Background: The microbiota–gut–brain axis has been proposed as a potential therapeutic target of PD. The effects of curcumin against Parkinson’s disease have been demonstrated; however, its neuroprotective mechanisms remain unknown. Our study investigated the potential mechanisms through which curcumin ameliorates Parkinson’s disease via the microbiota–gut–brain axis.Methods: Mice were randomly divided into four groups: control, Curcumin, MPTP, and MPTP + Curcumin. Motor deficits and gastrointestinal dysfunction were assessed using behavioral test, intestinal motility test, and fecal parameter measurement. The loss of dopaminergic neurons and intestinal barrier function was measured using Western blot and immunofluorescence. Shotgun metagenomic sequencing and LC-MS were parallelly performed on mice feces to investigate alterations in microbiota and metabolites.Results: Curcumin alleviated motor deficits and the loss of dopaminergic neurons in MPTP-induced mice. Curcumin ameliorated gastrointestinal and intestinal barrier dysfunctions in MPTP-induced mice. Curcumin reduced gut microbial dysbiosis and modulated carbohydrate metabolism in MPTP-induced mice. Curcumin restored short-chain fatty acid (SCFA) profiles in MPTP-induced mice.Conclusion: Concurrently, these results indicate that curcumin inhibits Parkinson’s disease by regulating the gut microbiota and short-chain fatty acids.

Ticks are small, blood-sucking arachnids, known vectors of various diseases, and found throughout the world. They are distributed basically in almost all regions of China. At present, there is not much information regarding tick species on Hainan Island. They were subjected to morphological identification and imaging on an individual basis. Molecular phylogenetic analyses, based on cox1 and 16S rRNA genes, were utilized to identify the species and determine their approximate phylogenetic origin and genetic diversity. The genomic DNA of tick species was extracted, and cytochrome oxidase subunit 1 (cox1) and 16S ribosomal RNA (rRNA) genes were amplified and sequenced. The identification of five tick species, namely Rhipicephalus microplus, Rhipicephalus sanguineus, Rhipicephalus haemaphysaloides, Haemaphysalis cornigera and Haemaphysalis mageshimaensis, was carried out by morphological analysis. When employing the cox1 and 16S rRNA phylogenetic tree, all isolates of R. microplus from Hainan Island were classified as clade A and B, respectively. R. sanguineus was recognized as a member of the tropical lineage by phylogenetic analysis on the cox1 and 16S rRNA genes. Three phylogenetic groups of R. haemaphysaloides were recognized and found to be related closely to strains from China. H. cornigera and H. mageshimaensis formed one phylogenetic group, presumably from tick strains prevalent in Japan and China. The haplotype network analysis indicated that R. microplus is classed into 26 and 6 haplotypes, which correspond to cox1 and 16S rRNA gene assemblages, respectively. In addition, four cox1 haplotypes were detected in R. sanguineus. This is the first evidence that suggests genetic diversity, host range and geographical distribution of hard ticks in Hainan Island, China.

Parkinson’s disease (PD) is a chronic progressive neurodegenerative disease commonly seen in aged people, in which gastrointestinal dysfunction is the most common nonmotor symptom and the activation of the gut–brain axis by intestinal inflammation may contribute to the pathogenesis of PD. In a previous study, curcumin was considered neuroprotective in PD, and this neuroprotective mechanism may act by inhibiting intestinal inflammation. Therefore, the aim of this study was to evaluate the effect of curcumin on motor dysfunction and the loss of dopaminergic neurons in a PD mouse model, induced by N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) using open field test and pole test behavioral assessments and the immunofluorescence and Western blot methods. Moreover, the effects of curcumin on gastrointestinal dysfunction, gastric barrier function, pro-inflammatory cytokines, and the SIRT1/NRF2 pathway in intestinal tissues in a PD mouse model were assessed using fecal parameters and intestinal dynamics, immunofluorescence, ELISA, and Western blot. A motor impairment study of an MPTP-induced mouse group prior to treatment with curcumin had a lower total movement distance and a slow average speed, while there was no statistical difference in the curcumin group. After treatment with curcumin, the total movement distance and average speed improved, the tyrosine hydroxylase (TH) rate in the substantia nigra pars compacta (SNpc) and striatum were reduced, the pyroptosis of AIM2 and caspase-1 activations were inhibited, and intestinal inflammatory factors and intestinal inflammation were reduced. Curcumin improved gastrointestinal disorders and gastrointestinal barrier function in the MPTP-induced mice and reversed MPTP-induced motor dysfunction and dopaminergic neuron loss in mice. The above effects may be partly dependent on curcumin activation of the SIRT1/NRF2 pathway in the colon. This study provides a potential opportunity to develop new preventive measures and novel therapeutic approaches that could target the gut–brain axis in the context of PD and provide a new intervention in the treatment of Parkinson’s disease.

