BMC Neuroscience[JOURNAL]
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200 papers
Retraction Note: Neuroprotective effects of Cerebrolysin in triple repeat Tau transgenic model of Pick's disease and fronto-temporal tauopathies.
Rockenstein E, Ubhi K, Mante M … +6 more , Florio J, Adame A, Winter S, Brandstaetter H, Meier D, Masliah E
BMC Neurosci · 2025 Mar · PMID 40065222 · Full text
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Esketamine attenuates traumatic brain injury by modulating STAT3-mediated Glycolysis and immune responses.
Liu Y, Gong Z, Zhang L … +4 more , Yang X, Zhu J, Zhou X, Liao X
BMC Neurosci · 2025 Mar · PMID 40055623 · Full text
BACKGROUND: Secondary injury following traumatic brain injury (TBI) involves neuroinflammation, immune cell infiltration, and metabolic dysregulation, leading to progressive neurological damage. This study evaluates the...
BACKGROUND: Secondary injury following traumatic brain injury (TBI) involves neuroinflammation, immune cell infiltration, and metabolic dysregulation, leading to progressive neurological damage. This study evaluates the potential of esketamine, an NMDA receptor antagonist, to modulate immune responses, inhibit glycolysis, and mitigate secondary brain injury in a TBI mouse model. METHODS: Male C57BL/6J mice were subjected to controlled cortical impact to induce TBI. Mice were treated with esketamine, either alone or combined with the STAT3 activator colivelin, or the glycolysis inhibitor 2-deoxyglucose (2-DG). Neurological function, BBB permeability, immune cell infiltration, macrophage polarization, and glycolytic activity were assessed using immunohistochemistry, flow cytometry, quantitative PCR, and enzyme-linked immunosorbent assay (ELISA). RESULTS: Esketamine treatment significantly reduced structural brain tissue damage, including contusions, tissue loss, and edema, while also improving neurological outcomes in TBI mice. Mechanistically, esketamine inhibited CD4 + T cell activation and suppressed Th17 differentiation both in vivo and in vitro. It also promoted a shift in macrophage polarization from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype. Further analysis revealed that esketamine blocked STAT3 activation, which in turn reduced the expression of glycolytic genes (e.g., Hk2, Pgk1, Aldoa) essential for Th17 cell proliferation and M1 polarization. Co-treatment with colivelin reversed esketamine's effects on STAT3-mediated glycolysis, while 2-DG enhanced its anti-inflammatory actions. CONCLUSION: Esketamine attenuates TBI-induced neuroinflammation and tissue damage by inhibiting STAT3-mediated glycolysis, thus reducing Th17 and M1 macrophage activity and promoting regulatory and reparative immune responses. These findings highlight esketamine's potential as a therapeutic option for TBI, targeting both immune modulation and metabolic pathways to alleviate secondary injury. CLINICAL TRIAL NUMBER: not applicable.
The changes of digestive system inflammatory, oxidative stress, and histopathology factors following oral mesenchymal stem cells administration in rats with traumatic brain injury.
Eslami M, Raji-Amirhasani A, Khaksari M … +6 more , Keshavarzi Z, Rostamzadeh F, Sabet N, Jafari E, Soltani Z, Karamouzian S
BMC Neurosci · 2025 Mar · PMID 40050727 · Full text
BACKGROUND AND AIMS: Mucous mesenchymal stem cells can migrate to damaged areas, and their use is proposed as a new approach to treating diseases. The present study aimed to investigate the effect of oral mesenchymal ste...
BACKGROUND AND AIMS: Mucous mesenchymal stem cells can migrate to damaged areas, and their use is proposed as a new approach to treating diseases. The present study aimed to investigate the effect of oral mesenchymal stem cells (OMSCs) on inflammatory, oxidative stress, and histopathological indices in the tissues of the stomach, intestine, and colon after traumatic brain injury (TBI). METHODS AND MATERIALS: Adult male rats were randomly divided into four groups: Sham, TBI, Vehicle (Veh), and Stem cell (SC). Intravenous injection of OMSCs was performed at 1 and 24 h after injury. The inflammatory, oxidative stress, and histopathological indices of the tissues of the stomach, small intestine, and colon were evaluated 48 h after injury. RESULTS: After TBI, IL-1β and IL-6 levels increased and IL-10 levels decreased in the tissues of the stomach, small intestine, and colon, but the administration of OMSCS prevented these changes to a large extent. Oxidative stress indices (MDA, PC, TAC, SOD, and CAT) showed an increase in oxidative stress after TBI, but oxidative stress was less severe in the OMSC group. The administration of OMSCs after TBI improved the histopathological outcome in the tissues of the stomach, small intestine, and colon. CONCLUSION: Administration of OMSCs in rats suffering from TBI can improve inflammatory, oxidative stress, and histopathological indices in the tissues of the stomach, small intestine, and colon, which shows the beneficial effect of using OMSCs in TBI.
