Search Results (424)

Among myrmecophilous insects, beetles represent the most specialised and diverse group. Myrmecophily is a complex evolutionary strategy encompassing a wide spectrum of interactions with ants, ranging from occasional to obligate relationships, and from mutualistic associations (e.g., trophobionts) to fully parasitic symbioses (social parasites). One of the most remarkable examples of an obligate ant parasite is Paussus favieri Fairmaire,1851 (Carabidae, Paussinae, Paussini), a West-Mediterranean ant-nest beetle. This species spends most of its life inside the nests of Pheidole pallidula (Nylander, 1849) (Hymenoptera, Formicidae), where it exploits the colony’s most valuable resources (ant larvae, pupae, and tenerals) through a suite of sophisticated chemical and structural adaptations that allow it to evade detection and integrate seamlessly into the host colony. For these reasons, P. favieri has recently emerged as a key model organism for studying host–parasite interactions in eusocial systems. In this study, we investigated possible correlations between the nervous system of P. favieri and its remarkable morphological and behavioural adaptations, shedding light on how an extreme environment such as the ant nest may have shaped the beetle’s brain. Our results, although requiring more in-depth analysis, reveal an exceptional development of the central body and the antennal lobes, which rank among the largest recorded across all insect species studied to date. We also report two previously undescribed morphological asymmetries affecting the optic lobes and mushroom bodies. Together, these findings provide new insights into the neuroanatomy of carabid beetles and, more broadly, into the biology of a unique model of ant parasitism, advancing our understanding of the evolutionary adaptations that characterise the highly specialised Paussinae subfamily, laying down the basis for further analysis. Full article

Background: Neuroinflammation contributes to the etiopathology and symptom severity of neurodegenerative and neuropsychiatric disorders. Glial cells, especially microglia and astrocytes, play a crucial role in neuroinflammation. It has been reported that ginseng (Panax ginseng) and its bioactive component ginsenoside Rg1 exhibit anti-inflammatory effects and can improve cognitive performance in various models. However, the exact underlying mechanisms remain unclear. Methods: Astrocyte–microglia co-culture models simulating physiological (M5, 5–10% microglia) and pathological/inflammatory (M30, 30–40% microglia) conditions were treated with different concentrations of ginsenoside Rg1 (15, 30, 45 µM) or ginseng extract (derived from Korean red ginseng) at low (12.5, 25, 37.5 µg/mL) or high doses (125, 250, 375 µg/mL) for 24 h. Cell viability was assessed using the MTT assay while microglial reactivity was examined using immunocytochemistry. Astrocytic gap-junctional coupling was investigated using the scrape-loading method, and connexin 43 (Cx43) expression was analyzed using immunocytochemistry and Western blot. Results: Both Rg1 and low-dose ginseng extract reduced microglial activation under inflammatory conditions by promoting a shift in microglia from an activated to homeostatic (resting) phenotype. Rg1 preserved astrocytic gap-junctional function by preventing the inflammation-induced downregulation of Cx43 expression and enhancing Cx43-mediated gap-junctional intercellular communication. Rg1 caused a significant reduction in glial cell viability, but only at high concentrations (30 and 45 µM), under inflammatory conditions. High-dose ginseng extract showed a significant concentration-dependent reduction in glial cell viability under physiological and pathological conditions, without comparable anti-inflammatory benefits. Conclusions: This study demonstrates that low-dose ginseng and its active compound Rg1 exert anti-inflammatory effects by modulating astrocytic coupling and microglial reactivity. These results provide a novel therapeutic perspective for the use of ginseng in the treatment of neurodegenerative and neuropsychiatric diseases related to neuroinflammation. Full article

