(continued from our coverage of yesterday’s sessions: A B)

This session was devoted to presentations by postdoctoral fellows and recipients of faculty startup grants — talks tended to be more data-intensive than the network-grant talks yesterday morning. Here are some of the highlights:

  • The cortex experiences significant synaptic loss in AD; Josh Trachtenberg (UCLA) has developed a method for imaging this loss as well as its repair in vivo in a mouse model of Alzheimer’s disease. This technology will be important in future studies of AD under the emerging paradigm of AD as a disease of neuronal connectivity (as opposed to cytotoxicity); more about this in yesterday’s coverage.
  • Speaking of connectivity in AD: Beth Stevens (Harvard Medical School) has asked whether Alzheimer’s is caused by re-activation of a developmental mechanism of synapse elimination. She is studying the effect of astrocytes (non-neuronal cells in the brain, each of which can ensheath and contact up to 100,000 synapses) on developing synapses, and observed that the complement protein C1q — involved in opsonization and clearance of foreign bodies in the blood — is expressed at synapses during the time period in early deveopment when “pruning” of superfluous connections is taking place. (In C1q knockout mice, pruning doesn’t occur efficiently.) Stevens hypothesizes that this process may be reactivated in AD (as well as other diseases that involve synapse loss), resulting in the targeting and destruction of (desirable) synapses.
  • I spoke during this session, partly about a paper about senescence-associated protein secretion that our lab has coming out in December and partly about my own studies of the relationship between micro-RNAs and cellular senescence. Oddly for an aging conference, my talk was one of only two about cancer and the only one about senescence.
  • Sun Hur (UCSF) spoke about the relationship between RNA modification and the human progeroid syndrome dyskeratosis congenita. The dyskerin protein is required for covalent modifications to a number of RNAs, including the telomerase RNA (aka TERC). Hur has crystallized several protein-RNA complexes, and is using their crystallographic structures to learn about the functional importance of RNA modification in the cell.
  • Ken Nakamura (UCSF) is studying Parkinson’s disease in a refreshingly original way: he has developed ways to monitor alpha-synuclein multimers in live cells, using fusion with fluorescent proteins. The pathological protein aggregates end up associating with membranes, including mitochondria — which then fragment, potentially contributing to cytotoxicity.