Short-term lipopolysaccharide treatment leads to astrocyte activation in LRRK2 G2019S knock-in mice without loss of dopaminergic neurons.
Ngo HKC, Srivastava A, Le H … +4 more , Ayer SJ, Crotty GF, Schwarzschild MA, Bakshi R
BMC Neurosci · 2025 Mar · PMID 40038582 · Full text
BACKGROUND: The G2019S mutation of LRRK2, which enhances kinase activity of the protein, confers a substantial risk of developing Parkinson's disease (PD). However, the mutation demonstrates incomplete penetrance, sugges...
BACKGROUND: The G2019S mutation of LRRK2, which enhances kinase activity of the protein, confers a substantial risk of developing Parkinson's disease (PD). However, the mutation demonstrates incomplete penetrance, suggesting the involvement of other genetic or environmental modulating factors. Here, we investigated whether LRRK2 G2019S knock-in (KI) mice treated with the inflammogen lipopolysaccharide (LPS) could model LRRK2 PD. RESULTS: We found that short-term (2 weeks) treatment with LPS did not result in the loss of dopaminergic neurons in either LRRK2 G2019S KI or wild-type (WT) mice. Compared with WT mice, LRRK2 G2019S-KI mice showed incomplete recovery from LPS-induced weight loss. In LRRK2 G2019S KI mice, LPS treatment led to upregulated phosphorylation of LRRK2 at the autophosphorylation site Serine 1292, which is known as a direct readout of LRRK2 kinase activity. LPS treatment caused a greater increase in the activated astrocyte marker glial fibrillary acidic protein (GFAP) in the striatum and substantia nigra of LRRK2 G2019S mice than in those of WT mice. The administration of caffeine, which was recently identified as a biomarker of resistance to developing PD in individuals with LRRK2 mutations, attenuated LPS-induced astrocyte activation specifically in LRRK2 G2019S KI mice. CONCLUSIONS: Our findings suggest that 2 weeks of exposure to LPS is not sufficient to cause dopaminergic neuronal loss in LRRK2 G2019S KI mice but rather results in increased astrocyte activation, which can be ameliorated by caffeine.
A systematic review of the therapeutic potential of nicotinamide adenine dinucleotide precursors for cognitive diseases in preclinical rodent models.
Qader MA, Hosseini L, Abolhasanpour N … +5 more , Oghbaei F, Maghsoumi-Norouzabad L, Salehi-Pourmehr H, Fattahi F, Sadeh RN
BMC Neurosci · 2025 Mar · PMID 40033213 · Full text
This systematic review sought to assess the impact of nicotinamide adenine dinucleotide (NAD) precursors on cognitive impairments in several diseases in rat/mouse models. Accumulating evidence suggests that inflammation,...
This systematic review sought to assess the impact of nicotinamide adenine dinucleotide (NAD) precursors on cognitive impairments in several diseases in rat/mouse models. Accumulating evidence suggests that inflammation, apoptosis, oxidative stress responses, and mitochondrial dysfunction are potential factors of cognitive deficits in aging, Alzheimer's disease (AD), diabetes, traumatic brain injury (TBI), vascular dementia (VAD), and schizophrenia. NAD precursors have received increased interest due to their unique molecular structure targets antioxidant and inflammatory pathways and mitochondrial function. The PubMed, Scopus, Google Scholar, Embase, and Web of Science databases were searched through May 30, 2024. Studies investigating the effect of NAD precursors on cognitive impairments in rodent models were included. Two reviewers independently extracted and evaluated the data. The PRISMA guidelines for reporting systematic reviews were followed. Thirty preclinical studies were included in the review. Studies have revealed that treatment with NAD rescues cognitive deficits by inhibiting inflammation, oxidative stress, and apoptosis and improving mitochondrial function. Preclinical evidence has demonstrated that treatment with NAD precursors may be more effective in learning and memory recovery in AD, TBI, diabetes, aging, VAD, and schizophrenia. The outcomes of this investigation may lead to additional studies on the use of NAD precursors for treating human cognitive decline.
Visualization of perivascular spaces in the human brain with 5-T magnetic resonance imaging.
Liu S, Li J, Hua R … +8 more , Xing Y, Wu J, Lin J, Wang J, Shan Y, Xu L, Shi F, Zeng M
BMC Neurosci · 2025 Mar · PMID 40033208 · Full text
BACKGROUND: To evaluate the effectiveness of 5-Tesla (T) magnetic resonance imaging (MRI) in the visualization of perivascular spaces (PVS). METHOD: A total of seventeen subjects underwent three-dimensional (3D) T1- and...
