Neural Dysfunction Research Articles

The activation of the piriform cortex to lateral septum pathway during chronic social defeat stress is crucial for the induction of behavioral disturbance in mice.

Chronic stress induces neural dysfunctions and risks mental illnesses. Clinical and preclinical studies have established the roles of brain regions underlying emotional and cognitive functions in stress and depression. However, neural pathways to perceive sensory stimuli as stress to cause behavioral disturbance remain unknown. Using whole-brain imaging of Arc-dVenus neuronal response reporter mice and machine learning analysis, here we unbiasedly demonstrated different patterns of contribution of widely distributed brain regions to neural responses to acute and chronic social defeat stress (SDS). Among these brain regions, multiple sensory cortices, especially the piriform (olfactory) cortex, primarily contributed to classifying neural responses to chronic SDS. Indeed, SDS-induced activation of the piriform cortex was augmented with repetition of SDS, accompanied by impaired odor discrimination. Axonal tracing and chemogenetic manipulation showed that excitatory neurons in the piriform cortex directly project to the lateral septum and activate it in response to chronic SDS, thereby inducing behavioral disturbance. These results pave the way for identifying a spatially defined sequence of neural consequences of stress and the roles of sensory pathways in perceiving chronic stress in mental illness pathology.

Glia-related Acute Effects of Risperidone and Haloperidol in Hippocampal Slices and Astrocyte Cultures from Adult Wistar Rats: A Focus on Inflammatory and Trophic Factor Release.

Antipsychotics are drugs commonly prescribed to treat a variety of psychiatric conditions. They are classified as typical and atypical, depending on their affinity for dopaminergic and serotonergic receptors. Although neurons have been assumed to be the major mediators of the antipsychotic pharmacological effects, glia, particularly astrocytes, have emerged as important cellular targets for these drugs. In the present study, we investigated the effects of acute treatments with the antipsychotics risperidone and haloperidol of hippocampal slices and astrocyte cultures, focusing on neuron-glia communication and how antipsychotics act in astrocytes. For this, we obtained hippocampal slices and primary astrocyte cultures from 30-day-old Wistar rats and incubated them with risperidone or haloperidol (1 and 10μM) for 30min and 24h, respectively. We evaluated metabolic and enzymatic activities, the glutathione level, the release of inflammatory and trophic factors, as well as the gene expression of signaling proteins. Haloperidol increased glucose metabolism; however, neither of the tested antipsychotics altered the glutathione content or glutamine synthetase and Na+K+-ATPase activities. Haloperidol induced a pro-inflammatory response and risperidone promoted an anti-inflammatory response, while both antipsychotics seemed to decrease trophic support. Haloperidol and risperidone increased Nrf2 and HO-1 gene expression, but only haloperidol upregulated NFκB and AMPK gene expression. Finally, astrocyte cultures confirmed the predominant effect of the tested antipsychotics on glia and their opposite effects on astrocytes. Therefore, antipsychotics cause functional alterations in the hippocampus. This information is important to drive future research for strategies to attenuate antipsychotics-induced neural dysfunction, focusing on glia.

Ferroptosis as a Therapeutic Target in Neurodegenerative Diseases: Exploring the Mechanisms and Potential of Treating Alzheimer's Disease and Parkinson's Disease.

Amidst the rising global burden of neurodegenerative diseases, such as Alzheimer's and Parkinson's diseases, there is an urgent need for novel therapeutic strategies to combat these debilitating conditions. These diseases are characterized by progressive neural dysfunction leading to cognitive impairments, for which current therapeutic strategies remain palliative at best. Recently, the discovery of ferroptosis, a novel cell death mode that is different from apoptosis and autophagy, has opened new avenues in the field of cognitive research. With in-depth research on ferroptosis, the clinical significance of iron homeostasis disorders and lipid peroxidation in the occurrence, development, and treatment of neurodegenerative diseases are gradually becoming apparent. This study aims to elucidate the roles of ferroptosis in the context of neurodegeneration and to explore its potential as a therapeutic target. By unraveling the intricate relationship between iron homeostasis disorders, oxidative damage, and lipid metabolism disturbances in these diseases, new intervention targets are revealed. It offers a new dimension to the management of neurocognitive impairments in Alzheimer's and Parkinson's diseases. The implications of these findings extend beyond just Alzheimer's and Parkinson's diseases. They also have relevance with other neurological conditions characterized by oxidative stress and iron dysregulation. This review contributes to increased knowledge of ferroptosis and provides a foundational understanding that could lead to the development of innovative therapeutic strategies. Ultimately, it may alleviate the development of neurodegenerative diseases and improve cognitive function by preventing ferroptosis, which has not only academic significance but also potential clinical significance.

