BMC Neuroscience[JOURNAL]
Sun
200 papers
Post-stroke butyrate treatment shows sex-dependent microglial responses but does not improve outcomes in a mouse model of endothelin-1 sensory motor stroke.
de Witte A, Montoya Sanchez J, Daniele E … +8 more , Chen J, Fan Y, Khatri P, Lozano Casasbuenas D, Zhang A, Todd KG, Faiz M, Churchward M
BMC Neurosci · 2025 Jul · PMID 40676515 · Full text
BACKGROUND: Stroke induces gut dysbiosis and reduces microbial production of short-chain carboxylic acids (SCCAs), which negatively correlates with stroke outcomes. Previous studies have demonstrated that SCCA supplement...
BACKGROUND: Stroke induces gut dysbiosis and reduces microbial production of short-chain carboxylic acids (SCCAs), which negatively correlates with stroke outcomes. Previous studies have demonstrated that SCCA supplementation can improve functional recovery, with one recent study suggesting this occurs via modulation of microglial responses. However, the effects of individual SCCAs on microglial responses remain unclear, particularly across sexes and following a more clinically relevant, post-stroke treatment protocol. To address this gap, we investigated the effect of post-stroke supplementation with butyrate on stroke outcomes and microglial responses in both male and female mice over time. RESULTS: Post-stroke butyrate treatment produced sex-specific microglial responses. In females, butyrate increased microglial ramification at chronic timepoints in vivo and enhanced IL6 release following IFNγ stimulation in vitro. These microglial changes were not observed in males. Despite the distinct microglial responses, butyrate treatment did not correlate with improved stroke outcomes in either sex, as measured by lesion volume and functional recovery. CONCLUSIONS: Our findings reveal previously unknown sex differences in microglial responses to butyrate following stroke. Despite these microglial changes in females, butyrate treatment did not improve functional outcomes in either sex, suggesting that sex-specific optimization of dosing and delivery may be needed for therapeutic efficacy.
Tamibarotene promotes differentiation of neuroblastoma SH-SY5Y cells into neurons, which is associated with activation of the PI3K/AKT signaling pathway.
Zhang J, XiangWei W, Zhang F … +5 more , Yi H, Yan W, Li X, Gao K, Jiang Y
BMC Neurosci · 2025 Jul · PMID 40665231 · Full text
Tamibarotene, a synthetic retinoid used in the treatment of acute promyelocytic leukemia, has been reported to induce differentiation in the SH-SY5Y cell line into neurons. However, the underlying mechanisms remain uncle...
Tamibarotene, a synthetic retinoid used in the treatment of acute promyelocytic leukemia, has been reported to induce differentiation in the SH-SY5Y cell line into neurons. However, the underlying mechanisms remain unclear. This study aimed to determine the optimal concentration of Tamibarotene (Am80) for promoting neuronal differentiation and to elucidate the underlying molecular mechanisms. SH-SY5Y cells were treated with Am80 at various concentrations, and the effects on cell morphology, gene expression, cell proliferation and apoptosis assessed using immunofluorescence, Western blotting, qPCR, and RNA sequencing. Results indicated that that 1µM Am80 effectively promoted neuronal differentiation, upregulating neuronal markers and the KCNT1 gene, while downregulating tumor-related genes MYC and CXCR4. The differentially expressed genes are predominantly enriched in the PI3K-Akt signaling pathway, with upregulation of genes related to neuronal development such as NTRK2, RET, and CNR1, and downregulation of tumor-related genes including MYC and CXCR4. Inhibition of the PI3K/Akt signaling pathway using LY294002 resulted in a decreased efficacy of AM80-induced differentiation in SH-SY5Y cells, along with downregulation of neuronal marker expression. These findings suggest that Am80 can effectively promote the differentiation of SH-SY5Y cells into neurons and reduce the proliferation of neuroblastoma cells, which is related to the PI3K/AKT pathway, providing a good model for the study of nervous system diseases.
Effects of arabinoxylan on BDNF/TrkB/p-CREB signaling pathway in the prefrontal cortex and intestinal microbiome in post-stroke depressed rats.
Bi BY, Lin L, Huang L … +5 more , Zhou J, Yan WJ, Huang L, Wang J, Li XB
BMC Neurosci · 2025 Jul · PMID 40653476 · Full text
AIM: To explore the effects of arabinoxylan on the BDNF/TrkB/p-CREB signaling pathway in the prefrontal cortex of post-stroke depressed rats, and to explore its neuronal protective effects through the microbial-gut-brain...
