Volume 32, Issue 1

Microparticles (MPs), a class of cell products with biological activities, have been found to participate in a series of vascular activities. The aim of this article is to investigate the changes in the concentrations of MPs after ischemic stroke by meta-analysis. According to pre-established criteria, a strict screening of articles was performed through the Medline and Embase databases. Subsequently, the included studies were subjected to quality assessment and data extraction. Finally, a meta-analysis was performed on seven major outcomes from 985 noncerebrovascular disease controls and 988 ischemic stroke patients. The pooled concentrations of total MPs (TMPs), endotheliocyte-derived MPs (EMPs), platelet-derived MPs (PMPs), erythrocyte-derived MPs (RMPs), leukocyte-derived MPs (LMPs), and monocyte-derived MPs (MMPs) were significantly increased in the ischemic stroke patients compared to the noncerebrovascular disease controls, with the results as follows: TMPs [standardized mean difference (SMD), 1.12; 95% confidence interval (CI), 0.26–1.97; p =0.01], EMPs (SMD, 0.90; 95% CI, 0.67–1.13; p <0.00001), PMPs (SMD, 1.15; 95% CI, 0.69–1.60; p <0.00001), RMPs (SMD, 1.14; 95% CI, 0.57–1.71; p <0.0001), LMPs (SMD, 1.42; 95% CI, 0.74–2.10; p <0.0001), and MMPs (SMD, 1.09; 95% CI, 0.59–1.60; p <0.0001). However, the pooled concentration of lymphocyte-derived MPs (LyMPs) demonstrated no significant difference between the patients and the controls (SMD, 0.22; 95% CI, −0.19 to 0.63; p =0.29). The available data indicated that the circulating MPs, except for LyMPs, play an important role in the development and prognosis of ischemic stroke.

The benefit of endovascular treatment (EVT) for patients with intracranial atherosclerosis–related large vessel occlusion (ICAS-LVO) in posterior circulation stroke (PCS) is inconsistent. This systematic review and meta-analysis were conducted to estimate the effect of ICAS-LVO in PCS treated by EVT. A systematic review was completed, tracking studies from their date of inception until February 2020. Clinical studies which compared outcomes after EVT for ICAS-LVO and non–ICAS-LVO in PCS were included. Data were synthesized and interpreted from meta-analysis. A total of 688 patients (352 ICAS-LVO and 336 non–ICAS-LVO) in the eight studies were included. The successful reperfusion rate (odds ratio [OR], 0.58; 95% confidence intervals [95% CIs], 0.37–0.93; P = 0.02) was lower in PCS with ICAS-LVO than non–ICAS-LVO. And for other clinical outcomes, there were no differences between both groups. Moreover, there were no statistical differences of any clinical outcome among subgroups stratified by nations and target vessel occlusion location. With respect to patients’ characteristics, age (mean difference [MD], −2.75; 95% CI, −4.62–−0.88; P  = 0.004), pc-Alberta Stroke Program Early CT Score (MD, −0.49; 95% CI, −0.94–−0.05; P  = 0.03), distributions of sex (male) (OR, 2.34; 95% CI, 1.53–3.56; P  < 0.001), prior or current smoking (OR, 1.85; 95% CI, 1.12–3.07; P  = 0.02), hypertension (OR, 2.06; 95% CI, 1.32–3.22; P  = 0.002), coronary artery disease (OR, 0.27; 95% CI, 0.11–0.66; P  = 0.004) and general anesthesia (OR, 2.89; 95% CI, 1.54–5.45; P  = 0.001) were statistically different between both groups. In conclusion , more targeted assessments are warranted for patients with ICAS-LVO–related PCS during clinical strategies, and the benefit of EVT for PCS with ICAS-LVO deserves further research.

The neonatal brain is susceptible to hypoxic-ischemic injury due to its developmental characteristics. Hypoxia-ischemia means a decreased perfusion of oxygen and glucose, which can lead to severe encephalopathy. Although early initiation of therapeutic hypothermia was reported to provide neuroprotection for infants after HI, hypothermia administered alone after the acute insult cannot reverse the severe damage that already has occurred or improve the prognosis of severe hypoxic-ischemic encephalopathy. Therefore, exploring new protective mechanisms for treating hypoxic-ischemic brain damage are imperative. Until now, many studies reported the neuroprotective mechanisms of hypoxic/ischemic preconditioning in protecting the hypoxic-ischemic newborn brains. After hypoxia and ischemia, hypoxia-inducible factor signaling pathway is involved in the transcriptional regulation of many genes and is also play a number of different roles in protecting brains during hypoxic/ischemic preconditioning. Hypoxic/ischemic preconditioning could protect neonatal brain by several mechanisms, including vascular regulation, anti-apoptosis, anti-oxidation, suppression of excitotoxicity, immune regulation, hormone levels regulation, and promote cell proliferation. This review focused on the protective mechanisms underlying hypoxic/ischemic preconditioning for neonatal brain after hypoxia-ischemia and emphasized on the important roles of hypoxia inducible factor 1 signaling pathway.

