J. Neurosci. Res. [JOURNAL]
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200 papers
A Nonhuman Primate Model to Evaluate Treatments for Long-Gap Ulnar Nerve Injury.
Shultz RB, Laimo FA, Lee HH … +7 more , Ali ZS, Huang R, Barnewall RE, Fetzek CG, Ledebur HC, Cullen DK, Katiyar KS
J Neurosci Res · 2025 Aug · PMID 40741899 · Full text
Among all upper extremity nerves, the ulnar nerve is both the most commonly injured and notoriously difficult to regenerate. Despite this, ulnar nerve injuries remain understudied. Nonhuman primates (NHPs) offer an ideal...
Among all upper extremity nerves, the ulnar nerve is both the most commonly injured and notoriously difficult to regenerate. Despite this, ulnar nerve injuries remain understudied. Nonhuman primates (NHPs) offer an ideal model for the human upper extremity, but existing NHP nerve trauma literature is biased towards median and radial injury models. To address this, a nonhuman primate ulnar nerve injury model was developed and regeneration assessed following sural nerve autografting using electrophysiological and histological techniques. Unilateral 4 cm ulnar nerve injuries were created at the mid-forearm level, sural nerve autografts were sutured into resulting defects (n = 3), and animals were survived for 6 months. At the terminal time point, intraoperative electrophysiological testing, tissue harvest, and tissue processing were performed. Naïve nerves (n = 5) served as controls. Animals appeared clinically normal throughout the study period, other than an expected decrease in fine hand muscle function. After 6 months, histological and electrophysiological evidence suggested that axons crossed the graft and reached distal muscle targets. However, regenerating nerves exhibited a reduced motor nerve conduction velocity, reduced compound action muscle potential (CMAP) amplitude and area under the curve, increased latency, and increased duration versus naïve controls as expected. Histological analysis revealed reduced axon diameters, thinner myelin sheaths, and smaller muscle fiber cross-sectional areas as compared to controls. At 6 months post-injury, 4 cm ulnar defects bridged with sural autografts show signs of ongoing regeneration and nascent reinnervation. Specific electrophysiological and histological benchmarks for ulnar nerve recovery following clinically relevant autografting are presented.
Transcriptomic Profiling Reveals Injury Responses of Peripheral Glial Cells in Sensory Neuron Microenvironment.
Xu J, Jin J, Lv S … +4 more , Pan Y, Wang D, Shen N, Wang Y
J Neurosci Res · 2025 Aug · PMID 40726253 · Publisher ↗
Schwann cells and satellite glial cells (SGCs) are important peripheral glial cells in the dorsal root ganglion (DRG) and commendable participants in regulating neuronal functions. Herein, through re-analysis of publicly...
Schwann cells and satellite glial cells (SGCs) are important peripheral glial cells in the dorsal root ganglion (DRG) and commendable participants in regulating neuronal functions. Herein, through re-analysis of publicly available single-nucleus RNA sequencing data from naïve and injured DRG at 1 and 3 days following sciatic nerve crush, we systematically characterized the transcriptomic alterations in Schwann cells and SGCs. Cell clustering and counting showed that peripheral glial cells occupied a large population after sciatic nerve crush injury. Using differentially expression analysis, we found that apoptosis and immune responses were involved in all these examined peripheral glial cells. Unique glial cells also responded differently to sciatic nerve crush injury, with myelinating Schwann cells characterized by enriched adenosine 5'-monophosphate activated protein kinase (AMPK) metabolic signaling, non-myelinating Schwann cells characterized by enriched tissue-remodeling-related signaling, and SGCs characterized by enriched ion channels. Using single-cell regulatory network inference and clustering (SCENIC) to determine essential transcription factors in specific cell type at the naïve state and at multiple time points after sciatic nerve crush injury, we found that Schwann cells and SGCs possessed their own elevated transcription factor-coding genes, with activating factor 3 (Atf3) commonly highly up-regulated in all peripheral glial cells. This study provides a profiling map of peripheral glial cells at the naïve and injured states, expands the acknowledgment of the molecular background of nerve injury, and can lead to novel strategies to promote sensory nerve regeneration.
Metabolic and Structural Alterations in the Motor System Following Spinal Cord Injury: An In-Vivo H-MR Spectroscopy Investigation.
Schading-Sassenhausen S, Lebret A, Şimşek K … +6 more , Gut P, Imhof S, Zörner B, Kreis R, Freund P, Seif M
J Neurosci Res · 2025 Jul · PMID 40704776 · Full text
Spinal cord injury (SCI) disrupts spinal tracts and neuronal pathways, including those in the primary motor cortex (M1) and the lumbar cord enlargement (LCE) involved in motor control. This study sought to determine whet...