Reverse engineering of feedforward cortical-Hippocampal microcircuits for modelling neural network function and dysfunction

Engineered biological neural networks are indispensable models for investigation of neural function and dysfunction from the subcellular to the network level. Notably, advanced neuroengineering approaches are of significant interest for their potential to replicate the topological and functional organization of brain networks. In this study, we reverse engineered feedforward neural networks of primary cortical and hippocampal neurons, using a custom-designed multinodal microfluidic device with Tesla valve inspired microtunnels. By interfacing this device with nanoporous microelectrodes, we show that the reverse engineered multinodal neural networks exhibit capacity for both segregated and integrated functional activity, mimicking brain network dynamics. To advocate the broader applicability of our model system, we induced localized perturbations with amyloid beta to study the impact of pathology on network functionality. Additionally, we demonstrate long-term culturing of subregion- and layer specific neurons extracted from the entorhinal cortex and hippocampus of adult Alzheimer’s-model mice and rats. Our results thus highlight the potential of our approach for reverse engineering of anatomically relevant multinodal neural networks to study dynamic structure-function relationships in both healthy and pathological conditions.

From Compression to Itch: Exploring the Link Between Nerve Compression and Neuropathic Pruritus.

Neuropathic itch is a type of chronic pruritus resulting from neural dysfunction along the afferent pathway. It is often accompanied by abnormal sensations such as paresthesia, hyperesthesia, or hypoesthesia. This condition, which may involve motor or autonomic neural damage, significantly impacts patients' quality of life, causing severe itch and associated comorbidities such as depression, disrupted sleep, and social strain. Neuropathic itch accounts for 8% of chronic pruritus cases, though this may be underestimated. This comprehensive review focuses on nerve impingement as the primary pathophysiological mechanism for various forms of neuropathic itch including brachioradial pruritus (BRP), notalgia paresthetica (NP), and anogenital itch. BRP, often seen in middle-aged white women, manifests as pruritus in the dorsolateral forearms typically exacerbated by ultraviolet (UV) exposure and related to cervical spine pathology. NP, prevalent in middle-aged women, presents as pruritus in the upper back due to thoracic spine nerve compression. Anogenital pruritus, affecting 1-5% of adults, is often linked to lumbosacral spine issues after ruling out dermatologic conditions such as lichen sclerosus or lichen simplex chronicus. The pathophysiology of neuropathic itch involves both peripheral and central mechanisms, with nerve damage being a key factor. Diagnosis requires a thorough history, physical examination, and potentially imaging studies. Topical agents such as menthol, capsaicin, and lidocaine are used for mild cases, while systemic medications such as gabapentin, pregabalin, and antidepressants are prescribed for moderate to severe cases; however, no USFood and Drug Administration (FDA)-approved therapies currently exist specifically for neuropathic itch. Understanding the underlying neural dysfunction and appropriate therapeutic strategies is crucial for managing neuropathic itch effectively.

Auditory and vestibular function in mitochondrial patients harbouring the m.3243A>G variant.

Hearing impairment is a frequent clinical feature in patients with mitochondrial disease harbouring the pathogenic variant, m.3243A>G. However, auditory neural dysfunction, its perceptual consequences and implications for patient management are not established. Similarly, the association with vestibular impairment has not yet been explored. This case-control study investigated in 12 adults with genetically confirmed m.3243A>G adults [9 females; 45.5 ± 16.3 years (range 18-66); 47.1 ± 21.5 hearing level, dB] compared with 12 age, sex and hearing level-matched controls with sensory (cochlear level) hearing loss [9 females; 46.6 ± 11.8 years (range 23-59); 47.7 ± 25.4 hearing level, dB]. Participants underwent a battery of electroacoustic, electrophysiologic and perceptual tests, which included pure tone audiometry, otoacoustic emissions, auditory brainstem responses, auditory temporal processing measures, monaural/binaural speech perception, balance and vestibular testing and self-reported questionnaires (dizziness and hearing disability). Our findings showed evidence of auditory neural abnormality and perceptual deficits greater than expected for cochlear pathology. Compared with matched controls with sensory hearing loss, adults with mitochondrial disease harbouring m.3243A>G had abnormal electrophysiologic responses from the VIII nerve and auditory brainstem (P = 0.005), an impaired capacity to encode rapidly occurring acoustic signal changes (P = 0.005), a reduced ability to localize sound sources (P = 0.028) and impaired speech perception in background noise (P = 0.008). Additionally, vestibular dysfunction (P = 0.011), greater perceived dizziness (P = 0.001) and reduced stance time (balance, P = 0.009) were also seen in participants with m.3243A>G mitochondrial disease when compared with matched counterparts. This pilot study revealed that auditory evaluation including evoked potential responses from the auditory nerve/brainstem and speech perception in noise tests should form an important part of the management for individuals with m.3243A>G-related mitochondrial disease. Those presenting with hearing impairment and symptoms concerning balance and dizziness should undergo vestibular testing and appropriate management.