The educational pathway for expertise in intraoperative neurophysiological monitoring (IONM) is complex and lengthy, requiring a solid foundation in neuroscience, neurophysiology, and neuroanatomy. It also demands direct familiarity with a broad range of neurosurgical scenarios, including supratentorial, infratentorial, and spinal procedures, gained through exposure to at least ten distinct surgical approaches. Intraoperative neurophysiology must be tailored to each patient’s preoperative assessments. It relies on a variety of methods to collect, analyze, and report neurophysiological signals that are relevant to the surgical procedure. Despite its importance, there remains a substantial shortage of training tools designed to support realistic practice and skill development. To address this gap, we developed a comprehensive framework (ION-Sim) that integrates all laboratory testing modalities and adapts them to the operating room environment. ION_sim supports the simulation and analysis of spontaneous EEG and EMG activity, a wide range of evoked potentials, and intraoperative stimulus–response testing protocols. The framework provides a unified environment for practicing, testing, and validating the core neurophysiological procedures employed during neurosurgical interventions. In addition, it incorporates a robust data-management architecture, maintaining a database with system setups, user profiles, educational performance metrics, and automatically generating reports. This structure enables the longitudinal tracking of objective skill acquisition and facilitates standardized assessments of trainee progress. ION_Sim is distributed both as a ready-to-use application, suitable for direct integration into teaching and training programs, and as a modular scientific library. Through its dedicated APIs, users can design customized configurations, create novel simulation scenarios, and extend the platform to support additional research or educational objectives. It is available upon request for educational purposes and is open-source and released under the GNU General Public License, ensuring transparency, reproducibility, and long-term accessibility for the scientific and clinical communities. Full article

Glioblastoma (GBM) is an extremely invasive and incurable tumor. We previously reported predominant ALDH1A3 expression at the invasive front of GBM tumors, which was associated with shorter patient survival, and further showed that ALDH1A3 promoted tumor angiogenesis involving plasminogen activator inhibitor-1 (PAI-1). Here, we investigated whether ALDH1A3 drives cell invasion through retinoic acid (RA) and PAI-1 signaling. Analysis of the TCGA-GBM dataset revealed a positive association between ALDH1A3 and PAI-1 (SERPINE1) expression. Overexpression of ALDH1A3 in GBM cells markedly increased PAI-1 mRNA and protein levels, with cellular colocalization of both proteins, accompanied by robust migration and invasion. These effects were reversed by treatment with a pan-RA receptor (RAR) antagonist AGN193109 (AGN), with a specific PAI-1 inhibitor tiplaxtinin (Tip) or by CRISPR/Cas9-mediated knockout of PAI-1. In a chick chorioallantoic membrane (CAM) model, ALDH1A3-overexpressing cells showed increased invasion, which was reduced by tiplaxtinin (Tip) treatment or PAI-1 knockout. Mechanistically, ChIP-qPCR demonstrated that RA treatment or ALDH1A3 overexpression increased RARα occupancy at the PAI-1 regulatory region, accompanied by increased PAI-1 expression, both of which were diminished by AGN. Collectively, the present study defines an ALDH1A3-RA-PAI-1 signaling axis that contributes to GBM cell motility and invasion. Full article

Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder characterized by amyloid-β (Aβ) and the accumulation of tau in the brain, which triggers robust innate immune responses. Growing evidence indicates that neuroinflammation contributes to AD progression by overactivating microglia through the release of cytokines and chemokines. In general, chemokines can disrupt neuronal communication and promote blood–brain barrier permeability. Peripheral immune cells are mobilized into the brain by a gradient of chemokines. These processes link peripheral immune responses with substantial T-cell infiltration into the CNS parenchyma, leptomeninges and cerebrospinal fluid of both AD mice and AD patients. This finding underscores the relevance of the adaptive immune system, particularly T and B cells, in AD neuropathology. T-cell infiltration into the brain can influence amyloid clearance through chemokine signalling. However, chemokines play a critical role in AD by either promoting or suppressing disease progression. The infiltration of peripheral T and B cells into the brain parenchyma can exacerbate neuronal loss, yet it may also exert neuroprotective effects. Despite the presence of CD4⁺ and CD8⁺ T cells in postmortem brains of AD patients, debate continues about their role in AD brains, in terms of whether they are protective or detrimental. Understanding the complex role of chemokines in controlling innate and adaptive immune responses by modulating neuron–glia interactions (involving astrocytes and microglia) may provide novel therapeutic approaches for AD. Targeting chemokine signalling or treating with drugs that can prevent the recruitment of immune cells may be promising strategies for treating AD neuropathology. Therapies that prevent the overactivation of T cells in the brain could lead to protective strategies against AD. In fact, regulatory T cells (Tregs) could delay the onset of cognitive symptoms, because they suppress inflammation and slow the accumulation of Aβ plaques and p-Tau in the brain. Complementary strategies, such as photobiomodulation, nanoparticle, and T-cell-based approaches, could mitigate AD progression in patients. Full article

