Endocannabinoid (eCB) signaling plays an important role in the central nervous system (CNS). α/β-Hydrolase domain-containing 6 (ABHD6) is a transmembrane serine hydrolase that hydrolyzes monoacylglycerol (MAG) lipids such as endocannabinoid 2-arachidonoyl glycerol (2-AG). ABHD6 participates in neurotransmission, inflammation, brain energy metabolism, tumorigenesis and other biological processes and is a potential therapeutic target for various neurological diseases, such as traumatic brain injury (TBI), multiple sclerosis (MS), epilepsy, mental illness, and pain. This review summarizes the molecular mechanisms of action and biological functions of ABHD6, particularly its mechanism of action in the pathogenesis of neurological diseases, and provides a theoretical basis for new pharmacological interventions via targeting of ABHD6.

Background: Acinetobacter baumannii intracranial infections, especially those caused by multidrug-resistant (MDR) or extensively drug-resistant (XDR) strains, have posed an increasing challenge to treatment because of poor drug permeability through the blood–brain barrier (BBB) and increased bacterial drug resistance. Therefore, we aimed to explore a therapeutic schedule for Acinetobacter baumannii intracranial infection. Case Presentation: We reported a case of intracranial infection caused by XDR A. baumannii after severe traumatic brain injury, cerebrospinal fluid (CSF) rhinorrhea, and severe pneumonia that was successfully treated with meropenem and cefoperazone sodium sulbactam. Conclusion: This case illustrated that meropenem combined with cefoperazone sodium sulbactam could still be a therapeutic option against intracranial XDR A. baumannii infection.

Background: Intracerebral hemorrhage causes high mortality and morbidity, but its therapy methods are limited. In the present study, pulsed electromagnetic fields (PEMFs) were demonstrated to have beneficial effects on an intracerebral hemorrhage (ICH) model. This study explored the effects and underlying mechanism of PEMFs in a mouse model of ICH and cultured BV2 cells.Methods: PEMFs were applied 24 hours after collagenase-induced ICH and 4 hours per day for seven consecutive days. The levels of proinflammatory factors were assessed by ELISA kits and western blotting. Hematoma volume was measured by histological analysis. The effects of PEMFs on phagocytosis of the erythrocytes was observed in cultured BV2 cells.Results: Seven days after ICH, the hematoma volume was significantly reduced in PEMF-treated animals compared to nontreated mice. We found that PEMFs decreased the hematoma volume and the levels of proinflammatory factors after ICH. To evaluate the mechanisms underlying the effects of PEMFs on ICH, we analyzed the transcriptome profile three days after ICH, and we found that PEMFs reversed the changes in inflammation-related pathways and alleviated neurological deficits. Furthermore, PEMFs enhanced the erythrophagocytosis of microglia via CD36. Thus, the PEMF-mediated promotion of neurological functions may at least partly involve anti-inflammatory processes and hematoma clearance.Conclusions: These results suggest that PEMF treatment is a possible adjuvant therapy for ICH patients.