2-Acetylacteoside improves recovery after ischemic stroke by promoting neurogenesis via the PI3K/Akt pathway

Ischemic stroke induces adult neurogenesis in the subventricular zone (SVZ), even in elderly patients. Harnessing of this neuroregenerative response presents the therapeutic potential for post-stroke recovery. We found that phenylethanoid glycosides (PhGs) derived from Cistanche deserticola aid neural repair after stroke by promoting neurogenesis. Among these, 2-acetylacteoside had the most potent on the proliferation of neural stem cells (NSCs) in vitro. Furthermore, 2-acetylacteoside was shown to alleviate neural dysfunction by increase neurogenesis both in vivo and in vitro. RNA-sequencing analysis highlighted differentially expressed genes within the PI3K/Akt signaling pathway. The candidate target Akt was validated as being regulated by 2-acetylacteoside, which, in turn, enhanced the proliferation and differentiation of cultured NSCs after oxygen-glucose deprivation/reoxygenation (OGD/R), as evidenced by Western blot analysis. Subsequent analysis using cultured NSCs from adult subventricular zones (SVZ) confirmed that 2-acetylacteoside enhanced the expression of phosphorylated Akt (p-Akt), and its effect on NSC neurogenesis was shown to be dependent on the PI3K/Akt pathway. In summary, our findings elucidate for the first time the role of 2-acetylacteoside in enhancing neurological recovery, primarily by promoting neurogenesis via Akt activation following ischemic brain injury, which offers a novel strategy for long-term cerebrological recovery in ischemic stroke.

Bioaccumulation, transformation and toxicity of imidacloprid and dinotefuran in Eisenia fetida under single and binary exposure scenarios

Earthworms (Eisenia fetida) were exposed to individual and binary mixture of imidacloprid (IMI) and dinotefuran (DIN) at 0.05 and 0.5 mg/kg for 28 days to investigate their bioaccumulation, transformation and toxicity. IMI was more easily absorbed by earthworms than DIN, and worms didn’t accumulate or generate toxic metabolites. The obvious accumulation of neonicotinoids during later period caused significant neural dysfunction, especially when exposed to high-concentration IMI. Meanwhile, oxidative stress indicated by decreased SOD/CAT activity (33.2 %-68.1 %) and increased MDA (38.4 %-55.0 %) was induced by binary exposure with high-concentration IMI. By contrast, coelomocytes responded earlier and more strongly than oxidative responses. Coelomocytes’ viability and mitochondrial membrane potential were inhibited (23.6 %-91.7 %) mainly by IMI and binary exposure. Coelomocytes’ lactate dehydrogenase activity exerted a fluctuating pattern, suggesting irregular disturbance on cellular functions. This study highlights the role of coelomocytes and the need to consider binary/multiple scenarios and transformation of neonicotinoids in their risk assessment to earthworms.

Methamphetamine-related working memory difficulties underpinned by reduced frontoparietal responses.

