failed, science seems to have found a way.

    The scientists started by genetically engineering mice to have a specific molecule in their senescent cells. Then they exposed these transgenic mice to a drug that stimulated the molecule, causing it to drill holes in the cells' outer membranes. Result? The cells self-destructed.

    What happened to the mice? Those that were given the drug over the long term were slower to develop cataracts and other aging-relating health problems, Time reported.

    "Mice that should have looked prematurely aged were essentially normal," Dr. Gary Kennedy, an expert on aging at Montefiore Medical Center in New York City, told USA Today.

    If future studies confirm the findings, the hope is that it may be possible to develop drugs that would kill senescent cells in humans - or to find ways to rev up a flagging immune system's ability to sweep away the cells, the New York Times reported. Another possibility might be to find ways to destroy the inflammatory substances the cells produce, according to Time.

    "I am very excited by the results," Dr. Norman E. Sharpless, University of North Carolina expert on aging, told the Times. "It suggests therapies that might work in real patients."

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