Spinal cord injury (SCI) disrupts spinal tracts and neuronal pathways, including those in the primary motor cortex (M1) and the lumbar cord enlargement (LCE) involved in motor control. This study sought to determine whether metabolite concentrations deviate between SCI and healthy controls (HC) in M1 and LCE using proton magnetic resonance spectroscopy (H-MRS) and structural MRI, and if these correlate with clinical impairment. Sixteen chronic SCI (mean age: 54.7 ± 14.8y) and 19 HCs (mean age: 53.2 ± 18.8y) underwent H-MRS to quantify metabolites along with T- and T*-weighted MRI to assess tissue structural changes. Associations between metabolic and structural changes and clinical impairment were also assessed. Patients showed significant atrophy in both white matter of the LCE (HC: 37.7 ± 4.7 mm, SCI: 33.9 ± 3.7 mm, Δ = -10.1%, p = 0.015) and gray matter (HC: 20.9 ± 2.1 mm, SCI: 19.4 ± 1.5 mm, Δ = -7.2%, p = 0.022). Total N-acetylaspartate (tNAA) with respect to total creatine (tCr) was reduced in M1 of SCI (HC: 1.94 ± 0.21, SCI: 1.77 ± 0.14, ∆ = -8.8%, p = 0.006) and in the LCE (HC: 2.48 ± 0.76, SCI: 1.81 ± 0.80, ∆ = -27.0%, p = 0.02). In conclusion, reduced tNAA/tCr in both the atrophied LCE and M1 suggests widespread neuronal changes including cell atrophy and/or cell loss after injury. These findings provide in vivo evidence for retrograde and trans-synaptic neurodegeneration, which may underline the atrophy observed in the motor system in SCI. Ultimately, this highlights the potential for metabolic and structural biomarkers to improve the monitoring of subtle neurodegeneration following SCI and to enhance future regenerative treatment strategies.
Hidden Markov Model-Based Behavioral Classification Reveals Visual Function Recovery After Retinal Organoid Transplantation in Mice.
Shuto H, Mandai M, Yamada T … +5 more , Sho J, Hayakawa C, Koike C, Takahashi M, Matsuyama T
J Neurosci Res · 2025 Jul · PMID 40698539 · Full text
Retinal degenerative diseases cause irreversible vision loss due to photoreceptor degeneration. Retinal organoid transplantation offers a promising strategy for restoring vision, but assessing functional recovery remains...
Retinal degenerative diseases cause irreversible vision loss due to photoreceptor degeneration. Retinal organoid transplantation offers a promising strategy for restoring vision, but assessing functional recovery remains challenging. Standard visual function tests provide binary or coarse measures that do not fully capture how visual input influences natural behavior. Here, we applied a Hidden Markov Model (HMM)-based behavioral analysis to the visual cliff test to track locomotor state transitions in wild-type (WT) and rd1-2 J (RD) mice, evaluating depth perception and its recovery following photoreceptor transplantation. WT mice exhibited a strong cliff avoidance response, while RD mice showed no response, confirming the model's sensitivity to depth perception. Over repeated trials, WT mice rapidly habituated, shifting from three behavioral states (Resting, Exploring, and Navigating) to just two (Resting and Navigating). Transplanted RD mice began responding to the cliff at 2 weeks posttransplantation, coinciding with early synapse formation between grafted photoreceptors and host bipolar cells. The avoidance response became robust by 16 weeks but disappeared by 18 weeks, accompanied by state collapse, a hallmark of habituation never observed in untreated RD mice. These findings demonstrate that behavioral state-based analysis provides a sensitive and dynamic measure of functional vision recovery, capturing not only the emergence of depth perception but also its integration into adaptive behavior. This approach may help refine clinical evaluations of vision restoration therapies, bridging the gap between sensory recovery and real-world functional outcomes.
Altered Effective Connectivity of the Numerical Brain in Children With Developmental Dyscalculia.
Schwizer Ashkenazi S, McCaskey U, O'Gorman Tuura R … +1 more , Kucian K
J Neurosci Res · 2025 Jul · PMID 40686324 · Full text
Numerical-order ability, a strong predictor of arithmetic, is often impaired in children with developmental dyscalculia (DD). While previous research has shown altered brain responses in number-processing regions in DD c...