Background: Growing evidence points to the pivotal role of vitamin D in the pathophysiology and treatment of major depressive disorder (MDD). However, there is a paucity of longitudinal research investigating the effects of vitamin D supplementation on the brain of MDD patients.Methods: We conducted a double-blind randomized controlled trial in 46 MDD patients, who were randomly allocated into either VD (antidepressant medication + vitamin D supplementation) or NVD (antidepressant medication + placebos) groups. Data from diffusion tensor imaging, resting-state functional MRI, serum vitamin D concentration, and clinical symptoms were obtained at baseline and after an average of 7 months of intervention.Results: Both VD and NVD groups showed significant improvement in depression and anxiety symptoms but with no significant differences between the two groups. However, a greater increase in serum vitamin D concentration was found to be associated with greater improvement in depression and anxiety symptoms in VD group. More importantly, neuroimaging data demonstrated disrupted white matter integrity of right inferior fronto-occipital fasciculus along with decreased functional connectivity between right frontoparietal and medial visual networks after intervention in NVD group, but no changes in VD group.Conclusions: These findings suggest that vitamin D supplementation as adjunctive therapy to antidepressants may not only contribute to improvement in clinical symptoms but also help preserve brain structural and functional connectivity in MDD patients.

Background: Aedes aegypti , the principal vector of dengue and other arboviruses, is widely distributed in Pakistan, yet its population genetics and endosymbiont status remain poorly characterized. This study aimed to investigate the genetic structure, haplotype diversity, and phylogeographic patterns of Ae. aegypti in dengue-endemic regions of Pakistan, and to screen for natural Wolbachia infections to provide baseline data for surveillance and vector control. Methods: Ovitrap collections were conducted in 2021 across the provinces of Punjab (Bakkar) and Khyber Pakhtunkhwa (Charsadda, DI Khan, Kohat, and two sites within Peshawar: Hayat Abad and Tarnab). Following the morphological identification of adult Ae. aegypti , we extracted genomic DNA from confirmed specimens to amplify and sequence a 658-bp fragment of the mitochondrial cytochrome c oxidase I ( COI ) gene. Phylogenetic analyses, haplotype network construction, and population differentiation statistics were performed. Additionally, 300 field-caught adult mosquitoes were screened for Wolbachia using validated conventional and quantitative PCR assays targeting the Wolbachia surface protein ( wsp ) gene. Results: Phylogenetic analysis of 166 COI sequences (92 from Pakistan) revealed a monophyletic Ae. aegypti clade with 99.65–100% sequence identity, with Pakistani isolates clustering with those from Saudi Arabia, Iran, and India. In total, 13 global haplotypes were identified, with Hap_3 dominating (53%) and shared across regions. Within Pakistan, eight haplotypes were detected, including region-specific variants, yielding high overall diversity (Hd 0.69; π = 0.007). District-level analysis showed that DI Khan and Bakkar had the highest haplotype diversity (Hd 0.73 and 0.71) but low nucleotide diversity ( π = 0.005–0.006), whereas Kohat exhibited no haplotype diversity. Population structure was higher in Pakistan (FST 0.26; Nm 0.7) than globally (FST 0.17; Nm 1.19), consistent with low gene flow among Pakistani populations. No natural Wolbachia infections were detected in Ae. aegypti . Conclusions: Aedes aegypti in Pakistan belong to a globally monophyletic lineage and show moderate mitochondrial diversity with higher population structure than the global population. The lack of detected Wolbachia infections suggests that natural strains are either absent or occur at very low prevalence. These findings provide a baseline for surveillance and support integrating Wolbachia -based biocontrol alongside conventional interventions in Pakistan. Graphical

Objectives: Altered expression of microRNAs (miRNAs) may contribute to disease vulnerability. Studies have reported the involvement of miRNA in the pathophysiology of ischemic stroke.Methods: We performed a meta-analysis of data from 6 studies that used a panel of miRNAs with altered expressions to diagnose ischemic stroke with the Bayesian framework. The I² test and Cochran's Q-statistic were used to assess heterogeneity. Funnel plots were generated and publication bias was assessed using Begg and Egger tests.Results: On summary receiver operating characteristics (SROC) curve analysis, the pooled sensitivity and specificity of altered miRNA expressions for diagnosis of ischemic stroke was 0.92 (95% confidence interval [CI] 0.80–0.97) and 0.83 (95% CI 0.71–0.90), respectively; the diagnostic odds ratio was 54.35 (95% CI 20.39–144.92), and the area under the SROC curve was 0.93 (95% CI 0.90–0.95).Conclusions: Our results showed a link between dysregulation of miRNAs and the occurrence of ischemic stroke. Abnormal miRNA expression may be a potential biomarker for ischemic stroke.