Disease Of Central Nervous System Research Articles

Exploring the feasibility of integrating ultra‐high field magnetic resonance imaging neuroimaging with multimodal artificial intelligence for clinical diagnostics

AbstractBackgroundThe integration of 7 Tesla (7T) magnetic resonance imaging (MRI) with advanced multimodal artificial intelligence (AI) models represents a promising frontier in neuroimaging. The superior spatial resolution of 7TMRI provides detailed visualizations of brain structure, which are crucial forunderstanding complex central nervous system diseases and tumors. Concurrently, the application of multimodal AI to medical images enables interactive imaging‐based diagnostic conversation.MethodsIn this paper, we systematically investigate the capacity and feasibility of applying the existing advanced multimodal AI model ChatGPT‐4V to 7T MRI under the context of brain tumors. First, we test whether ChatGPT‐4V has knowledge about 7T MRI, and whether it can differentiate 7T MRI from 3T MRI. In addition, we explore whether ChatGPT‐4V can recognize different 7T MRI modalities and whether it can correctly offer diagnosis of tumors based on single or multiple modality 7T MRI.ResultsChatGPT‐4V exhibited accuracy of 84.4% in 3T‐vs‐7T differentiation and accuracy of 78.9% in 7T modality recognition. Meanwhile, in a human evaluation with three clinical experts, ChatGPT obtained average scores of 9.27/20 in single modality‐based diagnosis and 21.25/25 in multiple modality‐based diagnosis. Our study indicates that single‐modality diagnosis and the interpretability of diagnostic decisions in clinical practice should be enhanced when ChatGPT‐4V is applied to 7T data.ConclusionsIn general, our analysis suggests that such integration has promise as a tool to improve the workflow of diagnostics in neurology, with a potentially transformative impact in the fields of medical image analysis and patient management.

Preclinical Evaluation of Dihydropyrazole-Cored Positron Emission Tomography (PET) Ligands for Imaging of Receptor-Interacting Serine/Threonine Protein Kinase 1 (RIPK1) in the Brain.

Receptor-interacting serine/threonine protein kinase 1 (RIPK1) has emerged as an important regulator of pathologic cell death and inflammation and is implicated in the pathologies of various central nervous system diseases. In this study, we reported the development of three potent dihydropyrazole-cored RIPK1 positron emission tomography (PET) ligands [18F]WL1-3. Among these, [18F]WL1 showed specific binding to RIPK1 in mouse brain sections in vitro through autoradiography and exhibited favorable brain kinetics in mice, characterized by a high initial uptake (brain2 min = 4.89% ID/g) and rapid washout (brain60 min = 0.21% ID/g). PET studies in rat brains revealed that [18F]WL1 could readily penetrate the brain with specific binding confirmed by inhibition effects of unlabeled WL1 and GSK'547. Notably, [18F]WL1 showed significant potential in imaging the alterations of RIPK1 in a rat brain of tumor necrosis factor α-induced systemic inflammatory response syndrome model. These findings may pave the way for the future design of potent RIPK1 PET ligands.

Advancements in the Controlled Delivery of Nanodrugs to the Central Nervous System: Challenges and Innovations.

About 1 million of the 6.8 million deaths attributed to disorders of the central nervous system (CNS) each year are caused by neurodegenerative diseases, which include Parkinson’s disease, Alzheimer’s disease, tumors, and ischemic stroke. Because of the complexity of the brain, CNS issues are a major concern. To address issues with toxicity, specificity, and delivery, several drugs are available to treat illnesses of the central nervous system (CNS). Therapeutic drugs are challenged by barriers such as the blood-brain barrier (BBB), which prevents them from reaching their intended target. Scholars have been investigating pathways for pharmaceuticals to cross the blood-brain barrier and reach their intended targets. These issues show how different cellular processes must be changed or manipulated by nanotechnology to obtain the required properties. Nanoparticles are an efficient replacement for drug delivery and other methods because of their nano size, which allows them to cross the blood-brain barrier. Effective drug transfer and enhanced CNS disease treatment and diagnosis are possible using nanotechnology. Drugs could be altered via nanoengineering to carry out tasks like transferring across the blood-brain barrier, modifying signaling pathways, focusing on certain cells, facilitating efficient gene transfer, and encouraging nerve cell regeneration and preservation.