Working memory difficulties are common, debilitating, and may pose barriers to recovery for people who use methamphetamine. Yet, little is known regarding the neural dysfunctions accompanying these difficulties. Here, we acquired cross-sectional, functional magnetic resonance imaging while people with problematic methamphetamine-use experience (MA+, n =65) and people without methamphetamine-use experience (MA-, n =44) performed a parametric n-back task (0-back through 2-back). Performance on tasks administered outside of the scanner, together with n-back performance, afforded to determine a latent dimension of participants' working memory ability. Behavioural results indicated that MA+ participants exhibited lower scores on this dimension compared to MA- participants (d = -1.39, p < .001). Whole-brain imaging results also revealed that MA+ participants exhibited alterations in load-induced responses predominantly in frontoparietal and default-mode areas. Specifically, while the MA- group exhibited monotonic activation increases within frontoparietal areas and monotonic decreases within default-mode areas from 0-back to 2-back, MA+ participants showed a relative attenuation of these load-induced activation patterns (d = -1.55, p < .001). Moreover, increased activations in frontoparietal areas from 0- to 2-back were related to greater working memory ability among MA+ participants (r = .560, p = .004). No such effects were observed for default-mode areas. In sum, reductions in working memory ability were observed alongside load-induced dysfunctions in frontoparietal and default-mode areas for people with problematic methamphetamine-use experience. Among them, load-induced activations within frontoparietal areas were found to have a strong and specific relationship to individual differences in working memory ability, indicating a putative neural signature of the working memory difficulties associated with chronic methamphetamine use.

Linear Monotonic Inter-electrode Associations as Quantitative EEG for Alcoholism Diagnosis

Alcohol use disorders (AUDs) are associated with alterations in EEG patterns that reflect underlying neural dysfunctions, such as impaired cognitive processing, reduced neural connectivity, and disrupted brain rhythms. These EEG alterations can be indicative of several brain disorders, including cognitive deficits, mood disorders, and neurodegenerative diseases, which are often exacerbated by chronic alcohol abuse. Cognitive impairment in alcoholic subjects is caused due to altered functional connectivity between brain regions that can be quantified using statistical measures such as correlation. This paper proposes novel Quantitative EEG (QEEG) features comprising the band-wise absolute value of inter-electrode correlations as a measure of brain functional connectivity to classify alcoholic and non-alcoholic EEG. The EEG signal is first decomposed into five frequency sub-bands. In each sub-band, the absolute value of the linear Pearson product-moment correlation coefficient is computed between time-series EEG recorded by electrode pairs placed over different brain regions. To reduce the dimensionality of the feature vector, an ensemble feature selection approach is adopted, utilizing ANOVA and Chi-square, in conjunction with greedy forward feature selection wrapper algorithm. Four classifiers, namely SVM, KNN, ANN and RF are utilized for the classification. Among them, the SVM classifier achieves the best classification accuracies of 100% on validation with test data and 99.58% on cross-validation with train data, respectively.

GABAergic dysfunction in postmortem dorsolateral prefrontal cortex: implications for cognitive deficits in schizophrenia and affective disorders.

The microcircuitry within superficial layers of the dorsolateral prefrontal cortex (DLPFC), composed of excitatory pyramidal neurons and inhibitory GABAergic interneurons, has been suggested as the neural substrate of working memory performance. In schizophrenia, working memory impairments are thought to result from alterations of microcircuitry within the DLPFC. GABAergic interneurons, in particular, are crucially involved in synchronizing neural activity at gamma frequency, the power of which increases with working memory load. Alterations of GABAergic interneurons, particularly parvalbumin (PV) and somatostatin (SST) subtypes, are frequently observed in schizophrenia. Abnormalities of GABAergic neurotransmission, such as deficiencies in the 67 kDA isoform of GABA synthesis enzyme (GAD67), vesicular GABA transporter (vGAT), and GABA reuptake transporter 1 (GAT1) in presynaptic boutons, as well as postsynaptic alterations in GABA A receptor subunits further contribute to impaired inhibition. This review explores GABAergic abnormalities of the postmortem DLPFC in schizophrenia, with a focus on the roles of interneuron subtypes involved in cognition, and GABAergic neurotransmission within presynaptic boutons and postsynaptic alterations. Where available, comparisons between schizophrenia and affective disorders that share cognitive pathology such as bipolar disorder and major depressive disorder will be made. Challenges in directly measuring GABA levels are addressed, emphasizing the need for innovative techniques. Understanding GABAergic abnormalities and their implications for neural circuit dysfunction in schizophrenia is crucial for developing targeted therapies.

