This study was designed to explore the potential mechanisms of electroacupuncture (EA) in treating inflammatory bowel disease‐ (IBD‐) related anxiety and mood disorders. A colitis model was induced in rats with 2, 4, 6‐trinitrohydrosulfonic acid (TNBS), followed by ST36 and SP6 targeted therapy by EA or sham EA treatment. The elevated plus maze (EPM) and open‐field test (OFT) were performed to assess the state of anxiety and depression‐like behavior. Tests were carried out by 16S rDNA amplification sequence, ¹H nuclear magnetic resonance (¹H NMR) spectroscopy, immunofluorescence staining, and enzyme‐linked immunosorbent assay (ELISA). The analyses detailed metabolic alterations and the Toll‐like receptor 4 (TLR4) signaling pathway/NOD‐like receptor protein 3 (NLRP3) inflammasome in rats’ hippocampal region. Furthermore, the activity of the hypothalamic‐pituitary adrenal (HPA) axis and gut microbiome was assessed. As a result of treatment, EA significantly improved in the behavioral tests and altered the composition of the gut microbiome through a significant increase in the density of short chain fatty acids (SCFAs) producers mainly including Ruminococcaceae, Phascolarctobacterium, and Akkermansiaceae. EA upregulated the metabolites of the hippocampus mainly containing l‐glutamine and gamma‐aminobutyric acid (GABA), as well as ZO‐1 expression. Whereas the treatment blocked the TLR4/nuclear factor‐ kappa B (NF‐κB) signaling pathways and NLRP3 inflammasomes, along with downregulating the interleukin‐ (IL‐) 1β level. The hyperactivity of the HPA axis was also diminished. In conclusion, EA at ST36 and SP6 attenuated anxiety and depression‐like behavior in colitis model rats through their effects on the gut microbiome by modulating the hippocampal inflammatory response and metabolic disorders, as well as the HPA axis. This study provides evidence for clinical application of EA to serve as an adjunctive treatment for IBD‐related anxiety and depression.

There is a pressing need to further our understanding of the mechanisms underlying the depression symptoms in patients with post-stroke depression (PSD) in order to inform targeted therapeutic approaches. While previous research has demonstrated a reorganization in the functional brain network of PSD, it remains uncertain whether, or not it also occurs in the structural brain network. We therefore aim to investigate the structural brain network of patients with PSD as compared to post-stroke non-depression (PSND) patients. In addition, our research considers the relationship between network metrics and functional measurements. Thirty-one PSD patients and twenty-three PSND patients were recruited. All patients underwent MRI and functional assessments, including the Barthel index, mini-mental state examination (MMSE), and Hamilton depression rating scale (HAMD). Diffusion tensor imaging was used to construct the structural brain network and to conduct the subsequent graph theoretical analysis. Network measures were computed and compared between PSD and PSND patients. Associations between functional assessments and network measures were studied as well. We successfully detected increased global and local efficiency in patients with PSD. Regions with disrupted local connections were located primarily in the cognitive and limbic systems. More importantly, PSD patients’ global and regional network measures were associated with depression severity, as measured by HAMD. These findings suggest that disrupted global and local network topologies might contribute to PSD patients’ depression symptoms. Therefore, connectome-based network measures could be potential bio-markers for evaluating stroke patients’ depression levels.

Background: Although there have been many magnetic resonance spectroscopy (MRS) studies of migraine, few have focused on migraines during an attack. Here, we aimed to assess metabolite changes in the brain of patients with migraine, both during an attack and in the interictal phase.Methods: Six patients (one man and five women, mean age: 39 ± 10 years) with migraine without aura during the attack (MWoA-DA), 13 patients (three men and 10 women, mean age: 31 ± 9 years) with migraine without aura during the interictal period (MWoA-DI), and 13 healthy controls (HC) (four men and nine women, mean age: 31 ± 9 years) were studied. All subjects underwent an MRS examination focusing on the occipital lobe. Metabolite changes were investigated among three groups.Results: The MWoA-DA patients had lower glutathione/total creatine ratio (GSH/tCr) than the MWoA-DI patients and HC. Furthermore, MWoA-DI patients showed lower total choline/total creatine ratio (tCho/tCr) than those in the other two groups. The GSH/tCr ratio was positively correlated with attack frequency in the MWoA-DI group. The tCho/tCr ratio was positively correlated with attack frequency and Migraine Disability Assessment Scale (MIDAS) scores in the MWoA-DA group.Conclusion: The present study suggests the existence of distinct pathophysiological states between the MWoA-DA and MWoA-DI groups. Neuronal dysfunction is a possible predisposing factor for migraine attack onset, along with oxidative stress and inflammation.

