Randi Reed - 2014 Spring Eagle SPUR Recipient


Vijay Rangachari




Investigating the Interaction between Human Granulin-E and Amyloid-β Proteins


Randi Reed’s research looks at the interaction between a human protein, granulin-E, and the proteins that aggregate in the human brain to cause Alzheimer’s disease.  Alzheimer’s disease is a condition that causes mild to severe dementia, particularly in individuals over age 60.  Much of the impaired cognitive function and memory loss results from the accumulation of a protein called amyloid-β, which leads to the formation of toxic oligomers and fibrils.  These toxic aggregates in turn can induce severe neuroinflammation as a secondary response.  Despite clinical evidence relating inflammation and Alzheimer’s disease, the underlying molecular events are largely unknown.  

Among the potential inflammatory mediators, Programulin (PGrn) is known to play a role in wound healing and repairing injuries.  Previous work with PGrn in Alzheimer’s patients has shown that during inflammatory events, PGrn is cleaved into smaller proteins called granulins.  In particular, Randi’s work investigates the possible molecular interactions between granulin-E and amyloid-β in the context of inflammation-triggered aggregation.