Abstract P229: Neurovascular and Cognitive Dysfunction in Hypertension at the Single-Cell Level

Hypertension (HTN) is the leading cause of vascular cognitive impairment, which has been attributed to altered microvascular regulation, neural network dysfunction and white matter (WM) damage. However, the neurovascular cells and cellular networks through which microvascular alterations lead to neuronal dysfunction and WM damage require elucidation. We employed unbiased single-cell RNA sequencing of the neocortex in 10-week-old C57BL/6 male mice treated with AngII (600ng/kg/min s.c.) or vehicle, to map out the transcriptomic changes induced by HTN. Transcriptomes (3 mice/group) were obtained for 39,451 cells before (day 3 after AngII) and after development of neurovascular and cognitive dysfunction (day 42). Profound transcriptional alterations were already seen at day 3 in venular endothelial cells (EC), GABAergic interneurons expressing neuronal nitric oxide synthase (nNOS), and oligodendrocyte precursors (OPC) (EdgeR; FDR&lt; 0.05, logFC&gt; 2). Gene ontology (GO) analysis (p &lt;0.05) revealed terms consistent with senescence of venular EC, validated by immunolabeling with senescence markers (β-galactosidase, p27, p21, p16). GO also flagged terms reflecting suppression of neuronal NO synthesis and synaptic dysfunction in interneurons, which were confirmed by demonstrating reduced NMDA-evoked NO release in brain slices (20±0.03% Veh vs. 0±0.03% AngII;p&lt;0.0001;n=60 neurons from 5 slices/group) and loss of the vesicular GABA transporter, VGAT. In addition, GO revealed early impairments in OPC differentiation, which could underlie later WM disruption. Consistent with this prediction, transcripts suggestive of impaired myelination were overrepresented at 42 days in mature oligodendrocytes (e.g., Hes5 ), and these WM alterations were confirmed in vivo by an increase in internodal distance (Nav1.6/CASPR) in axons (0.09±0.014 µm 3 Veh vs. 0.16±0.01 µm 3 AngII;n=4/group;p&lt;0.05). Ligand-receptor interaction analysis (CellChat) indicated molecular reprogramming of oligodendrocytes by senescent EC via suppression of signaling promoting myelination (CD39-AdeRA1) and upregulation of signaling arresting OPC development (Endothelin-ER2). These data reveal a previously unappreciated susceptibility of venular EC, OPC and nNOS interneurons to the deleterious effects of AngII HTN, and point to a novel pathogenic interaction between senescent EC and OPC, as well as to early nNOS interneuron dysfunction, the disease relevance and therapeutic potential of which requires validation.

Drp1 depletion protects against ferroptotic cell death by preserving mitochondrial integrity and redox homeostasis

Mitochondria are highly dynamic organelles which undergo constant fusion and fission as part of the mitochondrial quality control. In genetic diseases and age-related neurodegenerative disorders, altered mitochondrial fission-fusion dynamics have been linked to impaired mitochondrial quality control, disrupted organelle integrity and function, thereby promoting neural dysfunction and death. The key enzyme regulating mitochondrial fission is the GTPase Dynamin-related Protein 1 (Drp1), which is also considered as a key player in mitochondrial pathways of regulated cell death. In particular, increasing evidence suggests a role for impaired mitochondrial dynamics and integrity in ferroptosis, which is an iron-dependent oxidative cell death pathway with relevance in neurodegeneration. In this study, we demonstrate that CRISPR/Cas9-mediated genetic depletion of Drp1 exerted protective effects against oxidative cell death by ferroptosis through preserved mitochondrial integrity and maintained redox homeostasis. Knockout of Drp1 resulted in mitochondrial elongation, attenuated ferroptosis-mediated impairment of mitochondrial membrane potential, and stabilized iron trafficking and intracellular iron storage. In addition, Drp1 deficiency exerted metabolic effects, with reduced basal and maximal mitochondrial respiration and a metabolic shift towards glycolysis. These metabolic effects further alleviated the mitochondrial contribution to detrimental ROS production thereby significantly enhancing neural cell resilience against ferroptosis. Taken together, this study highlights the key role of Drp1 in mitochondrial pathways of ferroptosis and expose the regulator of mitochondrial dynamics as a potential therapeutic target in neurological diseases involving oxidative dysregulation.

Progress of researches on the mechanisms of acupuncture intervention underlying improvement of ischemic stroke by regulating microRNAs.