Numerical-order ability, a strong predictor of arithmetic, is often impaired in children with developmental dyscalculia (DD). While previous research has shown altered brain responses in number-processing regions in DD compared to typically developing children (TD), little is known about how these regions interact during number processing. This exploratory study examined the effective connectivity between six regions in the right parietal, frontal, and insular cortex as well as the vermis, using dynamic causal modeling (DCM). We investigated how number-order and number-identification tasks modulate connectivity within this network and the group differences related to DD. The number-order task led primarily to increased excitatory connectivity from the pre-supplementary motor area (preSMA) to all other regions, indicating an orchestrating role of the preSMA. DD, who exhibited deficits in number-order performance, demonstrated aberrant modulation of incoming connectivity to the ventral premotor cortex (vPMC) from the anterior intraparietal sulcus (aIPS), the preSMA, and the dorsal anterior insula (d-aINS). In TD, number-identification led to inhibitory modulation from the vPMC to the aIPS and the vermis. While behavioral performance in number-identification was unimpaired in DD, they showed increased excitatory connectivity from dorsal and ventral PMC to the d-aINS and from vPMC to the aIPS. Our results imply that, for both impaired and unimpaired number-related behavioral performance, neuronal number processing differs between DD and TD. This conclusion is further supported by the high predictive validity of the modulating connectivity group-effect parameters. We suggest the underlying explanation for this pattern may be related to decreased acuity of neuronal number representation in DD.
Piano Training Induces Dynamic Neuroplasticity of Bimanual Coordination but Not Auditory Processing in Young Adults.
Olszewska AM, Gaca M, Droździel D … +3 more , Jednoróg K, Marchewka A, Herman AM
J Neurosci Res · 2025 Jul · PMID 40650444 · Publisher ↗
Piano training enables the study of the interplay between the auditory and motor domains in the acquisition of complex skill. Here, we uniquely combine longitudinal and cross-sectional designs to show how the motor and a...
Piano training enables the study of the interplay between the auditory and motor domains in the acquisition of complex skill. Here, we uniquely combine longitudinal and cross-sectional designs to show how the motor and auditory brain systems respond in novice pianists over a 6-month training period. In the auditory domain, we found no differences in brain activation between novice pianists and a passive control group. In a specially designed piano task on an MRI-compatible keyboard, we demonstrate that the time course of neuroplastic reorganization in the cortical and subcortical regions reflects the shift from spatial attention to automated movements, but depends on task demands related to bimanual coordination. Importantly, no single model of brain plasticity can fully explain the observed dynamic time courses of functional changes. Finally, we demonstrate that the increased activation in the dorsal premotor and parietal cortices in novice pianists compared to skilled musicians while performing the motor task vanishes within the first 6 months of training. These results present converging evidence that the dynamic musical-training-related plasticity is highly contextual, and underscore the importance of ecological designs in research on skill acquisition.
Peripheral Nerve Repair: Historical Perspectives, Current Advances, and Future Directions in Natural and Synthetic Neural Conduits.
Tabatabai TS, Alizadeh M, Farahani MK … +3 more , Ehterami A, Kloucheh SG, Salehi M
J Neurosci Res · 2025 Jul · PMID 40626373 · Publisher ↗
Regenerative medicine aims to restore damaged tissues or organs using stem cells, biomaterials, and decellularized grafts. Peripheral nerve injuries (PNI), affecting 2.8% of patients, lead to severe functional impairment...
Regenerative medicine aims to restore damaged tissues or organs using stem cells, biomaterials, and decellularized grafts. Peripheral nerve injuries (PNI), affecting 2.8% of patients, lead to severe functional impairments with global socioeconomic costs exceeding $7 billion annually. Despite advancements in surgical techniques, full functional recovery remains elusive, particularly in critical gap injuries (> 3 cm). Autografts remain the gold standard but are hindered by donor tissue scarcity and complications like neuroma formation. Allografts face challenges due to the lack of Schwann cells and neurotrophic support. Emerging approaches in tissue engineering leverage synthetic materials, such as polycaprolactone (PCL) and polylactic acid (PLA), and biological scaffolds like decellularized nerve grafts. These innovations provide structural support, promote axonal regeneration, and retain extracellular matrix components, enabling cell adhesion and migration while minimizing antigenicity. However, barriers such as mechanical instability, scar tissue formation, and inadequate cellularization persist. This review explores the anatomy and clinical significance of the sciatic nerve, historical perspectives on peripheral nerve repair, and current treatment strategies. It evaluates biological and synthetic nerve conduits, highlighting FDA-approved products and their advantages in promoting nerve regeneration. Additionally, the paper discusses challenges in the field, including limited functional recovery and the need for more effective clinical solutions. By combining natural and synthetic materials with growth factor delivery and vascularization strategies, engineered scaffolds hold promise for improving outcomes in PNI repair. Further research is essential to optimize these technologies and bridge existing gaps in clinical practice.
Curcumin Prevents Neuronal Loss and Inhibits Development of Spontaneous Recurrent Seizures via the PPARγ/PTEN/Akt Pathway in Chronic Epilepsy.
Hong S, GuoYan L, JiaWen W … +5 more , Xin Y, ShuQin Z, HongWei R, MengYing C, YuXuan C
J Neurosci Res · 2025 Jul · PMID 40613145 · Publisher ↗
Chronic epilepsy is mainly characterized by spontaneous recurrent seizures (SRS). The peroxisome proliferator activated receptor gamma/phosphatase and tensin homolog/protein kinase B (PPARγ/PTEN/Akt) pathway is involved...