Background: Neurovascular compression syndromes (NVCS) represent a spectrum of disabling neurologic disorders caused by vascular or structural compression of cranial nerves, most commonly at the root entry zone. Conditions such as trigeminal neuralgia (TN), hemifacial spasm (HFS), and glossopharyngeal neuralgia (GN) are associated with significant pain, functional impairment, and reduced quality of life. This review provides a multidisciplinary, anatomically grounded overview of the pathophysiology, diagnosis, imaging, and contemporary management strategies for NVCS. Methods: A narrative review of the literature was conducted, synthesizing historical perspectives, neuroanatomy of the cerebellopontine angle, mechanisms of neurovascular conflict, advances in imaging and neuromonitoring, and current treatment modalities. Medical, percutaneous, surgical, radiosurgical, and neuromodulatory approaches were evaluated, with emphasis on patient selection and outcome considerations. Results: Neurovascular compression, most frequently arterial compression at the root entry zone, leads to focal demyelination, ephaptic transmission, and neuronal hyperexcitability. High-resolution Magnetic resonance imagin (MRI) remains the diagnostic gold standard. First-line management for TN and related syndromes typically includes pharmacotherapy, particularly sodium channel blockers. Refractory cases may benefit from percutaneous rhizotomy, balloon compression, stereotactic radiosurgery, or microvascular decompression (MVD), which offers the most durable relief in appropriately selected patients. Emerging technologies, including endoscopic visualization, advanced neuromodulation, and virtual reality-assisted surgical planning, continue to refine treatment precision and safety. Conclusions: Effective management of NVCS requires a comprehensive understanding of neuroanatomy, pathogenesis, and individualized risk–benefit profiles. A multidisciplinary, stepwise approach optimizes outcomes and improves quality of life in patients with these complex disorders. Full article

Background: The expanding interest in chatbots within the medical domain underscores the imperative for a comprehensive understanding of their capabilities and limitations, particularly in the context of anatomical education. Chatbots possess the potential to comprehend intricate anatomical concepts, deliver both advanced and contextually relevant information, and serve as a valuable resource for medical students and educators. This study aimed to evaluate the proficiency and constraints of chatbots in the domain of neuroanatomy. Methods: We developed 30 questions and administered them to ChatGPT-4, Google Gemini, Microsoft Copilot, and Perplexity.ai in their open versions. Questions were collaboratively constructed by the research team, selected through a semi-randomized process within the domain of neuroanatomy. Chatbots’ responses were evaluated in a blinded manner for validity and appropriateness, utilizing a 5-point Likert scale. Results: The highest observed performance among the evaluated chatbots was exhibited by ChatGPT-4 and Perplexity.ai, which achieved scores of 4.6 ± 0.5 and 4.5 ± 0.5, respectively. Microsoft Copilot (4.4 ± 0.5) and Google Gemini (4.1 ± 1.0) followed. The least successful performance was observed in the task of generating a neuroanatomical structure: only Microsoft Copilot attempted to fulfil the request, albeit with a dramatically flawed outcome. Conversely, Google Gemini and Perplexity.ai provided web links to anatomical illustrations. Conclusions: Despite technological advancements, AI models have not yet reached a level of sophistication sufficient to entirely supplant the role of educators or facilitators in a neuroanatomy course; however, they can serve as valuable adjunct tools for medical educators and students when utilized with careful consideration. Full article