AIM: To explore the effects of arabinoxylan on the BDNF/TrkB/p-CREB signaling pathway in the prefrontal cortex of post-stroke depressed rats, and to explore its neuronal protective effects through the microbial-gut-brain axis in the regulation of this pathway. METHODS: The rat model of post-stroke depression (PSD) was established by middle cerebral artery occlusion (MCAO) combined with chronic unpredictable mild stimulation (CUMS). They were randomly divided into 5 groups (blank control, post-stroke depression, arabinoxylan, fluoxetine hydrochloride, fluoxetine hydrochloride combined arabinoxylan). The rats were treated differently for 28 days according to their grouping. Body mass, sugar and water consumption experiments and open-field experiments were used to evaluate the behavior of rats. The pathological changes were observed by H&E staining. The expression levels of amine neurotransmitters were detected by ELISA. The expression levels of BDNF mRNA and BDNF, TrkB and p-CREB were detected by RT-PCR and Western blot. The analysis of intestinal metagenomics was conducted by 16 S rDNA sequencing. RESULTS: Compared with the post-stroke depression group, the body weight, activity and sugar water consumption rate of the arabinoxylan group were increased. The expression levels of 5-HT in the prefrontal cortex, colon and serum levels of 5-HT, DA and NE were increased. The expression levels of BDNF mRNA and BDNF, TrkB and P-CREB in the prefrontal cortex were also upregulated. The number of neurons in the prefrontal cortex increased; Colon mucosal injury and inflammatory cell infiltration decreased, the intestinal microbial diversity increased; The relative abundance of probiotics such as bifidobacterium, Christensenia, Dubosiella New York and ruminococcus increased. The relative abundance of Prevotella NK3B31 group was reduced. The level of 5-HT in the prefrontal cortex was negatively correlated with the abundance of Prevotellaceae NK3B31 group. CONCLUSION: Arabinoxylan improved depressive-like behavior in rats and its neuroprotective role was achieved by promoting the growth of intestinal probiotics, improving the intestinal barrier, affecting the BDNF/TrkB/p-CREB signaling pathway, and increasing the expression levels of monoamine neurotransmitters 5-HT, DA and NE.
Gut Microbiome rewiring via fecal transplants: Uncovering therapeutic avenues in Alzheimer's disease models.
Upadhyay P, Kumar S, Tyagi A … +3 more , Tyagi AR, Barbhuyan T, Gupta S
BMC Neurosci · 2025 Jul · PMID 40615821 · Full text
BACKGROUND: Emerging evidence implicates the gut microbiome in Alzheimer's disease (AD) pathogenesis, yet the underlying mechanisms remain elusive. This study elucidates the bidirectional relationship between gut microbi...
BACKGROUND: Emerging evidence implicates the gut microbiome in Alzheimer's disease (AD) pathogenesis, yet the underlying mechanisms remain elusive. This study elucidates the bidirectional relationship between gut microbiota and AD using fecal microbiota transplantation (FMT) in a mouse model. RESULT: Through meticulous experimentation, we conducted reciprocal FMT between AD (5xFAD) and healthy (C57BL/6) mice to unravel the impact of gut microbiome alterations on cognitive function and neuroinflammation. FMT from 5xFAD to C57BL/6 mice induced profound memory impairment and cognitive deficits, accompanied by elevated inflammatory cytokine levels, oxidative stress markers, and systemic inflammation, as evidenced by increased plasma cytokines. Conversely, transplanting healthy microbiota into 5xFAD mice yielded remarkable behavioral improvements, including enhanced spatial memory performance in the Morris water maze, directly correlating with cognitive recovery. Our findings underscore the pivotal role of the gut microbiome in AD pathogenesis and offer a promising therapeutic avenue. CONCLUSION: Targeted modulation of the gut microbiome through strategies like FMT may offer potential benefits in Alzheimer's disease by influencing neuroinflammation, oxidative stress, and cognitive function. This comprehensive study provides novel insights into the gut-brain axis dynamics and paves the way for innovative microbiome-based interventions in AD management.
Shikonin inhibits epithelial-mesenchymal transition in glioblastoma cells by upregulating p53 and promoting miR-361-5p level to suppress ZEB1 expression.
Zhang F, Liu Z, Wang Y … +5 more , Zuo L, Xu S, Liu Y, Liang H, Xue Y
BMC Neurosci · 2025 Jul · PMID 40597639 · Full text
OBJECTIVE: Shikonin, an active compound from the rhizome of Lithospermum erythrorhizon, exerts anti-tumor effects in various cancers, including glioblastoma multiforme (GBM). This study explored the mechanism of Shikonin...