Blood diagnostic and prognostic biomarkers in amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis is a devastating neurodegenerative disease for which the current treatment approaches remain severely limited. The principal pathological alterations of the disease include the selective degeneration of motor neurons in the brain, brainstem, and spinal cord, as well as abnormal protein deposition in the cytoplasm of neurons and glial cells. The biological markers under extensive scrutiny are predominantly located in the cerebrospinal fluid, blood, and even urine. Among these biomarkers, neurofilament proteins and glial fibrillary acidic protein most accurately reflect the pathologic changes in the central nervous system, while creatinine and creatine kinase mainly indicate pathological alterations in the peripheral nerves and muscles. Neurofilament light chain levels serve as an indicator of neuronal axonal injury that remain stable throughout disease progression and are a promising diagnostic and prognostic biomarker with high specificity and sensitivity. However, there are challenges in using neurofilament light chain to differentiate amyotrophic lateral sclerosis from other central nervous system diseases with axonal injury. Glial fibrillary acidic protein predominantly reflects the degree of neuronal demyelination and is linked to non-motor symptoms of amyotrophic lateral sclerosis such as cognitive impairment, oxygen saturation, and the glomerular filtration rate. TAR DNA-binding protein 43, a pathological protein associated with amyotrophic lateral sclerosis, is emerging as a promising biomarker, particularly with advancements in exosome-related research. Evidence is currently lacking for the value of creatinine and creatine kinase as diagnostic markers; however, they show potential in predicting disease prognosis. Despite the vigorous progress made in the identification of amyotrophic lateral sclerosis biomarkers in recent years, the quest for definitive diagnostic and prognostic biomarkers remains a formidable challenge. This review summarizes the latest research achievements concerning blood biomarkers in amyotrophic lateral sclerosis that can provide a more direct basis for the differential diagnosis and prognostic assessment of the disease beyond a reliance on clinical manifestations and electromyography findings.

Emerging Role of Extracellular Vesicles as Biomarkers in Neurodegenerative Diseases and Their Clinical and Therapeutic Potential in Central Nervous System Pathologies.

The emerging role of extracellular vesicles (EVs) in central nervous system (CNS) diseases is gaining significant interest, particularly their applications as diagnostic biomarkers and therapeutic agents. EVs are involved in intercellular communication and are secreted by all cell types. They contain specific markers and a diverse cargo such as proteins, lipids, and nucleic acids, reflecting the physiological and pathological state of their originating cells. Their reduced immunogenicity and ability to cross the blood-brain barrier make them promising candidates for both biomarkers and therapeutic agents. In the context of CNS diseases, EVs have shown promise as biomarkers isolable from different body fluids, providing a non-invasive method for diagnosing CNS diseases and monitoring disease progression. This makes them useful for the early detection and monitoring of diseases such as Alzheimer's, Parkinson's, and amyotrophic lateral sclerosis, where specific alterations in EVs content can be detected. Additionally, EVs derived from stem cells show potential in promoting tissue regeneration and repairing damaged tissues. An evaluation has been conducted on the current clinical trials studying EVs for CNS diseases, focusing on their application, treatment protocols, and obtained results. This review aims to explore the potential of EVs as diagnostic markers and therapeutic carriers for CNS diseases, highlighting their significant advantages and ongoing clinical trials evaluating their efficacy.

