Over at Ouroboros, you'll find a brace of posts reporting on the first Bay Area Aging Club meeting. There's actually quite a concentration of both mainstream and more ambitious biogerontologists and other life science researchers and advocates in that region, what with the Buck Institute for Age Research, Cynthia Kenyon's lab at UCSF, and the legacy of a few years of SENS-related conferences, fundraising meetings, and organizational work.
Today I’m attending the first Bay Area Aging Club at UCSF’s Gladstone Institute. BAAC is a meeting of local scientists working in biogerontology and related fields ... The idea is that the conference will be held regularly (every 6 months or so), allowing frequent discussion of recent progress and ongoing work, and encouraging networking and collaboration between Bay Area biogerontologists. The conference is drawing from a fairly big population - everyone at the Buck Institute, comprising the members of 15 or so labs, and at least as many from Berkeley, Stanford, UCSF; I’d estimate more than 300 scientists.
Networking is what makes the world go round, and the health of a field is measured by the frequency and quality of its conferences. Here are links to the meeting reports:
Adolfo Sanchez-Blanco began with the observation that lifespan [in nematode worms] is variable, even among clonally identical individuals kept under identical conditions. With genetics and environment taken out of the picture, what makes some individuals live longer than others? [He] has identified [several genes] whose expression at middle age strongly predicts remaining lifespan.
Jue Lin (Blackburn Lab, UCSF): Telomere length maintenance and aging-related diseases. This talk described work that builds on significant progress, from this lab and others, demonstrating relationships between telomere length and stress, psychological outlook, and lifespan. Lin reviewed evidence that perceived stress is correlated with telomere length in white blood cells (consistent with previous results showing a relationship with intrusive thoughts).
Protein aggregates are a hallmark of many age-related neurodegenerative diseases, leading to the hypotheses that the cellular mileu changes with age in a manner that causes native, aggregation-prone proteins to form aggregates. [Delia David] used mass spectrometry to identify a subset of normal worm proteins that aggregate as a function of age. As with the proteins associated with neurodegeneration, specific proteins aggregate in specific cell types. Mutations that extend lifespan (such as daf-2) decrease aggregation, and tend to downregulate the expression of genes encoding aggregation-prone proteins.
At the end of the meeting, Martin Brand and Stuart Kim led a group discussion about the free radical theory of aging. Martin began the discussion by pointing out that "after 50 years, you would expect a theory to accumulate enough evidence to convince us that it's true or false - but the fact that we're still discussing it today means that hasn't happened." I'm paraphrasing slightly, but that's the general idea.
Interesting stuff, and worth a look.