OBJECTIVE: Shikonin, an active compound from the rhizome of Lithospermum erythrorhizon, exerts anti-tumor effects in various cancers, including glioblastoma multiforme (GBM). This study explored the mechanism of Shikonin for inhibiting the migration and invasion of GBM cells, providing a rationale for developing novel glioma therapies. METHODS: The effects of Shikonin on GBM cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) were detected by CCK-8, scratch wound-healing, Transwell, and Western blot assays. The effect of Shikonin on miR-361-5p expression in GBM cells was examined by RT-qPCR and the effect of miR-361-5p inhibitor transfection on proliferation, migration, invasion, and EMT in Shikonin-treated GBM cells was examined. Shikonin's target genes were identified and validated using dual luciferase reporter gene assay and chromatin immunoprecipitation (ChIP) assay, focusing on its induction of miR-361-5p expression. The downstream target genes of miR-361-5p were also identified and validated under Shikonin action. A GBM cell nude mouse xenograft tumor was established to confirm the regulatory role of Shikonin. RESULTS: Shikonin inhibited cell proliferation, migration, invasion, and EMT and upregulated miR-361-5p expression in GBM cells. Shikonin upregulated the glioma-associated protein p53, which promoted miR-361-5p transcription. miR-361-5p inhibited ZEB1 expression. Therefore, Shikonin inhibited GBM cell proliferation, migration, invasion, and EMT via p53/ miR-361-5p/ ZEB1 axis in vitro and in vivo. CONCLUSION: Shikonin suppresses glioma cell proliferation, migration, invasion, and EMT by inhibiting ZEB1 expression through the p53/miR-361-5p axis.
Zebrafish mecp2 null-mutation increases anxiety and cortisol levels but no change in adult social preference and larval chemically-induced hyperlocomotion.
Shams S, Cronell P, Landin J … +4 more , Pietri T, Gimdal AE, Kettunen P, Westberg L
BMC Neurosci · 2025 Jul · PMID 40596833 · Full text
BACKGROUND: Methyl CpG binding protein 2 (MECP2) is an essential global modulator of transcription and mutations in MECP2 are the most common cause of Rett syndrome, an X-linked neurodevelopmental disorder. Patients diag...
BACKGROUND: Methyl CpG binding protein 2 (MECP2) is an essential global modulator of transcription and mutations in MECP2 are the most common cause of Rett syndrome, an X-linked neurodevelopmental disorder. Patients diagnosed with Rett syndrome have increased risk for epilepsy as well as problems with anxiety and social communication. Using the zebrafish mecp2 line, this study aimed to increase our understanding of the role of Mecp2 function in regulation of pharmacologically-induced hyperlocomotion, developmental social preference, and adult socialization, anxiety-related behaviour, and baseline cortisol levels. To determine responses of mecp2 zebrafish to a stimulating convulsant, general locomotor activity was measured at 5 days post-fertilization (dpf) in sibling mecp2, mecp2, and mecp2 fish after treatment with a GABA receptor antagonist pentylenetetrazol (PTZ) at varying concentrations. Responses to social stimulus were investigated in juvenile (21 dpf) and adult mecp2 and mecp2 fish. Anxiety responses to a novel tank and whole-body cortisol levels were also measured in adult mecp2 and control mecp2 zebrafish. RESULTS: The behavioural tests showed that mecp2 zebrafish displayed hypolocomotion at the larval stage, along with increased freezing time and thigmotaxis, and higher whole-body cortisol levels in adulthood. However, the hyper-locomotion response to PTZ at 5 dpf and social preference for visual social stimulus at 21 dpf and in adulthood were not affected by the lack of functional Mecp2. CONCLUSIONS: Functional Mecp2 modulated larval locomotion and behavioural anxiety at different ages and adult cortisol levels, but mecp2 null-mutation did not alter adult locomotion and socialization, and developmental sociability and PTZ-induced hyperlocomotion in zebrafish. Given the variability reported in patients and in rodent Mecp2 knockout models, studies using zebrafish can explore vital elements of MECP2's role across development and improve our understanding of neural mechanisms underlying neurodevelopmental disorders.
Memantine mitigates methamphetamine-induced impairments in social and recognition memories in rats.
Khodamoradi M, Allameh Y, Sarani M … +3 more , Zarei SA, Faaliat S, Ghazvini H
BMC Neurosci · 2025 Jun · PMID 40474066 · Full text
BACKGROUND: Methamphetamine (METH) is a widely abused neurotoxic substance that can lead to neurocognitive disabilities. Recent studies have shown that memantine (MEM), an NMDA receptor antagonist, can improve cognitive...
BACKGROUND: Methamphetamine (METH) is a widely abused neurotoxic substance that can lead to neurocognitive disabilities. Recent studies have shown that memantine (MEM), an NMDA receptor antagonist, can improve cognitive function across various disorders. Given that previous studies have revealed that exposure to METH leads to several social and cognitive impairments, this research aimed to investigate the effects of MEM on social memory, social behavior, and novel object recognition impairments caused by chronic METH exposure. Adult male Wistar rats received a regimen of METH, which causes neurotoxicity (four injections of 6 mg/kg, s.c., at 2-h intervals). After one week, the effects of MEM (5 mg/kg, i.p.) on novel object recognition memory and social behaviors in the experimental groups were examined. RESULTS: Animals exposed to the METH regimen exhibited significant impairments in the acquisition, consolidation, and retrieval stages of novel object recognition memory. However, treatment with MEM ameliorated the detrimental effects of METH on the acquisition, consolidation, and retrieval, but not the reconsolidation, of novel object recognition memory. Additionally, the results revealed that METH-triggered deficits in social interaction and behavior were improved by MEM treatment. CONCLUSIONS: In conclusion, this study demonstrated that MEM administration effectively ameliorated memory impairments induced by chronic METH exposure. These findings provide valuable insights into the neuroprotective effects of MEM on novel object memory, social memory, and social behaviors.