Chronic epilepsy is mainly characterized by spontaneous recurrent seizures (SRS). The peroxisome proliferator activated receptor gamma/phosphatase and tensin homolog/protein kinase B (PPARγ/PTEN/Akt) pathway is involved in the pathogenesis of SRS and neuronal loss. Curcumin is a natural compound, and previous studies have shown it provides neuroprotection via anti-inflammation and anti-oxidant effects in many central nervous system (CNS) diseases. In the present study, we show that curcumin regulates the abnormal expression of PTEN and Akt in the SRS phase, improves the neuronal loss in the hippocampus, and suppresses SRS development and seizure spike activity in epileptic rats. More importantly, these effects are reversed by the PPARγ antagonist, T0070907, suggesting that curcumin exerts neuroprotective and anti-epileptic effects through the PPARγ/PTEN/Akt signaling pathway. Other studies have shown that curcumin can cross the BBB and has a safety profiles and pleiotropic pharmacological effects. Thus, our data support the proposition that curcumin might be a potential neuroprotective and anti-epileptic agent for chronic epilepsy.
P2X7R: A Critical Regulator and Potential Therapeutic Target for Glioma.
Yan M, Zhao R, Xue Y … +3 more , Cao Y, Du Y, Peng X
J Neurosci Res · 2025 Jul · PMID 40607594 · Publisher ↗
Glioma is the most common primary brain tumor, characterized by high invasiveness and poor prognosis. The purinergic ligand-gated ion channel 7 receptor (P2X7R), an ion channel-type purinergic receptor with adenosine tri...
Glioma is the most common primary brain tumor, characterized by high invasiveness and poor prognosis. The purinergic ligand-gated ion channel 7 receptor (P2X7R), an ion channel-type purinergic receptor with adenosine triphosphate (ATP) as its ligand, is widely expressed in various tumor cells, including glioma. Moreover, it plays crucial biological functions in the progression of glioma. P2X7R promotes the proliferation, invasion, and metastasis of glioma by activating multiple signaling pathways, facilitating epithelial-mesenchymal transition (EMT), promoting the release of extracellular vesicles (EVs) and regulating the tumor microenvironment (TME) of glioma. However, the activation of P2X7R by high concentrations of ATP can induce cell necrosis or pyroptosis, exerting an anti-glioma effect. The bidirectional nature of its functions may be related to differences in the subtypes of P2X7R, cell types, as well as the TME. P2X7R antagonists can inhibit its effect in glioma, while the expression of P2X7R can enhance the efficacy of radiotherapy and chemotherapy. In this review, the structure and function of P2X7R, its role in tumor, especially its mechanism of action in glioma, and its latent capacity value as a target for therapeutic of glioma were reviewed in detail.
Unveiling the Neural Pathways of Empathic Pain: Implications for Modulation Strategies and Beyond.
Zhang Y, Zhang K, Gong H … +2 more , Zhao M, Luo L
J Neurosci Res · 2025 Jul · PMID 40590479 · Publisher ↗
Empathic pain, a core manifestation of empathy, encompasses an individual's perceptual sensitivity, evaluative judgment, and emotional responsiveness to the suffering of others. This capacity is vital for healthy social...
Empathic pain, a core manifestation of empathy, encompasses an individual's perceptual sensitivity, evaluative judgment, and emotional responsiveness to the suffering of others. This capacity is vital for healthy social interaction, as it fosters prosocial behavior, inhibits aggression, and upholds moral norms critical to social development. This article provides a comprehensive review of current research on empathic pain, examining its conceptual foundations and the underlying neural mechanisms. In particular, it explores the activation of key brain regions, including the anterior cingulate cortex, insula, amygdala, and cerebellum, as well as the neural circuits linking these areas. Additionally, the paper summarizes various influencing factors and modulatory strategies related to empathic pain. These insights enhance our understanding of emotional resonance and establish a solid basis for developing clinical modulation models. Future research should adopt a multidisciplinary approach, incorporating advanced neuroimaging techniques, behavioral experiments, and broader clinical trials to further elucidate empathic pain and inform the development of more effective treatment strategies.
Single-Neuron Discharges Correlating High-Frequency Oscillations Dynamics in Epileptogenesis and Epilepsy Development.
Li X, He S, Wang J … +8 more , Feng G, Li D, Xing Y, Yang Y, Dai W, Yan J, Yang X, Zhou L
J Neurosci Res · 2025 Jul · PMID 40589109 · Publisher ↗
The mechanism of epilepsy is still unclear. We aim to explore the relationship between high-frequency oscillations (HFOs) dynamics and epilepsy, with a focus on deciphering underlying mechanisms at the single-neuron leve...