BACKGROUND: To evaluate the effectiveness of 5-Tesla (T) magnetic resonance imaging (MRI) in the visualization of perivascular spaces (PVS). METHOD: A total of seventeen subjects underwent three-dimensional (3D) T1- and T2-weighted imaging on both 3-T and 5-T MRI systems. Twelve of these subjects underwent quantitative analysis of PVS in the semioval center (SOC) and basal ganglia (BG), with comparisons made between the two systems using paired-sample Wilcoxon tests. Additionally, high-resolution 5-T images were acquired for five other participants to examine the detailed anatomy of PVS in the SOC, BG, and cerebral cortex. RESULTS: Compared with 3-T MRI, 5-T MRI detected more PVS in the SOC and BG [39.5 (32.0-63.0) vs. 56.5 (44.0-75.5) and 49.5 (27.0-55.8) vs. 65.5 (53.0-72.0)] with p-values of 0.002 and 0.004, respectively. In these two regions, the PVS tortuosity, defined as the ratio of the actual path length to the straight-line distance between the start and end points of the PVS, was lower at 3-T compared to 5-T (p = 0.012 for the SOC and p = 0.006 for the BG). The length of PVS in the SOC on 5-T was longer than those on 3-T [4.6 mm (3.9-6.3 mm) vs. 5.1 mm (4.6-6.7 mm), p = 0.049]. In addition, the 5-T MRI provided enhanced visualization of the morphology of PVS in vivo, and improved the depiction of PVS across various brain regions, especially in the cortex, illustrating their course and associated small vessels. CONCLUSIONS: 5-T MRI notably enhanced the visualization of PVS compared to 3-T, particularly in its ability to depict PVS anatomy in the cortex using high-resolution images. This advancement may pave the way for further research into the physiological roles of PVS and their involvement in related diseases.
Effects of multisystem exercises on balance, postural stability, mobility, walking speed, and pain in patients with diabetic peripheral neuropathy: a randomized controlled trial.
Khurshid S, Saeed A, Kashif M … +2 more , Nasreen A, Riaz H
BMC Neurosci · 2025 Feb · PMID 40016658 · Full text
BACKGROUND: Diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus, is associated with peripheral nerve damage, leading to balance impairments, postural instability, and reduced mobility. Addres...
BACKGROUND: Diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus, is associated with peripheral nerve damage, leading to balance impairments, postural instability, and reduced mobility. Addressing these challenges requires comprehensive interventions that target multiple deficits simultaneously. Evidence suggests that exercise programs combining balance, proprioception, strength, and reaction time training can improve postural stability, enhance mobility, and alleviate pain in individuals with DPN. OBJECTIVE: The objective of this study was to compare the effects of multisystem exercises and conventional exercises on balance, postural stability, mobility, and walking speed and to reduce pain in patients with diabetic peripheral neuropathy. METHODS: This double-blinded, two-arm parallel design randomized controlled trial was conducted at DHQ Hospital, Pakpattan, Pakistan. A total of 50 participants who met the inclusion criteria were recruited using the nonprobability convenience sampling technique. They were randomly assigned to either a multisystem physical exercise (MPE) group (n = 26) and a conventional exercise group (n = 24). The MPE program included balance, proprioception, strength, and reaction time training, while the control group received conventional exercises, consisted of strength, balance, stretching, and range of motion exercises. Both groups underwent 30 min intervention sessions, 3 times per week, for 8 weeks. The outcome measures used for assessing the balance, postural stability, mobility, and pain included the Berg balance scale (BBS), functional reach test (FRT), time up and go test (TUG), 10 min walk test (10-MWT), and numeric pain rating scale (NPRS). The data was analyzed using SPSS version 26. RESULTS: Significant group and time interactions were observed for all outcome measures including BBS, FRT, TUG, 10-MWT, and NPRS (p < 0.001). The between-group analysis also revealed significant differences between the multisystem physical exercise group and the conventional exercise group at both the 4th week and 8th week for BBS, FRT, TUG, 10-MWT, and NPRS (p < 0.05). CONCLUSION: The study concluded that multisystem exercises resulted in significant improvement in balance, postural stability, mobility, and walking speed, along with reduction in pain, compared to conventional exercises in patients with diabetic peripheral neuropathy. TRIAL REGISTRATION: This randomized controlled study was registered prospectively on November 11th, 2023 with the ClinicalTrials.gov (NCT06130917).
Social isolation induces sexually aggressive behaviour in male Wistar rats.
Ngala ME, Hemmings SMJ, Womersley JS … +2 more , Shabangu TW, Qulu-Appiah L
BMC Neurosci · 2025 Feb · PMID 40011829 · Full text
BACKGROUND: Sexual violence, a pervasive global issue, significantly impacts individuals and societies, necessitating a deeper understanding of its underlying biological mechanisms. This study aimed to elucidate the role...