Pro-cognitive efficacy of Prospekta in a rat model of age-associated cognitive impairment.
Kardash E, Petrova N, Ganina K … +2 more , Tarasov S, Epstein O
BMC Neurosci · 2025 Jun · PMID 40468185 · Full text
BACKGROUND: Ageing is associated with lower levels of cognitive performance, and novel therapeutics are warranted to correct this defect. Aged rats represent a favourable model of human ageing. The aim of the present stu...
BACKGROUND: Ageing is associated with lower levels of cognitive performance, and novel therapeutics are warranted to correct this defect. Aged rats represent a favourable model of human ageing. The aim of the present study is to examine the effect of a novel neurotropic S100B-targeted drug, Prospekta, on the parameters of delayed alternation in the aged rats compared to responses in the young animals. METHODS: A spatial working memory task in an operant chamber, where aged and young animals (21 and 2 months old, respectively) needed to alternate between two retractable levers on a trial-by-trial basis to receive a food reward, was tested. We also assessed the Prospekta's effect on expression of some biomarkers of ageing by measuring their levels in the brains of aged rats using Western blot. RESULTS: Treatment with Prospekta ameliorated cognitive functions, which resulted in a significant reduction of simple and choice reaction times for aged rats. The drug also decreased the number of omission errors at the beginning of the acquisition phase, which indicated the influence of treatment on attention and decision-making process. At the same time, Prospekta did not affect the majority of parameters measured in young animals. The analysis of ageing biomarker expression did not reveal any significant differences between aged rats treated with Prospekta or placebo. CONCLUSIONS: The findings of this study underscore the potential of Prospekta as a promising pro-cognitive agent for the treatment of age-related cognitive decline. However, further research is imperative to elucidate the precise mechanisms underlying its therapeutic effects and validate its efficacy in vivo. CLINICAL TRIAL NUMBER: Not applicable.
Eosinophils differentially affect early and delayed neurological deterioration after mechanical thrombectomy in stroke.
Yu S, Yang J, Han X … +3 more , Shi J, Xiao G, Guo Z
BMC Neurosci · 2025 Jun · PMID 40461970 · Full text
BACKGROUND: To investigate the effect of eosinophils on early (END) and delayed neurological deterioration (DND) after mechanical thrombectomy (MT) in patients with acute ischemic stroke (AIS). METHODS: A total of 442 co...
BACKGROUND: To investigate the effect of eosinophils on early (END) and delayed neurological deterioration (DND) after mechanical thrombectomy (MT) in patients with acute ischemic stroke (AIS). METHODS: A total of 442 consecutive AIS patients experiencing MT between May 2017 and January 2023 were analyzed. END and DND were defined as a rise of ≥ 2 points on the National Institutes of Health Stroke Scale (NIHSS) or a fall of ≥ 1 point on the Glasgow Coma Scale or death from baseline to 24 h and from 24 to 72 h, respectively. Multivariate regression analysis, generalize additive models and mediation analysis were used to assess the effect of eosinophils on END and DND and the underlying mechanisms. RESULTS: 113 (25.17%) and 47 (10.63%) patients had END and DND, respectively. Eosinophils was independently associated with END after adjusting potential confounders (odds ratio, 0.00; 95% CI, 0.00-0.80; P = 0.0441), which is consistent with the result of eosinophils (dichotomous) as a categorical variable (odds ratio, 0.40; 95% CI, 0.24-0.68; P = 0.0006). In assessing the relationship between eosinophils and DND, the inflection point was found to be 0.02, and eosinophils were independently correlated with DND at less than 0.02 (odds ratio, 0.00, 95% CI: 0.00-0.00, P = 0.0038); however, eosinophils ceased to be independently correlated with DND after exceeding 0.02 (P = 0.3519). Mediation analyses confirmed that eosinophils contribute to END in patients through symptomatic intracranial hemorrhage (indirect effect: -0.463; 95%CI: -0.902-0.19; P < 0.001). CONCLUSIONS: The effects of eosinophils on END and DND are not identical.
Correction to: Association between apolipoprotein E Ε4 status and the risk of Alzheimer's disease: a meta-analysis.
Ren Z, Guan Z, Guan Q … +2 more , Guan H, Che H
BMC Neurosci · 2025 May · PMID 40420301 · Full text
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The short-term spinal cord stimulation improves the rates of tracheal decannulation in patients of brain injury with disorders of consciousness.
