Post-Injury Sleep Disruption Alters the Inflammatory Response to Traumatic Brain Injury
Abstract
Background: Traumatic brain injury (TBI) alters baseline neuroendocrine function and the process to restore homeostasis following a stressor. We predict that this altered post-injury stress response is a key mediator in long-term recovery. Sleep disruption (SD) is an environmental stressor that increases neuroinflammation, neuronal injury and loss, and behavioral impairment. To date, the role of post-injury SD is unclear and no studies have considered the interrelationship between TBI,SD, and neuropathology associated with Alzheimers disease (AD). We provide preliminary data showing that TBI reduces the corticosterone (CORT)-mediated stress response to acute SD in TBI mice. Mice exposed to SD displayed increased neuroinflammatory cytokine expression expressed by microglia/macrophages (CCL2, Trem2, TNF, IL1) and increased leukocyte accumulation in the brain. Finally, post-injury SD increased phosphorylation of microtubule associated protein tau(MAPT, tau) in TBI mice compared to all other groups, which occurred in close spatial proximity to reactive microglia/macrophages suggesting the two events are related. Hypothesis: SD after TBI impairs neuroendocrine (stress)signaling resulting in increased neuroinflammation, impaired functional recovery, and enhanced neurodegenerative pathology reflecting key features of AD.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 2021
- Accession Number
- AD1172210
Entities
People
- Olga N. Kokiko-cochran
Organizations
- Ohio State University