BACKGROUND: Sexual violence, a pervasive global issue, significantly impacts individuals and societies, necessitating a deeper understanding of its underlying biological mechanisms. This study aimed to elucidate the role of stress-induced dysregulation of the hypothalamus-pituitary-adrenocortical axis in sexual aggression in male Wistar rats. Employing a sexual aggression paradigm, we investigated the effects of social isolation on aggression, anxiety-like behaviour, and neurochemistry in virgin adult male Wistar rats. RESULTS: The results showed that social isolation significantly escalated aggressive behaviours and induced anxiety-like responses in male rats. The sexual aggression test revealed that socially isolated males exhibited heightened aggression towards non-receptive females. Neurochemical analyses indicated significant alterations in key markers, such as corticotrophin-releasing hormone, oxytocin, and arginine vasopressin, correlating with the observed behavioural changes. Gene expression analyses revealed significant findings, particularly in the expression of the oxytocin receptor (OXTR) and vasopressin receptor 1 A (AVPR1A) genes. Social isolation and the duration of aggressive behaviour prior to the sexual aggression test significantly influenced OXTR expression in the hippocampus and AVPR1A expression in both the prefrontal cortex and hippocampus, highlighting the complex interplay between environmental stressors, neurochemical responses, and gene expression in the manifestation of sexual aggression behaviour. CONCLUSIONS: This study underscores the critical impact of stress and social isolation on sexual aggression, providing valuable insights into possible neurobiological underpinnings of sexual violence. Understanding these mechanisms is crucial for developing effective interventions to mitigate the consequences of sexual aggression.
Ventromedial hypothalamic nucleus neuronal nitric oxide knockdown effects on GABAergic neuron metabolic sensor and transmitter marker gene expression in the male rat.
Roy SC, Pasula MB, Sapkota S … +1 more , Briski KP
BMC Neurosci · 2025 Feb · PMID 39994513 · Full text
The diffusible gas nitric oxide (NO) and amino acid γ-gamma-aminobutyric acid (GABA) exert contrary effects on glucose counterregulation in the male rat, but how these neurochemical signals integrate within ventromedial...
The diffusible gas nitric oxide (NO) and amino acid γ-gamma-aminobutyric acid (GABA) exert contrary effects on glucose counterregulation in the male rat, but how these neurochemical signals integrate within ventromedial hypothalamic nucleus (VMN) neural circuitries remains unclear. Female rat dorsomedial (VMNdm) and ventrolateral (VMNvl) GABAergic neurons express neuronal nitric oxide synthase (nNOS) mRNA; notably these subpopulations exhibit dissimilar nNOS transcriptional responses to insulin-induced hypoglycemia (IIH). Here, nNOS gene knockdown tools were used to examine whether one or both VMN GABA neuron groups may be a target for nitrergic control of basal and hypoglycemic counterregulatory hormone secretion in the male. Data show that VMN nNOS gene knockdown respectively up- or down-regulated counterregulatory hormone profiles in eu- versus hypoglycemic male rats. Single-cell multiplex qPCR analysis of laser-catapult-microdissected GABA neurons showed that IIH elevated nNOS gene expression in GABA neurons from each VMN division, yet nNOS siRNA pretreatment attenuated distinctive IIH-associated transmitter marker gene expression patterns in VMNdm versus VMNvl GABAergic neurons. nNOS gene silencing had similar effects on glucokinase and glucose transporter gene responses to IIH in each GABA neuron subpopulation but elicited division-specific effects on mRNA encoding 5-AMP-activated protein kinase (AMPK) alpha/catalytic subunits and the lactate membrane receptor GPR81/HCAR1. Current findings provide original evidence that VMN NO may impose bi-directional, glucose status-contingent control of counterregulatory hormone outflow in the male rat. Data moreover imply that during IIH, NO may control distinctive sources of metabolic sensory regulatory stimuli in VMNdm versus VMNvl GABA neurons and may shape unique counterregulation-controlling neurochemical transmission by each cell population.
Aerobic exercise training improves learning and memory performance in hypoxic-exposed rats by activating the hippocampal PKA-CREB-BDNF signaling pathway.
Luo S, Shi L, Liu T … +1 more , Jin Q
BMC Neurosci · 2025 Feb · PMID 39984845 · Full text
BACKGROUND: This study aims to investigate the effects of aerobic exercise training on learning and memory (L&M) performance in rats exposed to altitude hypoxia and its relationship with hippocampal plasticity and the PK...
BACKGROUND: This study aims to investigate the effects of aerobic exercise training on learning and memory (L&M) performance in rats exposed to altitude hypoxia and its relationship with hippocampal plasticity and the PKA-CREB-BDNF signaling pathway. METHODS: Male Sprague-Dawley rats were exposed to 14.2% hypoxia with or without 60 min of non-weight-bearing swimming training for 8 weeks. The L&M performance was evaluated using the Morris water maze, and the mRNA expression of PSD95, SYP, PKA, CREB, CBP, and BDNF in the hippocampus was detected. RESULTS: Chronic hypoxia exposure significantly impaired L&M performance and reduced the mRNA expression of hippocampal PSD95, SYP, PKA, CREB, CBP, and BDNF. Aerobic exercise training effectively reversed these changes by enhancing hippocampal synaptic plasticity through the activation of the PKA-CREB-BDNF signaling pathway. CONCLUSION: Aerobic exercise training can alleviate the decline in L&M performance caused by altitude hypoxia exposure, possibly through the activation of the hippocampal PKA-CREB-BDNF signaling pathway.