Introduction: Meckel’s diverticulum (MD) is the most common congenital anomaly of the gastrointestinal tract, resulting from incomplete involution of the vitelline duct during the fifth to seventh week of gestation. This study aimed to assess the prevalence, anatomical features, clinical manifestations, and heterotopic tissue of MD through a comprehensive meta-analysis of studies reporting on this anomaly. Methods: A systematic search of PubMed, Scopus, ScienceDirect, Web of Science, SciELO, BIOSIS, Current Contents Connect, and the Korean Journal Database was conducted up to March 2024 following PRISMA guidelines. Original studies with extractable data on Meckel’s diverticulum were included, while case reports, reviews, and studies with incomplete data were excluded. Outcomes included prevalence, anatomical features, clinical manifestations, complications, and postoperative outcomes. The study quality was assessed using CATAM and AQUA tools. Results: The results of the present meta-analysis comprised 172 studies. The pooled prevalence of MD was 1.56% (95% CI: 0.98–2.28%). Nausea and vomiting were the most frequent symptoms in the pediatric group, with an incidence of 52.34% (95% CI: 38.59–65.92%). In adults, wound infections or dehiscence or anastomotic leakage were the most common postoperative outcomes, with a pooled prevalence of 6.20% (95% CI: 4.02–8.79%). Conclusions: This systematic review and meta-analysis provide a comprehensive quantitative synthesis of MD characteristics. Symptomatic cases most frequently presented with intestinal obstruction, diverticulitis, and bleeding, each showing distinct age-related trends. Ectopic gastric mucosa was identified in over 40% of pediatric MD. Postoperative outcomes were generally favorable, particularly in elective settings, with low rates of morbidity and mortality. It is hoped that the findings of this study will aid clinicians in diagnosing, risk-stratifying, and managing patients with MD, particularly in guiding surgical decisions for incidentally discovered cases. Full article

The study of veterinary anatomy is gradually progressing with the combination of digital imaging and artificial intelligence (AI). This paper aimed to evaluate the potential use of AI tools for morphometric analysis and the anatomical identification of the ovine brain. Five adult specimens were used and approached through traditional dissection and fixation methods followed by digital photography and manual measurement with high-precision Vernier calipers. These results were compared against AI-based approaches, including DeeVid AI for 3D reconstruction, Imageonline for digital measurement, and ChatGPT/Artlist for anatomical nomenclature. The findings indicate that AI tools like DeeVid AI significantly enhance structural visualization, and Imageonline provides high-precision measurements comparable to manual tools (p > 0.05). However, AI-driven anatomical naming remains prone to significant errors, with ChatGPT and Artlist exhibiting error rates of 87.5% and 70.8%, respectively, in specific neuroanatomical labeling. This study concludes that while AI eases the reshaping and measurement of anatomical structures, human expertise remains indispensable for accurate anatomical identification. Full article

The visualization of embryonic and fetal brain development at mesoscopic resolution represents a critical frontier in developmental neuroscience. This review presents advances in high-field magnetic resonance imaging (HF-MRI) that achieve unprecedented spatial resolution in ex vivo human embryonic and fetal brain specimens. This mesoscopic imaging capability bridges the gap between conventional clinical MRI and histological microscopy, enabling three-dimensional visualization of transient developmental structures including cortical lamination, ganglionic eminences, and emerging white matter pathways. We review the technical foundations of HF-MRI, present methodological advances that enable mesoscopic resolution, demonstrate applications across gestation, and discuss validation through histological correlation. The integration of multimodal imaging approaches—including T1-weighted, T2-weighted, T2*-weighted, diffusion tensor imaging, and quantitative relaxometry—provides comprehensive characterization of tissue microstructure and connectivity during critical periods of neurodevelopment. These advances offer transformative potential for understanding normal brain development, identifying early markers of neurodevelopmental disorders, and establishing high-resolution atlases of human prenatal neuroanatomy. Full article

