Meagan M. Kitt

TL;DR: The mechanisms by which long-lasting elevations in pro-inflammatory cytokines in the hippocampus produce memory impairments are discussed, including dysregulations of the neuroendocrine system, potentiation of neuroinflammatory responses following an immune challenge, and the impairment of memories.

TL;DR: Findings demonstrate that microglia possess a circadian clock that influences inflammatory responses, and indicate time-of-day is an important factor to consider when planning inflammatory interventions such as surgeries or immunotherapies.

TL;DR: HMGB1 mediates neuroinflammatory priming in the aged brain by blocking the actions of HMGB1 appears to “desensitize” aged microglia to an immune challenge, thereby preventing exaggerated behavioral and neuroinflammatory responses following infection.

TL;DR: Intracisternal administration of mifepristone, a GR antagonist, effectively reduced immune-activated proinflammatory responses, specifically from hippocampal microglia and prevented Escherichia coli-induced memory impairments in aged rats, and voluntary exercise as a therapeutic intervention significantly reduced total hippocampal GR expression.

TL;DR: Whether stress-induced neuroinflammatory priming is regulated by the circadian system is tested and the importance of studying circadian rhythms to elucidate biological mechanisms of stress is highlighted.