01 Aug 2012

Beth Stevens, Children’s Hospital, Boston, was one of 96 scientists and engineers who received Presidential Early Career Award for Scientists and Engineers at a ceremony in the East Room of the White House on Tuesday, 31 July 2012. The award is the highest honor the government bestows on scientists in their early careers. Recipients typically are in the first five years of conducting independent research, explained Stevens, who told Alzforum that she was surprised to hear she was nominated, and excited and honored to receive the award. The President recognizes Stevens for her pioneering work investigating the regulation of synaptic pruning by the immune system. Her findings could have implications for neurodegenerative diseases, including Alzheimer’s, which is characterized by synaptic loss.

When she worked at Ben Barres’ lab at Stanford University, California, Stevens discovered that components of the complement cascade, a cornerstone of innate immunity, regulate synaptic pruning during development (see ARF related news story). More recently, Stevens and colleagues reported that microglia control postnatal pruning of synapses, and that glial complement receptors play an essential part in this triage (see Schafer et al., 2012). Microglia are often activated in AD and other neurodegenerative diseases.

“The fundamental focus of my lab is to understand the mechanism of synapse loss, which classically occurs during normal development,” said Stevens. Increasing evidence indicates synapse loss is fundamental in AD, and Stevens’ lab is moving to investigate that. Her group has begun to study if, and how, complement molecules and neuroimmune systems that normally drive developmental synaptic pruning become reactivated in the early stages of AD. “We will apply what we know to the normal brain, identify pathways and molecules involved in synaptic regulation, and then move on to AD models that feature clear synapse loss to see if blocking those pathways protects them,” she told Alzforum. Stevens also plans to cross AD mouse models with complement-deficient mice to see if complement loss protects against pathology.—Tom Fagan.