Melanoma is a heterogeneous, complex and aggressive disease that, despite recent advances in molecular-targeted drugs and molecular and genetic analysis, represents approximately 65% of skin cancer deaths, and unfortunately survival dramatically decreases in melanoma stages III/IV. In young people there is an increased incidence of developing melanoma; hence new therapeutic strategies must be urgently investigated. Peptidergic systems play a crucial role in these strategies to fight melanoma. The scope of this review is to show the enormous potential of targeting peptidergic systems alone or in combination therapy with standard therapeutic strategies currently used in clinical practice to treat melanoma. In this sense, key points such as peptidergic systems and anti-melanoma treatments, oncogenic/anti-melanoma peptides, peptide receptors, peptidergic systems, melanoma risk and immune system relationships, clinical relevance, peptidergic systems and delivery strategies in melanoma will be discussed. Peptides exert oncogenic, anti-melanoma and dual oncogenic and anti-melanoma effects in melanoma, showing a high functional complexity in regulating melanoma development. A plethora of anti-melanoma strategies have been developed or repurposed for potential clinical applications, including peptide/peptide receptor antibodies, peptide receptor antagonists or agonists, enzyme inhibitors, CAR-macrophages, microRNAs and vaccines. Strategies for peptide delivery and protection from enzymatic degradation have also been developed. Some of the previous anti-melanoma strategies are based on the expression/overexpression of peptide receptors in melanoma cells which is crucial for diagnosis, melanoma risk and progression and metastasis development and for the application of more specific and safer anti-melanoma strategies. A meticulous and in-depth study of the peptidergic systems may help to understand how peptidergic systems regulate melanoma progression and shed light on possible therapeutic applications that can be applied in clinical practice. This review shows the enormous potential of targeting peptidergic systems alone or in combination therapy with standard therapeutic strategies currently used in clinical practice to treat melanoma. The benefits to be gained from these studies will be enormous because the peptidergic systems are promising antitumor targets in melanoma, based on the numerous anti-melanoma strategies that have been developed until now. Full article

Peripheral nerve injuries often lead to incomplete recovery despite surgical repair. Vitamin B12 and folic acid have been implicated in nerve regeneration, but their comparative effects have not been systematically evaluated. Twenty-four male Wistar rats underwent femoral nerve transection and were assigned to three groups: control, vitamin B12 (2500 µg/kg weekly, subcutaneous), and folic acid (40 mg/L in drinking water). Functional recovery was assessed over eight weeks using foot-base angle (FBA) during beam walking. Histological analysis evaluated axon counts and myelination (g-ratio). Both treatments accelerated early gait recovery compared to controls, with significant FBA improvement at week 4 (p < 0.05). Vitamin B12 produced sustained functional benefits through week 8 and superior myelination (lower g-ratio, p < 0.0001), whereas folic acid increased axon numbers but did not enhance myelin thickness or late-phase recovery. High-dose vitamin B12 significantly improves structural and functional outcomes after femoral nerve injury, while folic acid primarily supports early axonal regrowth. Vitamin B12 represents a promising pharmacological adjunct for peripheral nerve repair. Further research should explore optimal dosing strategies and long-term effects in clinical settings. To our knowledge, no prior study has directly compared the effects of folic acid and vitamin B12 supplementation within the rat femoral-nerve model, providing the rationale for the present head-to-head design. Full article

Bovine spongiform encephalopathy (BSE) is a fatal transmissible spongiform encephalopathy caused by the misfolding of the host prion protein (PrP), representing a unique intersection between molecular pathology, neuroanatomy, and public health regulation. Although historically framed as a single feedborne epizootic, BSE is now recognized as a spectrum of strain-defined prion disorders encompassing classical and atypical forms with distinct origins, neuroanatomical trajectories, and surveillance implications. This review integrates advances in prion biology, neurodegenerative mechanisms, and anatomical pathways of neuroinvasion to reframe BSE as a heterogeneous disease entity. We synthesize evidence on PrP^C structure, trafficking, and proteolytic processing to explain how normal cellular physiology enables strain-specific conversion to pathogenic PrP^Sc and subsequent neurotoxicity. Distinct patterns of neuroinvasion and regional vulnerability are discussed for classical versus atypical (H- and L-type) BSE, highlighting differences in lymphoid involvement, brainstem targeting, and cortical or cerebellar tropism. We further examine how these biological differences translate into diagnostic sensitivity, surveillance design, and zoonotic risk assessment. By integrating molecular strain diversity with neuroanatomical connectivity, this review underscores the limitations of obex-centered surveillance for atypical BSE and emphasizes the need for proportionate yet precautionary monitoring strategies. These considerations should be interpreted in light of surveillance-dependent detection biases, which influence the apparent distribution of BSE forms. Ultimately, BSE emerges as a critical model for understanding how protein misfolding disorders bridge cellular mechanisms, animal health, and human public health policy. Full article