Evaluation of suitable reference genes for gene expression studies in the developing mouse cortex using RT-qPCR.
Uppalapati A, Wang T, Nguyen LH
BMC Neurosci · 2025 Feb · PMID 39966711 · Full text
BACKGROUND: Real-time quantitative PCR (RT-qPCR) is a widely used method to investigate gene expression in neuroscience studies. Accurate relative quantification of RT-qPCR requires the selection of reference genes that...
BACKGROUND: Real-time quantitative PCR (RT-qPCR) is a widely used method to investigate gene expression in neuroscience studies. Accurate relative quantification of RT-qPCR requires the selection of reference genes that are stably expressed across the experimental conditions and tissues of interest. While RT-qPCR is often performed to investigate gene expression changes during neurodevelopment, few studies have examined the expression stability of commonly used reference genes in the developing mouse cortex. RESULTS: Here, we evaluated the stability of five housekeeping genes, Actb, Gapdh, B2m, Rpl13a, and Hprt, in cortical tissue from mice at embryonic day 15 to postnatal day 0 to identify optimal reference genes with stable expression during late corticogenesis. The expression stability was assessed using five computational algorithms: BestKeeper, geNorm, NormFinder, DeltaCt, and RefFinder. Our results showed that B2m, Gapdh, and Hprt, or a combination of B2m/Gapdh and B2m/Hprt, were the most stably expressed genes or gene pairs. In contrast, Actb and Rpl13a were the least stably expressed. CONCLUSION: This study identifies B2m, Gapdh, and Hprt as suitable reference genes for relative quantification in RT-qPCR-based cortical development studies spanning the period of embryonic day 15 to postnatal day 0.
Platelet-rich fibrin and silver nano-particles loaded chitosan treatment for post- laminectomy epidural scar adhesions: in vivo rats study model.
Fouad S, Rizk A, Mosbah E … +5 more , Nabeeh MM, Awadin W, Elmezayyen AS, Elmorsy E, Zaghloul A
BMC Neurosci · 2025 Feb · PMID 39910448 · Full text
OBJECTIVE: Epidural scar fibrosis commonly leads to functional disability and pain following spinal surgery and is a prevalent manifestation of Failed Back Surgery Syndrome (FBSS). This study aimed to evaluate the use of...
OBJECTIVE: Epidural scar fibrosis commonly leads to functional disability and pain following spinal surgery and is a prevalent manifestation of Failed Back Surgery Syndrome (FBSS). This study aimed to evaluate the use of silver nano-articles (AgNPs) loaded on chitosan (Chi/Ag-NPs) with platelets-rich fibrin (PRF) gel for the reduction of post-laminectomy epidural scar adhesions. METHODS: A total of 90 male Sprague Dawley rats (255 ± 55gm) were randomized in-to six groups, each group with 15 rats: control group, laminectomy group, PRF group, Chi/Ag-NPs group, combined treatment group (PRF + Chi/Ag-NPs), and a group to prepare PRF. Lumbar laminectomy procedures were performed between L3-L5 in all rats except the control group. After a 30-days follow-up, macroscopic examination, histological studies, and mRNA evaluation for TGFβ-1and IL-6, were conducted. RESULTS: Data revealed that epidural scar adhesion, scaring, arachnoid involvement, dural thickness, as well as inflammation and TGFβ-1and IL-6 coding genes expression were significantly reduced in PRF group, Chi/Ag-NPs group, and combined group compared to the laminectomy group. Combined treatment showed more significant better outcomes. CONCLUSION: The use of PRF with Chi/Ag-NPs as nano biomaterials could be considered a combination therapy for the reduction of EF post-laminectomy in a rat model.
Neural progenitor cell-derived exosomes in ischemia/reperfusion injury in cardiomyoblasts.
Arvola O, Stigzelius V, Ampuja M … +1 more , Kivelä R
BMC Neurosci · 2025 Feb · PMID 39910431 · Full text
The physiologic relationship between the brain and heart is emerging as a novel therapeutic target for clinical intervention for acute myocardial infarction. In the adult human brain, vestigial neuronal progenitor stem c...
