Effectiveness of Mindfulness-Based Cognitive Therapy on Depressive Symptoms, Brain Potential, and Neuroimmunoinflammatory Factors in Depressed Patients.

OBJECTIVE: This study was aimed to investigate the effectiveness of mindfulness-based cognitive therapy (MBCT) on depressive symptoms, brain potential, and neuroimmunoinflammatory factors in patients with depression. METHODS: Sixty-four eligible patients according to the inclusion criteria were randomly divided into the control group and the observation group, with 32 patients in each group. The control group received conventional therapy, while the observation group received MBCT on top of conventional therapy. The depressive symptoms, brain potential, and neuroimmunoinflammatory factors were measured in the two groups. RESULTS: After treatment, the Hamilton Depression Rating Scale score, tumor necrosis factor α, and interleukin-6 levels were decreased, while the World Health Organization Quality of Life Scale score, total number of response execution score, and 5-hydroxy tryptamine level were increased in both groups. Moreover, the Hamilton Depression Rating Scale score, tumor necrosis factor α, and interleukin-6 levels were decreased more significantly, while the World Health Organization Quality of Life Scale score, total number of response execution score, and 5-hydroxy tryptamine level were increased more significantly in the observation group compare to the control group ( P < 0.01). In addition, the latency in the observation group was shorter and the amplitude was longer than those in the control group ( P < 0.01). CONCLUSIONS: Compared with conventional therapy, the use of MBCT combined with conventional therapy can effectively reduce depressive symptoms, suppresses inflammatory responses, and optimize attention and response to target stimulation and is worthy of wide clinical implementation.

NSC-derived exosomes enhance therapeutic effects of NSC transplantation on cerebral ischemia in mice.

Transplantation of neural stem cells (NSCs) has been proved to promote functional rehabilitation of brain lesions including ischemic stroke. However, the therapeutic effects of NSC transplantation are limited by the low survival and differentiation rates of NSCs due to the harsh environment in the brain after ischemic stroke. Here, we employed NSCs derived from human induced pluripotent stem cells together with exosomes extracted from NSCs to treat cerebral ischemia induced by middle cerebral artery occlusion/reperfusion in mice. The results showed that NSC-derived exosomes significantly reduced the inflammatory response, alleviated oxidative stress after NSC transplantation, and facilitated NSCs differentiation in vivo. The combination of NSCs with exosomes ameliorated the injury of brain tissue including cerebral infarction, neuronal death, and glial scarring, and promoted the recovery of motor function. To explore the underlying mechanisms, we analyzed the miRNA profiles of NSC-derived exosomes and the potential downstream genes. Our study provided the rationale for the clinical application of NSC-derived exosomes as a supportive adjuvant for NSC transplantation after stroke.

Aberrant Expression of Circulating MicroRNA Leads to the Dysregulation of Alpha-Synuclein and Other Pathogenic Genes in Parkinson's Disease.

A group of circulating microRNAs (miRNAs) have been implicated in the pathogenesis of Parkinson's disease. However, a comprehensive study of the interactions between pathogenic miRNAs and their downstream Parkinson's disease (PD)-related target genes has not been performed. Here, we identified the miRNA expression profiles in the plasma and circulating exosomes of Parkinson's disease patients using next-generation RNA sequencing. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses showed that the miRNA target genes were enriched in axon guidance, neurotrophin signaling, cellular senescence, and the Transforming growth factor-ß (TGF-ß), mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K)-protein kinase B (AKT) and mechanistic target of rapamycin (mTOR) signaling pathways. Furthermore, a group of aberrantly expressed miRNAs were selected and further validated in individual patient plasma, human neural stem cells (NSCs) and a rat model of PD. More importantly, the full scope of the regulatory network between these miRNAs and their PD-related gene targets in human neural stem cells was examined, and the findings revealed a similar but still varied downstream regulatory cascade involving many known PD-associated genes. Additionally, miR-23b-3p was identified as a novel direct regulator of alpha-synuclein, which is possibly the key component in PD. Our current study, for the first time, provides a glimpse into the regulatory network of pathogenic miRNAs and their PD-related gene targets in PD. Moreover, these PD-associated miRNAs may serve as biomarkers and novel therapeutic targets for PD.

Aberrant brain regional homogeneity in first-episode drug-naïve patients with major depressive disorder: A voxel-wise meta-analysis.

BACKGROUND: Resting-state functional magnetic resonance imaging studies have reported aberrant brain regional homogeneity (ReHo) in patients with major depressive disorder (MDD). However, the findings across studies were confounded by medication status and different depressive episodes. METHODS: A systematic literature search of the PubMed, Embase, and Web of Science databases was conducted. We conducted a quantitative voxel-wise meta-analysis of ReHo studies, using the Seed-based d Mapping approach, in first-episode drug-naïve patients with MDD. RESULTS: We identified 10 studies with 12 datasets suitable for inclusion, consisting of 402 first-episode drug-naïve patients with MDD and 330 healthy controls. The most consistent and robust findings were that patients with MDD relative to healthy controls exhibited increased ReHo in the left hippocampus and decreased ReHo in the left orbitofrontal cortex. LIMITATIONS: The patient samples included in our meta-analysis were all Chinese, thus limiting the applicability of the present findings to other populations. CONCLUSIONS: ReHo alterations in these brain regions are likely to reflect the core disease-related functional abnormalities, which are implicated in emotional dysregulation and cognitive impairment that are seen in the early stage of MDD. These findings contribute to a better understanding of the neurobiological underpinnings of MDD, and the left hippocampus and orbitofrontal cortex could serve as specific regions of interest for further investigations.

Alterations in resting-state local functional connectivity in obsessive-compulsive disorder.

BACKGROUND: Obsessive-compulsive disorder (OCD) is increasingly conceptualized as a brain connectivity disorder. Recently, abnormalities in remote resting-state functional connectivity (FC) have been well demonstrated in the frontoparietal areas that linked impairments in large-scale intrinsic brain networks with aberrant fronto-striatal interactions. Beyond the remote FC abnormalities in OCD, many studies using regional homogeneity (ReHo) analysis have reported local FC alterations. However, their results were not entirely consistent. METHODS: We conducted a voxel-wise meta-analysis of ReHo studies to identify consistent local FC abnormalities in patients with OCD. A seed-based d mapping approach was used. RESULTS: Eight studies that compared 200 patients with OCD and 187 healthy controls were included. Increased ReHo in the lateral orbitofrontal cortices and dorsomedial prefrontal cortices bilaterally, and decreased ReHo in the fusiform gyri bilaterally were the most consistent and reliable findings in patients with OCD relative to healthy controls. LIMITATIONS: The number of available studies included in the meta-analysis was relatively small. Many potential confounds on changes in ReHo warrant further attention. CONCLUSIONS: These regions are critically implicated in the pathophysiology of OCD. Our findings in local FC alterations are complementary to the abnormalities in remote FC in OCD, contributing to the modeling of brain functional connectomes in OCD.