Spinocerebellar Ataxia type 2 (SCA2) and Amyotrophic Lateral Sclerosis type 13 (ALS13) are triggered by polyglutamine expansion in Ataxin-2 (ATXN2). To understand these neurodegenerative disorders at the molecular level, the brains of 10-month-old Atxn2-CAG100-knockin mice were analyzed as microglial, astroglial and neuronal fractions via global RNA sequencing. Data were validated by comparison with the spinal cord oligonucleotide microarray profile or filtered by RNA-seq consistency. Here, we show that the mutation causes a massive inflammatory response in microglia and a reciprocal loss of neuronal transcripts in glial fractions, suggesting severe synapse loss. Beyond these general neurodegenerative signs, we identify pathognomonic changes in the machinery for protein translation and RNA splicing. Glial fractions showed upregulation of Gpnmb (to 2082%), Cst7, Clec7a, Axl, Csf1, Lgals3, Lgals3bp, Slc11a1, and Usp18 as an unspecific neuroinflammatory signature, versus downregulation of axonal Nefh (to <19%), and synaptic Scn4b, Camk2b, Rab15, and Grin1 mRNAs correlating with circuit disconnection. In all fractions, reductions in Kif5a, Rph3a, and Cplx1 were noted versus disease-specific inductions of ribosomal subunits, presumably mirroring the partial loss-of-function of ATXN2 as RNA translation modulator. Selective accumulations of embryonic factors Rnu1b2 and Eef1a1 versus downregulation of adult Eef1a2 specify the mutation impact on splicing and translation elongation. As a potential underpinning of toxic gain-of-function, the proteostasis transcript Rnf213 appeared increased in astroglial and microglial fractions. These transcriptome data suggest altered ribosomal and spliceosome machinery, with massive microgliosis versus mild astrogliosis, at the core of SCA2 and ALS13. Full article

Background: Severe trismus and post-oncologic maxillary defects often prevent conventional zygomatic implant placement. This study evaluates a novel implant specifically designed for reverse insertion (from the zygoma toward the oral cavity) and assesses its feasibility and accuracy in a cadaveric model. Materials and Methods: A Brown Class II maxillectomy was simulated in a fresh-frozen cadaver. Four custom reverse zygomatic implants were virtually planned and placed using CAD/CAM surgical guides. Superior and inferior orbital approaches were compared. Postoperative CT was superimposed onto the preoperative plan to measure linear and angular deviations, and a 3D-printed verification bar assessed prosthetic alignment. Results: All implants were successfully inserted with primary stability and without compromising critical structures. The superior orbital approach yielded lower deviations and better guide stability, which was reflected in the results: deviation at the zygomatic bone was 1.25 mm in the superior approach vs. 2.32 in the inferior approach, intraorally 4.7 mm vs. 7.3 mm, and angular deviation 1.85° vs. 5.63°. Despite minor distal deflection, intraoral emergence remained within clinically acceptable limits, allowing partial seating of the verification bar. Conclusions: Reverse-insertion zygomatic implants are technically feasible, anatomically safe, and compatible with fixed prosthetic rehabilitation in cases where conventional placement is impossible. Penetrating the orbit, injuring the skin or the infraorbital nerve could be possible but guided surgery seems to prevent them. A forthcoming clinical series of eight additional cases will further validate this protocol. Full article