"We are on the verge of a revolution in medicine: understanding, treating, and ultimately preventing the causes of degenerative aging. But medical revolutions only happen if we all stand up in support of funding and research. We did it for cancer. We're doing it for Alzheimer's. We can do it for aging - and create an era of longer, healthier lives!"

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The Causes of Aging
Accumulating AGEs
Buildup of Amyloid Between Cells
The Failing Immune System
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  • The Conservative View of Progress in Applied Cancer Research
  • More on Stem Cell Technology and the Rise of Medical Tourism
  • Resting Metabolic Rate and Aging, Another of Metabolism's Complexities
  • Capabilities in Stem Cell Science Are Advancing Rapidly
  • Incentives and Cryonics
  • Videos From the Foresight 2010 Conference
  • A Steady Flow of New Donors at the Methuselah Foundation
  • Manipulating Fat in the Context of Slowing Aging
  • On Medical Tourism For Stem Cell Therapies
  • Cells, Hearts, and Brains
  • Rapamycin Research Rolls Onward
  • Reversing Blindness in Retinitis Pigmentosa With Stem Cells
  • The Body Does Work to Break Down Damaging Aggregates
  • A Few Cancer Stem Cell Articles
  • The Latest on Mitochondrial Uncoupling
  • Longevity Research at the Science Network
  • Journalists Are In the Business of Gathering Eyeballs, Not Truth
  • @ging, a New Aging Science Blog
  • Redefining Bionics Again
  • Encouraging Transparency in Life Science Fundraising

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    Fight Aging! is published under the Creative Commons Attribution 3.0 license. In short, this means that you are encouraged to republish and rewrite Fight Aging! content in any way you see fit, the only requirements being that you (a) link to the original, (b) attribute the author, and (c) attribute Fight Aging!.

  • Saturday, April 15, 2006

    The Latest Rejuvenation Research

    Volume 9 issue 1 of Rejuvenation Research is up for perusal and your general edification - don't forget that the previous issue is presently free and open. Interestingly, the journal publisher is running an ad for Aubrey de Grey's GENcast interview from some weeks back (scroll down on that page to see it). The publisher's overview blurb is becoming more glowing too:

    Aubrey de Grey, at the helm of this multidisciplinary peer-reviewed journal, seeks to understand and ultimately defy the mechanisms of aging. He was featured in a recent 60 Minutes segment titled "The Quest for Immortality"; in a cover story on de Grey, MIT's Technology Review said, "His tireless efforts...have put him among the most prominent proponents of antiaging science in the world. ... De Grey has become more than a man; he is a movement."

    Dr. de Grey and his outstanding international editorial board have the opportunity to further explore and advance the science, and perhaps achieve the ultimate goal of slowing or reversing the process of aging.

    Someone in their marketing group has apparently decided to make this a project. But back to the scientific highlights from the latest issue:

    Analysis of Telomere Length and Telomerase Activity in Tree Species of Various Lifespans, and with Age in the Bristlecone Pine Pinus longaeva

    Normal somatic cells have a finite replicative capacity, and with each cell division telomeres progressively shorten, unless the telomerase enzyme is present. The bristlecone pine, Pinus longaeva, is the oldest known living eukaryotic organism, with the oldest on record turning 4770 years old in 2005. The results from our study of telomere length and telomerase activity [support the hypothesis] that both increased telomere length and telomerase activity may contribute to the increased lifespan and longevity evident in long-lived pine trees

    Mitochondrial Dysfunction and Cell Senescence: Cause or Consequence?

    The mitochondrial theory of aging remains to date one of the most popular theories of aging. ... Here, we review evidence supporting the involvement of mitochondria in replicative senescence and a possible link to telomere biology. Moreover, we suggest that this process might be more complex than originally formulated

    Immunorejuvenation in the Elderly

    Dysregulated T-cell–mediated immunity contributes materially to the increased susceptibility to infectious disease, and possibly cancer, in the elderly. One hallmark of this state of "immunosenescence" in humans is the predominance of large clones of peripheral T cells ... This excess of dysfunctional cells is indirectly immunosuppressive by filling the "immunologic space" and shrinking the T-cell repertoire for new antigens ... Therefore, it is hypothesized that deletion of such accumulations of dysfunctional cells would be beneficial to the individual.

    Conjecture: Can Continuous Regeneration Lead to Immortality? Studies in the MRL Mouse

    A particular mouse strain, the MRL mouse, has been shown to have unique healing properties that show normal replacement of tissue without scarring. The serendipitous discovery that the MRL mouse has a profound capacity for regeneration in some ways rivaling the classic newt and axolotl species raises the possibility that humans, too, may have an innate regenerative ability. We propose this mouse as a model for continuous regeneration with possible life-extending properties.

    MRL mice have been attracting more attention in the past year, and the broader - but still nascent - field interested in recreating lizard-like regeneration is moving forward and getting noticed. Researchers are starting to make progress in understanding and manipulating the processes underlying the serendipitous discovery of regeneration in MRL mice - you can find a little more background back in the Fight Aging! archives. Personally, I'm skeptical that MRL-like (or salamander-like) mechanisms in mammals could on their own net you something approximating physical immortality, as seen in lower animals like the hydra. Mammalian regeneration - even impressive, standout, amazing mammalian regeneration - comes from the actions of stem cell populations, and stem cells in mammals have a sell-by date due to the accumulation of genetic mutations. After a certain point, you're looking at cancer and ever more cancer, no matter how well you can regenerate.

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