Huang G, Wang D, Chen Q … +4 more , Zhong Q, Huang W, Zhou X, Jiang Q
BMC Neurosci · 2025 May · PMID 40419961 · Full text
OBJECTIVE: To evaluate the efficacy of short-term spinal cord stimulation (stSCS) in promoting tracheal decannulation among patients with brain injury-induced disorders of consciousness(DoC). METHODS: A retrospective coh...
OBJECTIVE: To evaluate the efficacy of short-term spinal cord stimulation (stSCS) in promoting tracheal decannulation among patients with brain injury-induced disorders of consciousness(DoC). METHODS: A retrospective cohort study was conducted on 81 tracheotomized brain injury patients with DoC treated at Ganzhou People's Hospital between June 2021 and June 2022.Patients were divided into two groups: the stSCS group (n = 46) receiving stSCS intervention and the control group (n = 35) receiving standard care. Decannulation success rates were compared using chi-square tests. RESULTS: The stSCS group demonstrated a significantly higher decannulation rate compared to the control group (50.0%vs.25.7%, χ²=5.24, p = 0.022). CONCLUSION: stSCS significantly enhances tracheal decannulation success in brain injury patients with DoC, suggesting its potential as a therapeutic neuromodulation strategy. CLINICAL TRIAL NUMBER: Not applicable.
The role of the contralesional primary motor cortex in upper limb recovery after stroke: a scoping review following PRISMA-ScR guidelines.
Suputtitada P, Costa V, Fregni F
BMC Neurosci · 2025 May · PMID 40414854 · Full text
BACKGROUND: Stroke often results in motor impairments, with recovery involving complex interactions between the lesioned (ipsilesional) and non-lesioned (contralesional) hemispheres. This scoping review investigates the...
BACKGROUND: Stroke often results in motor impairments, with recovery involving complex interactions between the lesioned (ipsilesional) and non-lesioned (contralesional) hemispheres. This scoping review investigates the role of the contralesional primary motor cortex (M1) in motor recovery of the paretic upper limb following stroke, examining its structural and functional changes and compensatory roles. METHODS: A systematic search for scoping review was conducted in PubMed, Embase, Web of Science, and Google Scholar following PRISMA-ScR guidelines. Studies examining contralesional M1 contributions to upper limb recovery in humans and animal models were included. Data were extracted, synthesized qualitatively, and assessed for risk of bias using SYRCLE and Cochrane tools. RESULTS: A total of 38 studies were included in the analysis, consisting of 34 focused on stroke patients and 4 utilizing animal models. The findings revealed the dual and task-specific role of the contralesional primary motor cortex (M1) in upper limb recovery after stroke. In patients with severe motor impairments, contralesional M1 supported recovery through compensatory mechanisms, such as increased neuronal recruitment and functional reorganization. However, in cases with mild impairments, its activation was associated with inhibitory effects on ipsilesional reorganization, potentially delaying optimal recovery. Animal studies provided evidence of structural and functional plasticity, including dendritic remodeling and enhanced neuronal connectivity, which paralleled improvements in motor function. In human studies, contralesional M1 activation was task-dependent, with pronounced engagement during demanding tasks and unimanual movements. Ipsilateral motor deficits, including reduced dexterity, strength, and coordination, were commonly reported and underscored the disrupted interhemispheric dynamics influencing recovery. Neuromodulation techniques showed promise in modulating interhemispheric interactions and enhancing motor outcomes. These results emphasize the complex interplay between compensatory and inhibitory processes mediated by contralesional M1 in stroke recovery. CONCLUSION: The contralesional M1 plays a complex, task-specific role in upper limb recovery after stroke, acting as both a compensatory resource and a potential inhibitory factor. Future research should stratify patients by impairment severity to refine therapeutic approaches. CLINICAL TRIAL NUMBER: Not applicable.
Body weight-supported treadmill training reduces glial scar overgrowth in SCI rats by decreasing the reactivity of astrocytes during the subacute phase.
Cai J, Wang Y, Zhai C … +8 more , Jiang K, Wang Z, Fang L, Li X, Zhu C, Liu W, Wang T, Wu Q
BMC Neurosci · 2025 Apr · PMID 40295901 · Full text
BACKGROUND: Spinal cord injury is followed by glial scar formation, which was long seen mainly as a physical barrier preventing axonal regeneration. Glial scar astrocytes lead to glial scar formation and produce inhibito...
