Rehana K. Leak

TL;DR: The results suggest that microglia/macrophages respond dynamically to ischemic injury, experiencing an early “healthy’ M2 phenotype, followed by a transition to a “sick” M1 phenotype, which suggests that stroke therapies should be shifted from simply suppressing microglIA/ Macrophage toward adjusting the balance between beneficial and detrimental microglio-macrophage responses.

TL;DR: It is argued that therapeutic approaches targeting cerebral inflammation should shift from broad suppression of microglia and macrophages towards subtle adjustment of the balance between their phenotypes, and breakthroughs in the identification of regulatory molecules that control these phenotypic shifts could ultimately accelerate research towards curing brain disorders.

TL;DR: A detailed quantitative analysis of the organization of the SCN core and shell in the rat is presented and place this in the context of the functional significance of the subdivisions in the circadian control of regulatory systems.

TL;DR: There is a need to summarize the current literature on phase II genes in the central nervous system (CNS) to help guide future studies on phase I, II and III genes as therapeutic targets in neurological diseases.

TL;DR: It is found that microglia/macrophages respond dynamically to TBI, experiencing a transient M2 phenotype followed by a shift to the M1 phenotype, which may propel WMI progression and represents a rational target for TBI treatment.