The physiologic relationship between the brain and heart is emerging as a novel therapeutic target for clinical intervention for acute myocardial infarction. In the adult human brain, vestigial neuronal progenitor stem cells contribute to neuronal repair and recovery following cerebral ischemic injury, an effect modulated by secreted exosomes. Ischemia conditioned neuronal cell derived supernatant and experimental stroke has been shown to be injurious to the heart. However, whether unconditioned neuronal progenitor cell derived-exosomes can instead protect myocardium represents a profound research gap. We investigated the effects of unconditioned neural stem cell derived exosomes as post-injury treatment for cardiomyoblasts from three neuronal culture conditions; adherent cultures, neurosphere cultures and bioreactor cultures. Small extracellular vesicles were enriched with serial ultracentrifugation, validated via nanoparticle tracking analysis, transmission electron microscopy and Western blot analysis prior to utilization as post-injury treatment for H9c2 cardiomyoblasts following oxygen and glucose deprivation. LDH assay was used to assess viability and Seahorse XF high-resolution respirometry analyzer to investigate post-injury cardiomyocyte bioenergetics. We found no evidence that unconditioned neural stem cell derived exosomes are cardiotoxic nor cardioprotective to H9c2 cardiomyoblasts following ischemia-reperfusion injury. Based on our findings, utilizing unconditioned neural stem cell derived exosomes as post-injury treatment for other organs should not have adverse effects to the damaged cardiac cells.
Molecular assessment of NMDAR subunits and neuronal apoptosis in the trigeminal ganglion in a model of male migraine-induced rats following Moringa oleifera alcoholic extract administration.
Vafaeian A, Vafaei A, Parvizi MR … +3 more , Chamanara M, Mehriardestani M, Hosseini Y
BMC Neurosci · 2025 Feb · PMID 39905292 · Full text
INTRODUCTION: Migraine, a common disorder marked by severe and repetitive headaches, has been linked to the involvement of the NMDA receptor (NMDAR), a receptor responsible for glutamate signaling. Moringa oleifera (M. o...
INTRODUCTION: Migraine, a common disorder marked by severe and repetitive headaches, has been linked to the involvement of the NMDA receptor (NMDAR), a receptor responsible for glutamate signaling. Moringa oleifera (M. oleifera), recognized for its anti-inflammatory properties and therapeutic potential in various conditions, has been investigated. This study aims to assess the efficacy and precise mechanisms of M. oleifera for the treatment of migraine, for which evidence is limited. METHODS: Rats were stratified into four distinct groups. The control group did not undergo the migraine-induction protocol. Post-induction, the "sumatriptan" group was administered sumatriptan injections, the "treatment" group received oral M. oleifera extract, and the "vehicle" group was provided with oral solvent treatment. Behavioral evaluations encompassing Von Frey's and hot plate assessments, in addition to qPCR analysis targeting Nr2a, Nr2b, Bax, Bcl-2, and Caspase-3, were conducted. RESULTS: Von Fery's and hot plate tests revealed a notable decrease in triggering pressure and temperature within the vehicle group when compared to the other groups (both ps < 0.001). The Nr2a expression levels in both the vehicle and treatment cohorts exhibited significantly higher values than those observed in the control group (p < 0.001, p = 0.001) and the sumatriptan group (p < 0.001, p = 0.002). Conversely, no substantial alterations in Nr2b or Bcl-2 expression levels were observed across the study groups (p = 0.404, p = 0.976). Notably, heightened expressions of Caspase-3 and Bax were evident in the vehicle group relative to the other groups (p = 0.013, p = 0.010). CONCLUSIONS: Moringa oleifera extract appears to mitigate symptoms of migraine by inhibiting apoptosis, suggesting potential efficacy in migraine treatment; however, additional research investigating a wider range of pathways is necessary. CLINICAL TRIAL NUMBER: Not applicable.
NPT100-18A rescues mitochondrial oxidative stress and neuronal degeneration in human iPSC-based Parkinson's model.
Alecu JE, Sigutova V, Brazdis RM … +9 more , Lörentz S, Bogiongko ME, Nursaitova A, Regensburger M, Roybon L, Galler KM, Wrasidlo W, Winner B, Prots I
BMC Neurosci · 2025 Jan · PMID 39875842 · Full text
BACKGROUND: Parkinson's disease (PD) is a neurodegenerative disorder characterized by protein aggregates mostly consisting of misfolded alpha-synuclein (αSyn). Progressive degeneration of midbrain dopaminergic neurons (m...