The mechanism of epilepsy is still unclear. We aim to explore the relationship between high-frequency oscillations (HFOs) dynamics and epilepsy, with a focus on deciphering underlying mechanisms at the single-neuron level. Using a rat model of chronic focal cortical epilepsy induced by cobalt-wire implantation, we monitored the seizures and HFO dynamics, as well as the cross-frequency coupling trends between HFOs and theta activities. Additionally, excitatory and inhibitory neurons' discharges were recorded by 16-channel tetrode electrode, with comparisons made between the discharge rates and changes from baselines during different bands of HFOs (ripple:80-200 Hz; fast ripple, FRs:200-500 Hz). All rats (8/8) with cobalt-wire implantation developed spontaneous seizures within 4 to 8 days post-surgery, in contrast to the control group (3/3) with steel-wire insertion remaining seizure-free. HFOs exhibited a progressive increase over time post-surgery in the epilepsy model, while minimal HFOs was observed in the control group. HFOs recorded during the peak-seizure periods showed a propensity to synchronize with the trough of theta activity, coinciding with heightened seizure frequency. A substantial augmentation showed in the discharge rates of both putative excitatory and inhibitory neurons during HFO occurrences. The change ratios between putative excitatory and inhibitory neurons during ripples were smaller than those during FRs. In conclusion, we found that HFO dynamics reflect epileptogenic network formation, with implications for early seizure prediction and therapeutic interventions. Our data provide novel insights at cellular and cross-frequency level into the mechanistic underpinnings of HFO emergence and network reorganization offering potential strategies for targeting pathological network activity in epilepsy.
Lanthionine Ketimine Ethyl Ester Induces Proliferation and Maturation and Regulates Calcium Flux in Primary Mouse Oligodendrocyte Progenitor Cells.
Cheli VT, Tumuluri SG, McDonald Z … +4 more , Denton TT, Dupree JL, Paez PM, Feinstein DL
J Neurosci Res · 2025 Jul · PMID 40579839 · Full text
Previous studies have shown that lanthionine ketimine ethyl ester (LKE), a semi-synthetic derivative of the endogenous amino acid lanthionine, can induce proliferation and maturation of oligodendrocyte progenitor cells (...
Previous studies have shown that lanthionine ketimine ethyl ester (LKE), a semi-synthetic derivative of the endogenous amino acid lanthionine, can induce proliferation and maturation of oligodendrocyte progenitor cells (OPCs) in vivo. In the current study, we examined the effects of LKE on Ca influx in primary mouse OPCs, as intracellular Ca can regulate those processes. Treatment with LKE stimulated proliferation of OPCs and increased the number of Olig2+, CC1+, and PLP+ cells. LKE also reduced cell death (caspase-3 expressing cells). Measurements of Ca flux showed that LKE increased basal Ca levels, reduced Ca influx following stimulation with glutamate or ATP, and increased Ca flux because of depolarization with KCl. Reduced Ca responses were also observed following treatment with a peptide that disrupts interactions of collapsin response mediated protein 2 (CRMP2), a primary target of LKE. These findings demonstrate regulation of Ca levels in OPCs by LKE and suggest that these actions may be mediated, in part, by CRMP2. LKE or related analogs could therefore be of benefit for the treatment of multiple sclerosis as well as other demyelinating conditions.
Characteristics and Changes of Cingulate Gyrus Function and Perfusion in Patients With Anti-N-Methyl-D-Aspartate Receptor Encephalitis.
Guo Y, Zhao Y, Li C … +6 more , Zhang J, Wei L, Wei Q, Zhou N, Wang K, Tian Y
J Neurosci Res · 2025 Jun · PMID 40556132 · Publisher ↗
Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is an autoimmune condition associated with neuropsychiatric and cognitive deficits. Changes in the cingulate cortex may be central to this disorder. This study inve...
Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is an autoimmune condition associated with neuropsychiatric and cognitive deficits. Changes in the cingulate cortex may be central to this disorder. This study investigates subregional alterations in the cingulate cortex of patients with anti-NMDAR encephalitis and their relationship to cognitive deficits using functional and perfusion imaging. Thirty-eight patients with anti-NMDAR encephalitis and 30 healthy controls (HC) underwent resting-state MRI and neuropsychological assessments. We measured low-frequency amplitude (fALFF), degree centrality (DC), and cerebral blood flow (CBF) in the cingulate cortex, and performed functional connectivity (FC) and CBF connectivity analyses. We also analyzed the relationship between subregional changes and cognitive impairment. Finally, we applied support vector machines (SVM) to classify patients and controls based on functional and perfusion features. Patients with anti-NMDAR encephalitis showed significant cognitive impairments in memory and executive function, along with anxiety symptoms. Neuroimaging revealed decreased fALFF, DC, and CBF in the left pregenual anterior cingulate cortex (pgACC.L). FC between pgACC.L and several brain regions, including the parahippocampal gyrus and precuneus, was reduced. Additionally, pgACC.L exhibited altered CBF connectivity patterns with other brain regions. Moreover, the changes of fALFF, DC, and FC are related to the impaired cognitive function of patients. SVM classification based on fALFF, DC, and CBF features successfully distinguished patients from controls. Our findings suggest that pgACC abnormalities play a key role in the pathomechanism of anti-NMDAR encephalitis and may serve as biomarkers for disease monitoring.