BACKGROUND: Spinal cord injury is followed by glial scar formation, which was long seen mainly as a physical barrier preventing axonal regeneration. Glial scar astrocytes lead to glial scar formation and produce inhibitory factors to prevent axons from growing through the scar, while inhibiting the conversion of reactive astrocytes into glial scar-forming astrocytes may represent an ideal treatment for CNS injury. Exercise is a non-invasive and effective therapeutic intervention for clinical rehabilitation of spinal cord injury. However, its precise therapeutic mechanisms still need to be continuously explored. METHODS: 30 rats were randomly assigned to three groups (Sham, SCI, SCI + BWSTT; n = 10 rats per group). In this study, we employed the BBB scales and gait analysis system to examine the behavioral functions of the rats in each group. Furthermore, we utilized immunoblotting of spinal cord tissue at the injury site, in addition to histological staining and immunofluorescence staining, to explore glial scar aggregation and axonal regeneration in each group of rats. RESULTS: Our results revealed that hindlimb motor function was significantly improved in SCI rats after a sustained subacute period of BWSTT, accompanied by the promotion of histological repair and nerve regeneration. Subsequent immunofluorescence staining and immunoblotting showed diminished astrocyte reactivity in the region surrounding the spinal cord injury as well as reduced expression and distribution of collagen fibers near the lesion after BWSTT. Additionally, a significant decrease in the expression of MMP-2/9, which is closely related to astrocyte migration, was observed in the vicinity of spinal cord tissue lesions. CONCLUSION: Our study demonstrates that a sustained BWSTT intervention during the subacute phase of spinal cord injury can effectively reduce astrocyte reactivity and glial scarring overgrowth, thereby facilitating functional recovery after SCI.
CHIRP-Seq: FOXP2 transcriptional targets in zebra finch brain include numerous speech and language-related genes.
Gedman GL, Kimball TH, Atkinson LL … +5 more , Factor D, Vojtova G, Farias-Virgens M, Wright TF, White SA
BMC Neurosci · 2025 Apr · PMID 40281419 · Full text
BACKGROUND: Vocal learning is a rare, convergent trait that is fundamental to both human speech and birdsong. The Forkhead Box P2 (FOXP2) transcription factor appears necessary for both types of learned signals, as human...
BACKGROUND: Vocal learning is a rare, convergent trait that is fundamental to both human speech and birdsong. The Forkhead Box P2 (FOXP2) transcription factor appears necessary for both types of learned signals, as human mutations in FOXP2 result in speech deficits, and disrupting its expression in zebra finches impairs male-specific song learning. In juvenile and adult male finches, striatal FOXP2 mRNA and protein decline acutely within song-dedicated neurons during singing, indicating that its transcriptional targets are also behaviorally regulated. The identities of these targets in songbirds, and whether they differ across sex, development and/or behavioral conditions, are largely unknown. RESULTS: Here we used chromatin immunoprecipitation followed by sequencing (ChIP-Seq) to identify genomic sites bound by FOXP2 in male and female, juvenile and adult, and singing and non-singing birds. Our results suggest robust FOXP2 binding concentrated in putative promoter regions of genes. The number of genes likely to be bound by FOXP2 varied across conditions, suggesting specialized roles of the candidate targets related to sex, age, and behavioral state. We interrogated these binding targets both bioinformatically, with comparisons to previous studies, and biochemically, with immunohistochemistry using an antibody for a putative target gene. Gene ontology analyses revealed enrichment for human speech- and language-related functions in males only, consistent with the sexual dimorphism of song learning in this species. Fewer such targets were found in juveniles relative to adults, suggesting an expansion of this regulatory network with maturation. The fewest speech-related targets were found in the singing condition, consistent with the well-documented singing-driven down-regulation of FOXP2 in the songbird striatum. CONCLUSIONS: Overall, these data provide an initial catalog of the regulatory landscape of FOXP2 in an avian vocal learner, offering dozens of target genes for future study and providing insight into the molecular underpinnings of vocal learning.
Retraction Note: MK801 attenuates secondary injury in a mouse experimental compression model of spinal cord trauma.
Esposito E, Paterniti I, Mazzon E … +5 more , Genovese T, Galuppo M, Meli R, Bramanti P, Cuzzocrea S
BMC Neurosci · 2025 Apr · PMID 40229701 · Full text
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Hippocampal functional imaging-derived radiomics features for diagnosing cognitively impaired patients with Parkinson's disease.
Zeng W, Liang X, Guo J … +6 more , Cheng W, Yin Z, Hong D, Li F, Zhou F, Fang X
BMC Neurosci · 2025 Mar · PMID 40155831 · Full text
PURPOSE: The aim of this retrospective study was to investigate whether radiomics features derived from hippocampal functional imaging can effectively differentiate cognitively impaired patients from cognitively preserve...
