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Posted on Nov 07, 2006, 11 a.m.
By Bill Freeman
The meeting itself was at the same time exciting and grueling: There
I spent last week at the Cold Spring Harbor meeting on the Molecular Genetics of Aging.
The meeting itself was at the same time exciting and grueling: There’s so much happening in the field right now; one has the feeling of drinking from a firehose…all day long…after staying up very late the night before, talking science on the deck of the Lab bar.
I’ve been struggling to find a way to summarize the event, and the contents of the meeting, but I’ve decided that a thorough conference review is beyond the scope of a blog entry. With a few days’ remove from the experience, however, I keep returning to one theme: This field has exploded in the last dozen years.
Without in any way meaning to denigrate the progress in study of aging prior the early 90’s, the specific field in question at this conference (molecular genetics of aging) barely existed then. Excellent work had been performed on the contribution of oxidative damage to the aging process, but while a broad consensus about oxidation’s significance had emerged, the specific details were often murky. Many believed that the eagerly anticipated identification of genes mutated in progeroid syndromes (e.g., Werner’s) would provide an entry point for work in humans and shorter-lived organisms, but at the time we were very short on genes and model systems.
Starting in 1993, however, that began to change. I want to single out two papers that mark the beginning of the era of a true molecular genetics of aging (for me, i.e., I don’t mean to discredit any other work done during the same period; I’m just able to see a pattern and tell a story about it, and that story involves these two papers, which I read as a graduate student). Both have had tremendous impact on the field over the ten years since — at the CSHL meeting, more than half of the talks were in some way based on the founding observations in these two papers.