Concomitant Increases in Brain-Derived Neurotrophic Factor and Lactate Post-Exercise Do Not Demonstrate a Direct Correlation.
Ashcroft SK, Basclain K, Woolnough C … +6 more , Hoon MW, Walsh SJ, Starc LC, Johnson L, Kuys SS, Thompson-Butel AG
J Neurosci Res · 2025 Jun · PMID 40552481 · Full text
The aim of this study was to determine the relationship between BDNF and lactate concentration, accounting for genotype and sex, before and after a submaximal graded exercise test in 31 adults (37.5 ± 14.0 years, 54.8% f...
The aim of this study was to determine the relationship between BDNF and lactate concentration, accounting for genotype and sex, before and after a submaximal graded exercise test in 31 adults (37.5 ± 14.0 years, 54.8% female). The presence of the Val66Met polymorphism was identified at baseline, and BDNF and lactate concentrations were measured before and after exercise. Pearson's correlation coefficient was used to determine the relationship between BDNF and lactate concentration at pre- and post-exercise, and change in concentration (post- minus pre-exercise). The Val66Met polymorphism was identified in 11 participants (35%, seven females). An increase in BDNF and lactate concentration was observed from pre- to post-exercise (p < 0.001), but no significant correlation between the two measures was observed at pre-exercise (r = -0.256, p = 0.164), post-exercise (r = 0.112, p = 0.549), and change in concentration (r = 0.019, p = 0.921). A moderate inverse correlation was observed in participants with the Val66Met polymorphism (r = -0.744, p = 0.009) and males (r = -0.695, p = 0.006) at pre-exercise. The results show that while BDNF and lactate concentrations increased following a submaximal graded exercise test, there is little evidence to suggest a relationship exists between BDNF and lactate.
Protective Effect of Resveratrol Against Intracranial Aneurysm Rupture in Mice.
Dang DNP, Kamio Y, Kawakatsu T … +8 more , Makino H, Hokamura K, Imai R, Suzuki Y, Hiramatsu H, Zhitong L, Umemura K, Kurozumi K
J Neurosci Res · 2025 Jun · PMID 40546125 · Publisher ↗
Resveratrol is a polyphenol and potent antioxidant that has anti-inflammatory effects in conditions such as atherosclerosis, aortic aneurysm, and inflammatory bowel disease. In this study, we investigated whether resvera...
Resveratrol is a polyphenol and potent antioxidant that has anti-inflammatory effects in conditions such as atherosclerosis, aortic aneurysm, and inflammatory bowel disease. In this study, we investigated whether resveratrol exerts anti-inflammatory effects and protects against intracranial aneurysm formation and rupture in male mice. Intracranial aneurysms were induced in mice using a combination of elastase injection into the cerebrospinal fluid and deoxycorticosterone acetate-salt (DOCA-salt)-induced hypertension. Male mice were divided into two groups: a resveratrol diet group and a normal diet group. The dietary intervention lasted for 6 weeks, starting 3 weeks prior to elastase injection. The overall incidence of aneurysms did not differ significantly between the normal diet and resveratrol diet groups (71% vs. 59%, p = 0.497). However, resveratrol significantly reduced the rate of aneurysmal rupture compared with that in the normal diet group (88% vs. 40%, p = 0.026). Furthermore, resveratrol supplementation increased the mRNA levels of Sirtuin 1 (Sirt1) and decreased the mRNA levels of nuclear factor kappa B subunit 1 (Nfkb1) and Tumor necrosis factor (Tnf). Our findings demonstrate that resveratrol reduces intracranial aneurysm rupture in a mouse model, indicating its therapeutic potential in this condition.
Abnormal Static and Dynamic Functional Connectivity in Tension-Type Headache: A Support Vector Machine Analysis.
Li M, Zhang S, Chu F … +6 more , Zhan Y, Zhao M, Hao Z, Zhan L, Ren J, Jia X
J Neurosci Res · 2025 Jun · PMID 40519127 · Publisher ↗
Tension-type headache (TTH) is a primary headache with the highest prevalence. Previous studies have revealed the local brain abnormalities of TTH patients. However, little is known about its brain connectivity disruptio...