PURPOSE: The aim of this retrospective study was to investigate whether radiomics features derived from hippocampal functional imaging can effectively differentiate cognitively impaired patients from cognitively preserved patients with Parkinson's disease (PD). METHODS: The study included a total of 89 clinically definite PD patients, comprising 55 who werecognitively impaired and 34 who were cognitively preserved. All participants underwent functional magnetic resonance imaging and clinical assessments. Preprocessed functional data were utilized to derive the amplitude of the low-frequency fluctuations (ALFF), regional homogeneity (ReHo), voxel-mirrored homotopic connectivity (VMHC), and degree centrality (DC). A standardized set of radiomics features was subsequently extracted from the bilateral hippocampi, resulting in a total of 819 features. Following feature selection, the radiomics score (rad-score) and logistic regression (LR) models were trained. Additionally, the Shapley additive explanations (SHAP) algorithm was employed to elucidate and interpret the predictions made by the LR models. Finally, the relationships between the radiomics features derived from hippocampal functional imaging and the scores of the clinical measures were explored to assess their clinical significance. RESULTS: The rad-score and LR algorithm models constructed using a combination of wavelet features extracted from ReHo and VMHC data exhibited superior classification efficiency. These models demonstrated exceptional accuracy, sensitivity, and specificity in distinguishing cognitively impaired PD patients (CI-PD) from cognitively preserved PD (CP-PD) patients, with values of 0.889, 0.900, and 0.882, respectively. Furthermore, SHAP values indicated that wavelet features derived from ReHo and VMHC were critical for classifying CI-PD patients. Importantly, our findings revealed significant associations between radiomics wavelet features and scores on the Hamilton Anxiety Scale, Non-Motor Symptom Scale, and Montreal Cognitive Assessment in CI-PD patients (P < 0.05, with Bonferroni correction). CONCLUSIONS: Our novel rad-score model and LR model, which utilize radiomics features derived from hippocampal functional imaging, have demonstrated their value in diagnosing CI-PDpatients. These models can enhance the accuracy and efficiency of functional MRI diagnosis, suggesting potential clinical applications. CLINICAL TRIAL NUMBER: Not applicable.
Experimental orthodontic pain drives anxiety state through the induction of alterations to the neuronal architecture in hippocampus.
Que H, Wang Y, Feng Y … +6 more , Tu S, Wei J, Cheung C, Wei N, Chen Z, Ai H
BMC Neurosci · 2025 Mar · PMID 40114067 · Full text
BACKGROUND: To explore the effect and mechanism of hippocampus on experimental orthodontic pain-induced anxiety. METHODS: Herein, we document a novel modeling method whereby the nickel-titanium (Ni-Ti) orthodontic wire w...
BACKGROUND: To explore the effect and mechanism of hippocampus on experimental orthodontic pain-induced anxiety. METHODS: Herein, we document a novel modeling method whereby the nickel-titanium (Ni-Ti) orthodontic wire was fixed stably in the oral cavity of mice with a ligation technique to induce stable distal movement of maxillary incisors to mimic orthodontic tooth movement. At the experimental endpoint, serum corticosterone assay, Golgi staining and Micro-CT were performed in each group after oral-facial mechanical pain sensitivity assessment and open field test. RESULTS: The mechanical pain sensitivity of experimental tooth movement pain (ETMP) mice had an apparent increased elicited following tooth movement. And anxiety-like behavior was developed: reduced the time proportion of center zone and the total moving distance in the open field test and the elevated serum corticosterone levels in ETMP mice relative to control group mice. The Golgi staining in ventral hippocampal CA1 revealed that neural spine density, dendritic length and number of dendrites are reduced markedly in ETMP mice compared with the control group. CONCLUSION: Experimental orthodontic pain drives emotional anxiety through the plasticity changes in decreased neuronal complexity and reduced spine density in ventral hippocampal CA1 in mice.
Risk taking behaviour predicts consistent and heritable coping styles in zebrafish.
Koets L, van der Kwaak T, Schaaf M … +1 more , Tudorache C
BMC Neurosci · 2025 Mar · PMID 40114049 · Full text
BACKGROUND: Coping styles are individually coherent sets of behavioural and physiological responses to stress. Coping styles are thought to remain consistent across context and time, and display a certain level of herita...
BACKGROUND: Coping styles are individually coherent sets of behavioural and physiological responses to stress. Coping styles are thought to remain consistent across context and time, and display a certain level of heritability. Here, we examined whether risk taking is a predictor for consistency and heritability of stress coping styles in both larval and adult zebrafish (Danio rerio). RESULTS: A group emergence test where fish emerge from a familiar housing compartment into a potentially dangerous novel environment, established the level of risk taking of F0 generation adult zebrafish. The degree of risk taking appeared to be consistent over time and context. Then, the F0 risk taking degree was further correlated with various behavioural parameters related to stress coping of the F1 and F2 generations. In larval fish, these parameters were measured during a light dark challenge which elicits an anxiety like response. In adults, they were measured during a single emergence test and a combined open field and mirror biting test, estimating the degree of risk taking and the level of explorativeness and aggressiveness. The results show that (i) parental risk taking behaviour is a good predictor for a large number of larval and adult behavioural parameters, within and between generations; (ii) a number of these parameters are consistent over ontogenetic (larval and adult) stages within the same generation, and (iii) four of these parameters representing risk taking, aggressiveness, and swimming behaviour, were correlated over multiple generations, establishing heritability of coping styles. CONCLUSION: We conclude that risk taking behaviour is a strong predictor of coping style within and between generations and behavioural parameters associated with risk taking are consistent over time and heritable over generations.