Background. Resting-state functional MRI is widely used in migraine research. However, the pathophysiology and imaging markers specific for migraine pathologies are not well understood. In this study, we combined both structural and functional images to explore the concurrence and process of migraines. Methods. Thirty-four patients with a history of migraine without aura presenting during the interictal period (MwoA-DI), 10 patients with migraine without aura presenting during the acute attack (MwoA-DA), and 32 healthy controls (HCs) were recruited in this study. All participants underwent scanning via MRI. Voxel-based morphometry (VBM) and seed-based resting-state functional connectivity (rs-FC) analysis were used to detect the brain structural and associated brain functional connectivity. Results. In VBM analysis, a decrease of gray matter volume (GMV) in the middle frontal cortex was found in MwoA patients compared with HCs. The GMV of the middle frontal cortex had a negative correction with the duration of disease. In rs-FC analysis, the left middle frontal cortex (lower, VBM result) in both the MwoA-DA and the HC groups showed significantly increased functional connectivity with the left middle frontal cortex (upper) and left superior frontal cortex compared with MwoA-DI. The left middle frontal cortex (lower) in the MwoA-DI group also showed decreased functional connectivity in the left posterior cingulate cortex (PCC) compared with the HC group. The left middle frontal cortex (lower) in the MwoA-DA group demonstrated significantly increased functional connectivity in the left cerebellum lobule VI compared with the HC group. Conclusions. Our results demonstrated that the middle frontal cortex may serve as an important target in the frequency and severity of migraines due to its role in pain regulation through the default mode network, especially in the PCC. In addition, the cerebellum may modulate the pathophysiology of migraines by serving as a communication point between the cortex and the brainstem.

Migraine is a prevalent neurological disorder affecting 14.1% of the global population. Despite advances in genetic research, further investigation is needed to identify therapeutic targets and better understand its mechanisms. In this study, we aimed to identify drug targets and explore the relationships between gene expression, protein levels, and migraine pathophysiology. We utilized cis-pQTL data from deCODE Genetics, combined with migraine GWAS data from the GERA + UKB cohort as the discovery cohort and the FinnGen R10 cohort as the replication cohort. SMR and MR analyses identified migraine-associated protein loci. Brain eQTL data from GTEx v8 and BrainMeta v2 were used to explore causal relationships between gene expression, protein levels, and migraine risk. Mediation analysis assessed the role of metabolites, and PheWAS evaluated potential side effects. Four loci were identified: PNKP, MRVI1, CALCB, and INPP5B. PNKP and MRVI1 showed a high level of evidence and opposing effects at the gene and protein levels. PNKP gene expression in certain brain regions was protective against migraine, while its plasma protein levels were positively associated with migraine risk. MRVI1 showed protective effects at the protein level but had the opposite effect at the gene expression level. Mediation analysis revealed that the glutamate to pyruvate ratio and 3-CMPFP mediated PNKP’s effects on migraine. PheWAS indicated associations between PNKP and body composition traits, suggesting drug safety considerations. PNKP and MRVI1 exhibit dual mechanisms of action at the gene and protein levels, potentially involving distinct mechanistic pathways. Among them, PNKP emerges as a promising drug target for migraine treatment, supported by multi-layered validation.

To investigate the value of diffusion weighted imaging (DWI) in predicting the clinical progression of perforator artery cerebral infarction. The magnetic resonance imaging (MRI) data of patients with perforator artery cerebral infarction hospitalized in our hospital from October 2015 to February 2022 were analyzed retrospectively. Then we compared the differences of apparent diffusion coefficient (ADC) value, maximal size, location of cerebral infarction, clinical data and treatment plan between the two groups. A total of 81 patients with perforating artery cerebral infarction were included, with 33 patients in the progressive cerebral infarction (PCI) group and 48 patients in the non-progressive cerebral infarction (NPCI) group. The ADC value in the progressive group was lower than that in the non-progressive group (P < 0.001), and ADC value was an independent factor influencing the clinical progression (OR = 0.974, 95 %CI = 0.960–0.989, P = 0.001); The average area of cerebral infarction in the progressive group was larger than that in the non-progressive group (P = 0.004). There was no difference between the two groups (P > 0.05) in terms of clinical data and treatment plan. The ADC value and maximal size of infarction were correlated with the clinical Progression. ADC value was an independent factor influencing the clinical progression of perforating artery cerebral infarction, which could be used for the prediction of clinical progress and provide guidance for the development of individualized treatment.