This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.The study purpose is to improve our understanding of the etiology of cognitive dysfunction by using a well-established acute tryptophan depletion paradigm to alter central serotonin neurotransmission in women with breast cancer. This study will augment a currently funded study using the same acute tryptophan depletion paradigm focusing on hot flash response (Dr. Carpenter, PI, Grant # DAMD BC043199). The amino acid tryptophan is a precursor to serotonin. Serotonin may be involved in cognitive dysfunction. The main hypothesis is that alterations in dietary tryptophan and serotonin levels are involved in cognitive dysfunction in women with breast cancer and that variability in response to tryptophan manipulation can be partly explained by genetic variations in the serotonin receptors and transporters. A within-subjects, balanced, crossover design is proposed, with each participant taking part in two similar 9-hour test days, 1 week apart, at the Indiana University General Clinical Research Center. If data support our hypothesis, we will have strong physiological rationale to pursue an intervention involving increasing dietary availability of tryptophan in women with cognitive dysfunction following breast cancer treatment. This dietary intervention may eradicate cognitive dysfunction as a frequent, severe and bothersome breast cancer treatment related condition, and ultimately improve overall quality of life.
Showing the most recent 10 out of 767 publications