Effects of repetitive transcranial magnetic stimulation on learning and memory cognitive function in rats with vascular cognitive impairment and its neural induction mechanism.
Wang J, Gao H
BMC Neurosci · 2025 Mar · PMID 40102718 · Full text
BACKGROUND: The treatment of vascular cognitive impairment (VCI) is challenging, and its neurological mechanisms are not yet fully understood. Repetitive transcranial magnetic stimulation (rTMS) offers a new non-invasive...
BACKGROUND: The treatment of vascular cognitive impairment (VCI) is challenging, and its neurological mechanisms are not yet fully understood. Repetitive transcranial magnetic stimulation (rTMS) offers a new non-invasive treatment approach. METHODS: One hundred male SD rats were grouped: intervention group (IG), model group (MG), sham group (SG), and control group (CG), to prepare the rat model of VCI. The Morris water maze (MWM) test was conducted, and oxidative stress (OS) markers, neurotrophic factors, apoptosis factors, and the amplitude of postsynaptic potential (PSP) in the hippocampus of rats were measured. RESULTS: Post-intervention, IG's escape latency was lower than MG but higher than SG and CG. IG's hippocampal malondialdehyde (MDA) content, Bax, and Caspase-3 (Cas-3) were lower than MG but higher than SG and CG, while the tendency was opposite for Bcl-2 expression and the content of glutathione (GSH) and superoxide dismutase (SOD). IG's brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF), and N-methyl-D-aspartate receptor 1 (NMDAR1) in the hippocampus were higher than MG but lower than SG and CG; The changes in the amplitude of PSP in the hippocampal region of IG at 10, 30, and 60 min were all higher than those in MG but lower than those in SG and CG (P < 0.05). CONCLUSION: Low-frequency rTMS visibly improved the learning and memory abilities of VCI rats and reduced OS levels.
Epigallocatechin -3- gallate mitigates diazinon neurotoxicity via suppression of pro-inflammatory genes and upregulation of antioxidant pathways.
Onukak CE, Femi-Akinlosotu OM, Obasa AA … +12 more , Folarin OR, Ajibade TO, Igado OO, Esan OO, Oyagbemi TO, Adeogun AV, Oyagbemi AA, Ola-Davies OE, Omobowale TO, Olopade JO, Oguntibeju OO, Yakubu MA
BMC Neurosci · 2025 Mar · PMID 40065246 · Full text
Diazinon is a commonly used organophosphate (OP) insecticide especially in developing countries for the control of insect pests, however, exposure to its toxic impact especially in humans and other non-target species rem...
Diazinon is a commonly used organophosphate (OP) insecticide especially in developing countries for the control of insect pests, however, exposure to its toxic impact especially in humans and other non-target species remains an important public health concern. The study aimed to investigate the effect of epigallocatechin -3- gallate (EGCG), abundant in green tea plants on neurobehavioural, biochemical, and pathological changes in the brain of male Wistar rats following exposure to diazinon toxicity. Sixty adult male Wistar rats were acclimatized for seven days and subsequently randomly assigned into six treatment groups as follows: Group I: Control group (0.2 mL distilled water); Group II: Diazinon at 3 mg/kg (1% LD50); Group III: Diazinon (3 mg/kg) + EGCG (50 mg/kg, ~ 2% of LD50); Group IV: Diazinon (3 mg/kg) + EGCG (100 mg/kg, ~ 5% of LD50); Group V: EGCG (50 mg/kg) and Group VI: EGCG (100 mg/kg). All treatments were administered orally once daily for 14 days. Neurobehavioural studies, biomarkers of oxidative stress, histology, immunohistochemistry, and quantitative polymerase chain reaction (RT qPCR) were performed. Diazinon alone impaired recognition memory, increased oxidative stress markers and altered antioxidant defense in the brain. It upregulated TNF-α and IL-6 genes and repressed GPx 4 gene expressions. It was also associated with increased GFAP, Tau, and α-SN immunoreactivity. Microscopic examination revealed loss of Purkinje and hippocampal cells in brain. Co-treatment with EGCG however improved cognition, lowered oxidative stress markers, improved antioxidant status and suppressed TNF-α and IL-6. In conclusion, findings from this study demonstrated that EGCG offered protection against diazinon-induced neurotoxicity. Hence, natural sources of epigallocatechin -3- gallate such as fruits and vegetables could offer immense benefits by protecting against oxidative stress and inflammation in neurodegenerative disease conditions.Clinical trial number Not applicable.
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