BACKGROUND: Parkinson's disease (PD) is a neurodegenerative disorder characterized by protein aggregates mostly consisting of misfolded alpha-synuclein (αSyn). Progressive degeneration of midbrain dopaminergic neurons (mDANs) and nigrostriatal projections results in severe motor symptoms. While the preferential loss of mDANs has not been fully understood yet, the cell type-specific vulnerability has been linked to a unique intracellular milieu, influenced by dopamine metabolism, high demand for mitochondrial activity, and increased level of oxidative stress (OS). These factors have been shown to adversely impact αSyn aggregation. Reciprocally, αSyn aggregates, in particular oligomers, can impair mitochondrial functions and exacerbate OS. Recent drug-discovery studies have identified a series of small molecules, including NPT100-18A, which reduce αSyn oligomerization by preventing misfolding and dimerization. NPT100-18A and structurally similar compounds (such as NPT200-11/UCB0599, currently being assessed in clinical studies) point towards a promising new approach for disease-modification. METHODS: Induced pluripotent stem cell (iPSC)-derived mDANs from PD patients with a monoallelic SNCA locus duplication and unaffected controls were treated with NPT100-18A. αSyn aggregation was evaluated biochemically and reactive oxygen species (ROS) levels were assessed in living mDANs using fluorescent dyes. Adenosine triphosphate (ATP) levels were measured using a luminescence-based assay, and neuronal cell death was evaluated by immunocytochemistry. RESULTS: Compared to controls, patient-derived mDANs exhibited higher cytoplasmic and mitochondrial ROS probe levels, reduced ATP-related signals, and increased activation of caspase-3, reflecting early neuronal cell death. NPT100-18A-treatment rescued cleaved caspase-3 levels to control levels and, importantly, attenuated mitochondrial oxidative stress probe levels in a compartment-specific manner and, at higher concentrations, increased ATP signals. CONCLUSIONS: Our findings demonstrate that NPT100-18A limits neuronal degeneration in a human in vitro model of PD. In addition, we provide first mechanistic insights into how a compartment-specific antioxidant effect in mitochondria might contribute to the neuroprotective effects of NPT100-18A.
Age predicts peak gamma frequency and N1 amplitude of visual evoked potential.
Dawood AB
BMC Neurosci · 2025 Jan · PMID 39856596 · Full text
The current study investigated whether the age of healthy adults could predict the peak gamma frequency and the peak amplitudes of VEP components (N1, P2). 49 healthy participants (aged between 19 and 52 years) underwent...
The current study investigated whether the age of healthy adults could predict the peak gamma frequency and the peak amplitudes of VEP components (N1, P2). 49 healthy participants (aged between 19 and 52 years) underwent EEG recordings during a visual task eliciting clear gamma frequency oscillations and VEP activities. After eliminating noisy and outlier data, data from 41 participants were analysed using simple linear regression. The results indicated that age was a significant predictor of peak gamma frequency and the peak amplitude of VEP-N1 but not the peak amplitude of VEP-P2. Age was negatively associated with peak gamma frequency and the peak amplitude of VEP-N1. These findings support previous research indicating that ageing is associated with decreased cortical inhibition, highlighting the importance of GABA in maintaining cortical E-I balance.
Effects of subclinical hypothyroidism during pregnancy on mtDNA methylation in the brain of rat offspring.
Xie L, Huang Y, Ma X … +4 more , Ma X, Wang J, Gao T, Chen W
BMC Neurosci · 2025 Jan · PMID 39856545 · Full text
OBJECTIVE: This study aims to investigate the impact of subclinical hypothyroidism (SCH) during pregnancy on mitochondrial DNA (mtDNA) methylation in the brain tissues of rat offspring. MATERIALS AND METHODS: Sixteen SD...
OBJECTIVE: This study aims to investigate the impact of subclinical hypothyroidism (SCH) during pregnancy on mitochondrial DNA (mtDNA) methylation in the brain tissues of rat offspring. MATERIALS AND METHODS: Sixteen SD rats were randomly divided into two groups: control group (CON) and SCH group. BS-seq sequencing was used to analyze mtDNA methylation levels in the offspring's brain tissues; the 2,7-dichlorofluorescin diacetate (DCFH-DA) probe method was employed to detect reactive oxygen species (ROS) levels in brain tissues; electron microscopy was utilized to observe the mitochondrial structure in the hippocampal tissues of the offspring. RESULTS: In the analysis of differentially methylated regions (DMRs), the mitochondrial chromosome in the SCH group exhibited 23 DMRs compared to the control group. ROS levels in the brain tissues of the SCH group were significantly higher than those in the control group (P < 0.05). The mitochondrial structure in the hippocampus of the SCH group was less intact compared to the CON group. CONCLUSION: Subclinical hypothyroidism in pregnant rats may alter the mtDNA methylation pattern in the brains of their offspring, potentially affecting mitochondrial function and structure.
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 Jan · PMID 39856540 · Full text
BACKGROUND: The apolipoprotein E ε4 (APOE ε4) status has a controversial role in predicting Alzheimer's disease (AD) factors. This meta-analysis assessed AD event risk in patients with APOE ε4 status. MATERIALS AND METHO...
