Molecular and cellular mechanisms underlying sickle cell disease pain
Approximately 100,000 Americans suffer from a genetic blood disorder known as sickle cell disease (SCD). Under stress, dehydration, and reduced oxygen conditions, SCD patients experience intense pain crises that often lead to hospitalization. In addition to these acute crises, approximately 40% of SCD patients also develop persistent chronic pain as the disease progresses. In my research, I am investigating the neurobiological mechanisms, particularly those of the peripheral nervous system, that mediate the acute and chronic pain associated with SCD as well as the transition between the two states.
Kate was recently awarded an NINDS Ruth L. Kirchstein National Research Service Award (NRSA) for Training of Postdoctoral Fellows (F32). Kate’s proposal entitled “Fibroblast-to-neuron communication in muscle pain” will explore the extent and mechanisms through which muscle support cells communicate with sensory neurons to relay both painful and non-painful signals to the central nervous system. This unique award is presented to promising, early-stage postdoctoral fellows and will fund Kate’s position until January 2020.