Tension-type headache (TTH) is a primary headache with the highest prevalence. Previous studies have revealed the local brain abnormalities of TTH patients. However, little is known about its brain connectivity disruption. Based on rs-fMRI data from 33 TTH patients and 30 healthy controls (HCs), static functional connectivity (FC) and dynamic FC were calculated between the default mode network (DMN) and the whole brain. Regions of interest (ROIs)-wise FC was performed to explore the connectivity pattern of the circuit established by the static and dynamic FC methods. The support vector machine (SVM) model was applied to distinguish the TTH patients from HCs. Compared with the HCs, TTH patients showed increased FC between the left posterior cingulate cortex (PCC) and the left parahippocampal and left middle frontal gyrus (MFG). Decreased dynamic FC was observed between the left PCC and right middle occipital gyrus (MOG), left precuneus, left inferior parietal gyrus (IPG), right median cingulate and paracingulate gyri (DCG) and right supplementary motor area (SMA) in TTH patients. The ROI-wise FC results showed that left precuneus-left IPG, left precuneus-right DCG, and left IPG-right SMA generated higher FC in TTH patients. SVM obtained a total accuracy of 70.476%, and the area under the curve (AUC) value was 0.658. TTH patients showed abnormal static and dynamic connectivity in multiple brain regions, and abnormal brain activity was also identified within these brain regions. This novel classification model using the brain connectivity could be useful in detecting neuro-markers for clinical applications in TTH patients.
Abscisic Acid Enhances Motor and Cognitive Function in the 3-Acetylpyridine Mouse Model of Cerebellar Ataxia.
Soti M, Ilaghi M, Ranjbar H … +3 more , Kohlmeier KA, Sabzalizadeh M, Shabani M
J Neurosci Res · 2025 Jun · PMID 40519112 · Publisher ↗
Cerebellar ataxia is a debilitating neurodegenerative disorder characterized by impaired motor coordination and balance with limited treatment options. Abscisic acid (ABA), a phytohormone detected in mammalian brains, ha...
Cerebellar ataxia is a debilitating neurodegenerative disorder characterized by impaired motor coordination and balance with limited treatment options. Abscisic acid (ABA), a phytohormone detected in mammalian brains, has shown neuroprotective properties. This study investigated the effects of ABA on motor, cognitive, and affective deficits in a mouse model of cerebellar ataxia in which male Swiss mice received a single intraperitoneal injection of 3-acetylpyridine (3-AP; 60 mg/kg), which leads to the loss of climbing fiber input to Purkinje neurons leading to cerebellar degeneration. In ABA-treated groups, ABA (10 or 15 μg/mouse) was intracerebroventricularly applied for four consecutive days. Behavioral testing consisted of open field, footprint analysis, wire grip, rotarod, tail suspension, elevated plus maze, Morris water maze, and the passive avoidance assay. Cerebellar brain-derived neurotrophic factor (BDNF) levels were measured using ELISA. As expected, 3-AP-treated mice exhibited significant motor impairments, increased anxiety-like and depressive-like behaviors, and cognitive deficits. ABA treatment, particularly at the 15 μg/mouse dose, significantly improved motor coordination, locomotor activity, memory, and spatial and passive avoidance learning as well as reduced anxiety-like and depressive-like behaviors. Behavioral changes were associated with normalization of the 3-AP-induced increases in cerebellar BDNF levels. This study demonstrates that ABA can ameliorate motor, cognitive, and affective deficits in a mouse model of cerebellar ataxia, which could involve BDNF and be due to neuroprotective effects in the cerebellum. By extension, our data suggest that ABA may have therapeutic potential in the management of cerebellar ataxia and other cerebellar disorders.
Attention Regulation Among Sleep-Deprived Air-Force Pilots.
Dolev T, Maoz I, Zubedat S … +7 more , Aga-Mizrachi S, Levkovsky A, Nakdimon I, Ben-Ari O, Grinstein D, Gordon B, Avital A
J Neurosci Res · 2025 Jun · PMID 40491070 · Full text
Short sleep duration is associated with adverse physical and mental events. However, it is quite challenging to objectively quantify its impact on human cognitive performance. Thus, we aim to examine the effects of sleep...
Short sleep duration is associated with adverse physical and mental events. However, it is quite challenging to objectively quantify its impact on human cognitive performance. Thus, we aim to examine the effects of sleep deprivation on physiological measures of emotional and attention regulation, in terms of recovery dynamics among sleep-deprived air force pilots. Ninety-one pilots participated in a sleep deprivation workshop held by an aeromedical center. The Auditory Sustained Attention Test (ASAT) and the Psychomotor Vigilance Test were applied to evaluate emotional and attention performance at baseline, post 24-h of sleep deprivation, following recovery of 3- and 8-h of sleep. Machine learning was used to predict the aerial professions based on the physiological measures. The results indicate that 24 h of sleep deprivation induced impairments in both attention and emotional regulation; however, while 3 h of sleep recovery have ameliorated emotional regulation and latency to response inhibition, attention performance required 8 h of sleep to ameliorate the observed 70% impairment. The physiologically measured adverse effects induced by sleep deprivation were distinctive among aerial professions, thus allowing machine learning prediction with high accuracy, sensitivity, and specificity. The effects of sleep-deprivation-induced fatigue were detected by the ASAT measures, which may be utilized as an objective, non-invasive physiological measure to quantify emotional and attention regulation. The ability to monitor sleep effects in a fast and accurate manner may be beneficial for the competence assessment of pilots and promote safety, and the differentiation across the aerial professions may potentially improve individual suitability assessment, together with the consequences of sleep deprivation.
