"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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  • Wednesday, November 14, 2007

    From the 2007 Hillblom Foundation Scientific Meeting

    Researcher Chis Patil of Ouroboros has been blogging this year's scientific meeting of the Larry L. Hillblom Foundation, a gathering of scientists involved aging (and longevity) research and other medicine funded by the Foundation. Links and a few highlights:

    2007 Hillblom Meeting: Morning session 1:

    Getting down to brass tacks and emphasizing the real-world applications of the work, Kenyon described a brave new world in which the 40-year-old men of the future will find themselves unwittingly, but enthusiastically, hitting on 90-year-old hotties in singles bars.

    2007 Hillblom meeting: Morning session 2:

    Bill Mobley (Stanford) began with the bold claim that all neurodegenerative illnesses are ultimately breakdowns of neural circuitry - if not etiologically, then symptomologically. He went on to summarize and review the body of evidence supporting the view that axonal dysfunction contributes to Alzheimer’s Disease (AD) pathology, focusing especially on the idea that decreases in neurotrophic factor signaling and retrograde transport play a causative role in AD.

    2007 Hillblom meeting: Afternoon session:

    Lithgow begins from a simple premise: Given that genetic manipulations have revealed significant plasticity in the rate of aging, shouldn’t we be able to discover drugs that phenocopy, simulate or even outstrip the effects of longevity-extending mutations? Thus far, early screens for both stress resistance and lifespan extension per se have generated several lead compounds that delay aging in yeast, worms and flies (and in at least one case, both species). Studies from multiple labs are beginning to converge, with the ultimate goal of testing multi-species hits in mouse models of aging and age-related diseases. In closing, Lithgow acknowledged that understanding of the mechanism of action of these compounds is lagging behind their discovery, in part because some of the most promising molecules have mystifyingly large numbers of candidate targets.

    Interesting stuff; that last quote is an excellent summation of the metabolic manipulation school of longevity science, the presently dominant view of that part of the aging research mainstream that supports initiatives to extend the healthy human life span.

    Patil is off to the Keck Futures Initiative meeting on "The Future of Human Healthspan" next - more of what you get to do when you're one of the scientists actually working on aging and longevity research.

    Posted by Reason

     
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