BACKGROUND: The apolipoprotein E ε4 (APOE ε4) status has a controversial role in predicting Alzheimer's disease (AD) factors. This meta-analysis assessed AD event risk in patients with APOE ε4 status. MATERIALS AND METHODS: The relevant English-language articles were identified by searching the Cochrane Library, EMBASE, and PubMed databases. The prognostic significance of APOE ε4 status in AD patients was examined on the basis of pooled hazard ratios (HRs). RESULTS: A total of 22 studies published after 1987, including 571,800 patients, were included. Consequently, APOE ε4 status was a risk factor for disease-free survival (DFS, HR = 2.033; 95% confidence interval [CI] = 1.589-2.602; P = 0.000; I 2 = 93.1%) in patients with AD. Additionally, subgroup analysis suggested that the ROC curve was the main risk factor among patients with AD. CONCLUSIONS: AD patients with different events are managed via different methods; however, the present meta-analysis suggests an increased risk of AD events in patients with different APOE ε4 statuses.
Delta opioid receptors affect acoustic features of song during vocal learning in zebra finches.
Singh UA, Iyengar S
BMC Neurosci · 2025 Jan · PMID 39844074 · Full text
Delta-opioid receptors (δ-ORs) are known to be involved in associative learning and modulating motivational states. We wanted to study if they were also involved in naturally-occurring reinforcement learning behaviors su...
Delta-opioid receptors (δ-ORs) are known to be involved in associative learning and modulating motivational states. We wanted to study if they were also involved in naturally-occurring reinforcement learning behaviors such as vocal learning, using the zebra finch model system. Zebra finches learn to vocalize early in development and song learning in males is affected by factors such as the social environment and internal reward, both of which are modulated by endogenous opioids. Pairs of juvenile male siblings (35-day-old) were systemically administered a δ-OR-selective antagonist naltrindole or vehicle (controls) for a period of 10 days. The acoustic structure of songs differed across treated and control groups at adulthood (120 days). Naltrindole-treated birds had a significantly lower pitch, mean frequency, and frequency modulation than controls, whereas there was no difference in the number of songs in naltrindole-treated and control siblings. Since the opioid and dopaminergic systems interact, we decided to study whether blocking δ-ORs during the sensitive period led to changes in dopaminoceptive neurons in Area X, a song control nucleus in the basal ganglia. Interestingly, compared with controls, naltrindole-treated birds had higher numbers of DARPP-32-positive medium spiny neurons and potentially excitatory synapses in Area X. We show that manipulating δ-OR signaling during the learning phase resulted in alterations in the acoustic features of song and had long term effects on dopaminergic targets within the basal ganglia in adulthood. Our results suggest that endogenous opioids regulate the development of cognitive processes and the underlying neural circuitry during the sensitive period for learning.
Identification of key genes associated with oxidative stress in ischemic stroke via bioinformatics integrated analysis.
Li G, Cheng Y, Ding S … +4 more , Zheng Q, Kuang L, Zhang Y, Zhou Y
BMC Neurosci · 2025 Jan · PMID 39806309 · Full text
BACKGROUND: Ischemic stroke (IS) is a common cerebrovascular disease. Although the formation of atherosclerosis, which is closely related to oxidative stress (OS), is associated with stroke-related deaths. However, the r...
BACKGROUND: Ischemic stroke (IS) is a common cerebrovascular disease. Although the formation of atherosclerosis, which is closely related to oxidative stress (OS), is associated with stroke-related deaths. However, the role of OS in IS is unknown. METHODS: OS-related key genes were obtianed by overlapping the differentially expressed genes (DEGs) between IS and normal control (NC) specimens, IS-related genes, and OS-related genes. Then, we investigated the mechanism of action of key genes. Subsequently, protein-protein interaction (PPI) network and machine learning algorithms were utilized to excavate feature genes. In addition, the network between feature genes and microRNAs (miRNAs) was established to investigate the regulatory mechanism of feature genes. Finally, quantitative PCR (qPCR) was utilized to validate the expression of feature genes with blood specimens. RESULTS: A total of 42 key genes related to OS were acquired. Enrichment analysis indicated that the key genes were associated with oxidative stress, reactive oxygen species, lipid and atherosclerosis, and cell migration-related pathways. Then, 6 feature genes (HSPA8, NCF2, FOS, KLF4, THBS1, and HSPA1A) related to OS were identified for IS. Besides, 6 feature genes and 255 miRNAs were utilized to establish a feature genes-miRNA network which contained 261 nodes and 277 edges. At last, qPCR results revealed that there was a trend for higher expression of FOS, KLF4, and HSPA1A in IS specimens than in NC specimens. Additionally, HSPA8 expression was significantly decreased in the IS specimens, which was consistent with the findings of the GEO database analysis. CONCLUSION: In conclusion, 6 feature genes (HSPA8, NCF2, FOS, KLF4, THBS1, and HSPA1A) related to OS were mined by bioinformatics analysis, which might provide a new insights into the evaluation and treatment of IS. CLINICAL TRIAL NUMBER: Not applicable.
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