MicroRNAs play an important role in the occurrence and development of ischemic stroke (IS). A lot of researches have shown that acupuncture intervention can improve IS-induced neural dysfunction by regulating miRNA. In the present paper, we summarized the current progress of researches on the mechanisms of acupuncture underlying improvement of IS via regulation of miRNA from 1) promoting angiogenesis and increasing cerebral blood flow, 2) inhibiting inflammatory response, 3) maintaining blood-brain barrier homeostasis and relieving brain edema, 4) regulating programmed cell death, 5) promoting neuron regeneration, and 6) improving synaptic plasticity. These miRNA -related mechanisms may provide a reference for the follow-up research .

Targeting high-affinity nicotinic receptors protects against the functional consequences of β-amyloid in mouse hippocampus.

The accumulation of β-amyloid oligomers is a hallmark of Alzheimer's disease, inducing neural and network dysfunction in the early stages of pathology. The hippocampus is affected early in the pathogenesis of AD, however the impact of soluble β-amyloid on the dentate gyrus (DG) subregion of the hippocampus and its interaction with nicotinic acetylcholine receptors (nAChRs) within this region are not known. Using a localized model of over-expression, we show that β-amyloid induces early-onset neuronal hyperactivity and hippocampal-dependent memory deficits in mice. Further, we find the DG region to be under potent and sub-type specific nicotinic control in both healthy and pathophysiological conditions, with targeted receptor inhibition leading to a mnemonic rescue against localized amyloidosis. We show that while neurogenesis and synaptic functions are not severely affected in our model, reducing β2-containing nAChR function is associated with the promotion of young adult-born neurons within the pathological network, suggesting a possible protective mechanism. Our data thus reveal the DG network level changes which occur in the early-stages of β-amyloid accumulation and highlight the downstream consequences of targeted nicotinic neuromodulation.

Insulin restores retinal ganglion cell functional connectivity and promotes visual recovery in glaucoma.

Dendrite pathology and synaptic loss result in neural circuit dysfunction, a common feature of neurodegenerative diseases. There is a lack of strategies that target dendritic and synaptic regeneration to promote neurorecovery. We show that daily human recombinant insulin eye drops stimulate retinal ganglion cell (RGC) dendrite and synapse regeneration during ocular hypertension, a risk factor to develop glaucoma. We demonstrate that the ribosomal protein p70S6 kinase (S6K) is essential for insulin-dependent dendritic regrowth. Furthermore, S6K phosphorylation of the stress-activated protein kinase-interacting protein 1 (SIN1), a link between the mammalian target of rapamycin complexes 1 and 2 (mTORC1/2), is required for insulin-induced dendritic regeneration. Using two-photon microscopy live retinal imaging, we show that insulin rescues single-RGC light-evoked calcium (Ca2+) dynamics. We further demonstrate that insulin enhances neuronal survival and retina-brain connectivity leading to improved optomotor reflex-elicited behaviors. Our data support that insulin is a compelling pro-regenerative strategy with potential clinical implications for the treatment and management of glaucoma.

BRAIN TUMOR AND EPILEPSY IN CHILDREN: CLINICAL COMPLICATIONS AND SURGICAL TREATMENT

Introduction: Brain tumors in children often present a complex intersection with epilepsy, creating significant challenges for diagnosis and treatment. The presence of brain tumors can lead to the development of epilepsy, which may manifest in various forms depending on the tumor's location and type. Clinical complications include refractory epileptic seizures, neuropsychomotor development impairment, and deterioration in quality of life. Surgical treatment can be crucial for both tumor removal and seizure control, offering the possibility of seizure remission and improving overall prognosis. Objective: The systematic literature review aimed to evaluate the relationship between brain tumors and epilepsy in children, focusing on clinical complications and surgical treatment strategies. Methodology: The methodology followed the PRISMA checklist to ensure a comprehensive and rigorous review. Databases such as PubMed, Scielo, and Web of Science were consulted using descriptors like "pediatric brain tumor," "epilepsy in children," "clinical complications," "surgical treatment," and "pediatric neurosurgery." Inclusion criteria were studies on brain tumors in children, research addressing epilepsy as a symptom or complication, and articles describing surgical treatment. Articles not available in full text, studies outside the pediatric scope, and publications prior to 2014 were excluded. Results: The review revealed that brain tumors can cause epilepsy due to cortical irritation and neural dysfunction. Surgical treatment is often effective in reducing or eliminating epileptic seizures but can be challenging due to the tumor's location and characteristics. Additionally, the results showed that complete tumor resection is associated with better clinical outcomes in terms of seizure control. The literature also highlighted the importance of postoperative monitoring to detect and manage complications. Conclusion: Brain tumors in children frequently lead to epilepsy, and surgical treatment is essential for seizure control and improving quality of life. Complete tumor removal is crucial for positive outcomes, and ongoing monitoring is necessary to manage potential complications. The review highlighted the importance of a multidisciplinary approach to optimize clinical outcomes and patient quality of life.