Executive Function Decline and Its Association With TNF-α in the Later Stages of Post-Acute Sequelae of COVID.
Varenya A, Vijayalakshmi K, Babu MR
J Neurosci Res · 2025 Jun · PMID 40485151 · Publisher ↗
Beyond the immediate impact of the COVID-19 pandemic, survivors often grapple with incapacitating post-infection symptoms, referred to as Post-Acute Sequelae of COVID (PASC) when persistent beyond 90 days. Cognitive mani...
Beyond the immediate impact of the COVID-19 pandemic, survivors often grapple with incapacitating post-infection symptoms, referred to as Post-Acute Sequelae of COVID (PASC) when persistent beyond 90 days. Cognitive manifestations, encompassing attention, memory, and executive functions (EF), collectively termed brain fog, contribute to functional challenges in PASC. This infection also elicits a long-lasting pro-inflammatory response that persists even after viral clearance, potentially correlated with brain fog. However, it is unclear whether pro-inflammatory responses and cognitive sequelae persist beyond 1 year after the onset of infection. Thus, this study sought to investigate the long-term consequences of PASC on EFs as well as a potential association with markers of inflammation. Forty individuals with PASC who passed performance validity testing (PVT) and 40 matched healthy controls (HC) underwent neuropsychological assessments, including the Montreal Cognitive Assessment to assess global cognition, Victoria Stroop Test to assess inhibitory control, Wisconsin Card Sorting Test to assess cognitive flexibility, Digit Span Task to assess working memory, and Mackworth Clock Test to assess sustained attention on the Psychology Experiment Building Language (PEBL) toolkit. Serum was assayed for tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10). Results indicate significant EF decline in PASC, inversely correlated with serum TNF-α concentrations, approximately 562 ± 225 days after the onset of infection. Thus, there exists protracted EF decline in PASC, persistent even beyond 1 year after the onset of infection. Increased levels of TNF-α are observed to be associated with poorer executive functioning in PASC.
Adenylyl Cyclase Activator: Forskolin Mediates CREB ser133 Phosphorylation in the Hippocampus, Alleviates Autism-Like Deficits in a Valproic Acid Model of Wistar Rats.
Jain A, Dhir N, Prabha PK … +11 more , Raja A, Sharma AR, Kaundal T, Charan S, Bhatia A, Banerjee D, Saikia B, Zohmangaihi D, Goyal MK, Medhi B, Prakash A
J Neurosci Res · 2025 Jun · PMID 40457879 · Publisher ↗
Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by social deficits, restricted interest, and repetitive behaviors. The prevalence is higher in males (4:1). FDA-approved drugs, Aripi...
Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by social deficits, restricted interest, and repetitive behaviors. The prevalence is higher in males (4:1). FDA-approved drugs, Aripiprazole, and risperidone, only target comorbid conditions and have significant side effects. Dysregulation in cAMP-responsive element-binding protein (CREB) signaling is reported in autistic individuals. Forskolin is traditionally used in Ayurvedic medicine with lesser side effects. It is a potent adenylyl cyclase (AC) activator, increases intracellular cyclic adenosine monophosphate (cAMP) levels, thereby activating the protein kinase A (PKA)/CREB pathway with clinically proven benefits as an anticancer, anti-asthmatic, and in metabolic disorder, and crosses the blood-brain-barrier (BBB) junction. The present study aimed to investigate the impact of Forskolin and sought to explore the role of estrogen beta (ERβ/ESR2) receptors in a valproic acid (VPA) model of ASD. Pregnant Wistar rats received VPA or an equal volume of saline on gestational day (GD) 12.5. From postnatal day (PND) 23, male and female rats were divided separately into control, VPA, risperidone, and Forskolin (10-30 mg/kg) groups. Systemic administration of Forskolin ameliorated anxiety, social deficit, repetitive behavior, spatial recognition memory, motor coordination, gastrointestinal (GIT) motility, brain edema, and BBB permeability in a dose-dependent manner. Moreover, chronic Forskolin treatment significantly alleviated VPA-induced neuronal damage in the prefrontal cortex (PFC), hippocampus (HC), and cerebellum, and increased the intracellular CREB ser133 protein phosphorylation. Forskolin upregulated the mRNA expression of CREB signaling, which was altered by prenatal VPA administration. Our findings indicate that Forskolin provides neuroprotection through CREB signaling, suggesting its therapeutic potential for ASD.
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