Filtering by
- All Subjects: Stress
- Creators: Department of Psychology
- Status: Published
Past studies have shown that exercise in the form of high intensity interval training (HIIT) is the "ideal form of exercise to improve health and performance without overstressing the immune system" (Fisher et. al, 2011, p. 5). Additionally, HIIT has been found to promote cardiovascular health and immunity (Fisher et. al, 2011). The proposed study will evaluate the neuropsychological effects of HIIT on breast cancer patients undergoing anthracycline-based chemotherapy. The intervention group (n = 17) will receive a HIIT protocol concurrent with chemotherapy treatment. There will also be a control group (n= 17) to compare the effects of the intervention. Breast cancer survivorship is often ridden with various health and mental problems, the implementation of HIIT procedures could help to reduce these issues. It is expected that knowledge from this study will be useful in the healthcare setting to benefit breast cancer patients. This study will uniquely add to the limited research base by introducing an intervention for neuropsychological declines in breast cancer patients.
This hypothesis is supported by previous studies demonstrating that stress-induced elevation of glucocorticoids increases the transcription of C4. I propose that activated glucocorticoid receptors directly increase C4 protein expression as a transcription factor activator. Additionally, I propose that activated glucocorticoid receptors inhibit the expression of the transcription factor nuclear factor-light-chain-enhancer of activated B cells (NF-κB), thereby leading to decreased expression of the C4 inhibitor CUB and Sushi multiple domains 1 (CSMD1).
Glucocorticoid receptors and C4 are richly expressed in the hippocampus, a region critical in memory consolidation, spatial, and declarative memory. I propose that stress-induced upregulation of C4 activity in the hippocampus promotes excessive synaptic pruning, contributing to specific deficits and hippocampal shrinkage seen in schizophrenia. Stress exposure during fetal development and adolescence likely acts through the proposed mechanisms to increase hippocampal C4 activity and subsequent schizophrenia risk. These mechanisms may reveal novel interactions between environmental and genetic risk factors in the etiology of schizophrenia through complement activation.