KineWheel-DeepLabCut Automated Paw Annotation Using Alternating Stroboscopic UV and White Light Illumination.

Uncovering the relationships between neural circuits, behavior, and neural dysfunction may require rodent pose tracking. While open-source toolkits such as DeepLabCut have revolutionized markerless pose estimation using deep neural networks, the training process still requires human intervention for annotating key points of interest in video data. To further reduce human labor for neural network training, we developed a method that automatically generates annotated image datasets of rodent paw placement in a laboratory setting. It uses invisible but fluorescent markers that become temporarily visible under UV light. Through stroboscopic alternating illumination, adjacent video frames taken at 720 Hz are either UV or white light illuminated. After color filtering the UV-exposed video frames, the UV markings are identified and the paw locations are deterministically mapped. This paw information is then transferred to automatically annotate paw positions in the next white light-exposed frame that is later used for training the neural network. We demonstrate the effectiveness of our method using a KineWheel-DeepLabCut setup for the markerless tracking of the four paws of a harness-fixed mouse running on top of the transparent wheel with mirror. Our automated approach, made available open-source, achieves high-quality position annotations and significantly reduces the need for human involvement in the neural network training process, paving the way for more efficient and streamlined rodent pose tracking in neuroscience research.

Exploring viral neuropathic pain: Molecular mechanisms and therapeutic implications.

As the Coronavirus Disease 2019 (COVID-19) pandemic continues, there is a growing concern regarding the relationship between viral infections and neuropathic pain. Chronic neuropathic pain resulting from virus-induced neural dysfunction has emerged as a significant issue currently faced. However, the molecular mechanisms underlying this phenomenon remain unclear, and clinical treatment outcomes are often suboptimal. Therefore, delving into the relationship between viral infections and neuropathic pain, exploring the pathophysiological characteristics and molecular mechanisms of different viral pain models, can contribute to the discovery of potential therapeutic targets and methods, thereby enhancing pain relief and improving the quality of life for patients. This review focuses on HIV-related neuropathic pain (HNP), postherpetic neuralgia (PHN), and neuropathic pain caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infections, examining rodent models and relevant cellular molecular pathways. Through elucidating the connection between viral infections and neuropathic pain, it aims to delineate the current limitations and challenges faced by treatments, thereby providing insights and directions for future clinical practice and research.

Advances in Brain Stimulation, Nanomedicine and the Use of Magnetoelectric Nanoparticles: Dopaminergic Alterations and Their Role in Neurodegeneration and Drug Addiction.

Recent advancements in brain stimulation and nanomedicine have ushered in a new era of therapeutic interventions for psychiatric and neurodegenerative disorders. This review explores the cutting-edge innovations in brain stimulation techniques, including their applications in alleviating symptoms of main neurodegenerative disorders and addiction. Deep Brain Stimulation (DBS) is an FDA-approved treatment for specific neurodegenerative disorders, including Parkinson's Disease (PD), and is currently under evaluation for other conditions, such as Alzheimer's Disease. This technique has facilitated significant advancements in understanding brain electrical circuitry by enabling targeted brain stimulation and providing insights into neural network function and dysfunction. In reviewing DBS studies, this review places particular emphasis on the underlying main neurotransmitter modifications and their specific brain area location, particularly focusing on the dopaminergic system, which plays a critical role in these conditions. Furthermore, this review delves into the groundbreaking developments in nanomedicine, highlighting how nanotechnology can be utilized to target aberrant signaling in neurodegenerative diseases, with a specific focus on the dopaminergic system. The discussion extends to emerging technologies such as magnetoelectric nanoparticles (MENPs), which represent a novel intersection between nanoformulation and brain stimulation approaches. These innovative technologies offer promising avenues for enhancing the precision and effectiveness of treatments by enabling the non-invasive, targeted delivery of therapeutic agents as well as on-site, on-demand stimulation. By integrating insights from recent research and technological advances, this review aims to provide a comprehensive understanding of how brain stimulation and nanomedicine can be synergistically applied to address complex neuropsychiatric and neurodegenerative disorders, paving the way for future therapeutic strategies.