Mitochondrial diseases are predominantly caused by mutations of mitochondrial or nuclear DNA, resulting in multisystem defects. Current treatments are largely supportive, and the disorders progress relentlessly. Nutritional supplements, pharmacological agents and physical therapies have been used in different clinical trials, but the efficacy of these interventions need to be further evaluated. Several recent reviews discussed some of the interventions but ignored bias in those trials. This review was conducted to discover new studies and grade the original studies for potential bias with revised Cochrane Collaboration guidelines. We focused on seven published studies and three unpublished studies; eight of these studies showed improvement in outcome measurements. In particular, two of the interventions have been tested in studies with strict design, which we believe deserve further clinical trials with a large sample. Additionally, allotopic expression of the ND4 subunit seemed to be an effective new treatment for patients with Leber hereditary optic neuropathy.

Extensive research has gone into proposing a promising link between melatonin administration and attenuation of epileptic activity, the majority of which suggest its propensity as an antiseizure with antioxidant and neuroprotective properties. In the past few years, a number of studies highlighting the association of the melatonergic ligands with epilepsy have also emerged. In this context, our review is based on discussing the recent studies and various mechanisms of action that the said category of drugs exhibit in the context of being therapeutically viable antiseizure drugs. Our search revealed several articles on the four major drugs i.e. melatonin, agomelatine, ramelteon and piromelatine along with other melatonergic agonists like tasimelteon and TIK-301. Our review is suggestive of antiseizure effects of both melatonin and its analogues; however, extensive research work is still required to study their implications in the treatment of persons with epilepsy. Further evaluation of melatonergic signaling pathways and mechanisms may prove to be helpful in the near future and might prove to be a significant advance in the field of epileptology.

Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder. Its three core symptoms are social communication disorder, communication disorder, narrow interest and stereotyped repetitive behavior. The proportion of male and female autistic patients is 4:1. Many researchers have studied this phenomenon, but the mechanism is still unclear. This review mainly discusses the related mechanism from the perspective of gut microbiota and introduces the influence of gut microbiota on the difference of ASD between men and women, as well as how gut microbiota may affect the gender dimorphism of ASD through metabolite of microbiota, immunity, and genetics, which provide some useful information for those who are interested in this research and find more gender-specific treatment for autistic men and women.

Smoking is the leading preventable cause of death worldwide and tobacco addiction has become a serious public health problem. Nicotine is the main addictive component of tobacco, and the majority of people that smoke regularly develop nicotine dependence. Nicotine addiction is deemed to be a chronic mental disorder. Although it is well known that nicotine binds to the nicotinic acetylcholine receptors (nAChRs) and activates the mesolimbic dopaminergic system (MDS) to generate the pleasant and rewarding effects, the molecular mechanisms of nicotine addiction are not fully understood. Brain-derived neurotrophic factor (BDNF) is the most prevalent growth factor in the brain, which regulates neuron survival, differentiation, and synaptic plasticity, mainly through binding to the high affinity receptor tyrosine kinase receptor B (TrkB). BDNF gene polymorphisms are associated with nicotine dependence and blood BDNF levels are altered in smokers. In this review, we discussed the effects of nicotine on BDNF expression in the brain and summarized the underlying signaling pathways, which further indicated BDNF as a key regulator in nicotine dependence. Further studies that aim to understand the neurobiological mechanism of BDNF in nicotine addcition would provide a valuable reference for quitting smoking and developing the treatment of other addictive substances.

This review highlights recent data concerning the synthesis of brain metabolic DNA (BMD) by cytoplasmic reverse transcription and the prompt acquisition of the double-stranded configuration that allows its partial transfer to nuclei. BMD prevails in the mitochondrial fraction and is present in presynaptic regions and astroglial processes where it undergoes a turnover lasting a few weeks. Additional data demonstrate that BMD sequences are modified by learning, thus indicating that the modified synaptic activity allowing proper brain responses is encoded in learning BMD. In addition, several converging observations regarding the origin of BMD strongly suggest that BMD is reverse transcribed by mitochondrial telomerase.

The neurophysiological basis of consciousness is still unknown and one of the most challenging questions in the field of neuroscience and related disciplines. We propose that consciousness is characterized by the maintenance of mental representations of internal and external stimuli for the execution of cognitive operations. Consciousness cannot exist without working memory, and it is likely that consciousness and working memory share the same neural substrates. Here, we present a novel psychological and neurophysiological framework that explains the role of consciousness for cognition, adaptive behavior, and everyday life. A hypothetical architecture of consciousness is presented that is organized as a system of operation and storage units named platforms that are controlled by a consciousness center (central executive/online platform). Platforms maintain mental representations or contents, are entrusted with different executive functions, and operate at different levels of consciousness. The model includes conscious-mode central executive/online and mental time travel platforms and semiconscious steady-state and preconscious standby platforms. Mental representations or contents are represented by neural circuits and their support cells (astrocytes, oligodendrocytes, etc.) and become conscious when neural circuits reverberate, that is, fire sequentially and continuously with relative synchronicity. Reverberatory activity in neural circuits may be initiated and maintained by pacemaker cells/neural circuit pulsars, enhanced electronic coupling via gap junctions, and unapposed hemichannel opening. The central executive/online platform controls which mental representations or contents should become conscious by recruiting pacemaker cells/neural network pulsars, the opening of hemichannels, and promoting enhanced neural circuit coupling via gap junctions.