GAS6 as a potential target to alleviate neuroinflammation during Japanese encephalitis in mouse models

Viral encephalitis is characterized by inflammation of the brain parenchyma caused by a variety of viruses, among which the Japanese encephalitis (JE) virus (JEV) is a typical representative arbovirus. Neuronal death, neuroinflammation, and breakdown of the blood brain barrier (BBB) constitute vicious circles of JE progression. Currently, there is no effective therapy to prevent this damage. Growth arrest specific gene 6 (GAS6) is a secreted growth factor that binds to the TYRO3, AXL, and MERTK (TAM) family of receptor tyrosine kinases and has been demonstrated to participate in neuroprotection and suppression of inflammation in many central nervous system (CNS) diseases which has great potential for JE intervention. In this study, we found that GAS6 expression in the brain was decreased and was reversely correlated with viral load and neuronal loss. Mice with GAS6/TAM signalling deficiency showed higher mortality and accelerated neuroinflammation during peripheral JEV infection, accompanied by BBB breakdown. GAS6 directly promoted the expression of tight junction proteins in bEnd.3 cells and strengthened BBB integrity, partly via AXL. Mice administered GAS6 were more resistant to JEV infection due to increased BBB integrity, as well as decreased viral load and neuroinflammation. Thus, targeted GAS6 delivery may represent a strategy for the prevention and treatment of JE especially in patients with impaired BBB.

Progress of Astrocyte-Neuron Crosstalk in Central Nervous System Diseases.

Neurons are the primary cells responsible for information processing in the central nervous system (CNS). However, they are vulnerable to damage and insult in a variety of neurological disorders. As the most abundant glial cells in the brain, astrocytes provide crucial support to neurons and participate in synapse formation, synaptic transmission, neurotransmitter recycling, regulation of metabolic processes, and the maintenance of the blood-brain barrier integrity. Though astrocytes play a significant role in the manifestation of injury and disease, they do not work in isolation. Cellular interactions between astrocytes and neurons are essential for maintaining the homeostasis of the CNS under both physiological and pathological conditions. In this review, we explore the diverse interactions between astrocytes and neurons under physiological conditions, including the exchange of neurotrophic factors, gliotransmitters, and energy substrates, and different CNS diseases such as Alzheimer's disease, Parkinson's disease, stroke, traumatic brain injury, and multiple sclerosis. This review sheds light on the contribution of astrocyte-neuron crosstalk to the progression of neurological diseases to provide potential therapeutic targets for the treatment of neurological diseases.

Buprenorphine with Bupivacaine 0.5% Heavy Versus Clonidine with Bupivacaine 0.5% Heavy Versus Bupivacaine 0.5% Heavy Alone in Patients Undergoing Total Abdominal Hysterectomy: A Comparative Study

Background and Aims: This research aimed to determine which of three spinal anaesthetic medication combinations—clonidine–bupivacaine, buprenorphine–bupivacaine and bupivacaine alone—is the most effective for total abdominal hysterectomy. Material and Methods: In this prospective study, approved by the Institutional Ethical Committee, 120 patients aged 35–60 years scheduled for elective total abdominal hysterectomy under spinal anaesthesia were included, following informed consent. Comprehensive pre-anaesthetic assessments, including detailed medical histories, clinical examinations and routine surgical investigations, were conducted. The study, spanning 24 months, utilised purposive sampling and a cross-sectional design. The inclusion criteria encompassed ASA I and II patients aged 35–60 years, undergoing elective total abdominal hysterectomy with a weight exceeding 45 kg, height over 150 cm, and valid informed consent. Exclusion criteria involved ASA Class III or higher, patient unwillingness for spinal anaesthesia, gross spinal deformities, bleeding diathesis, known allergy to the test drug, history of cardiac, respiratory, or central nervous system disease, hepatic or renal dysfunction and elevated intracranial pressure. Results: The onset time of sensory blockade was faster in the Bupivacaine + Buprenorphine group than in the Clonidine + Bupivacaine group, with the Bupivacaine group exhibiting the slowest onset. The Bupivacaine + Buprenorphine group had a significantly faster onset of motor block than the Clonidine + Bupivacaine and Bupivacaine groups. The total duration of motor block was shorter in both the Bupivacaine + Buprenorphine and Bupivacaine groups than in the Clonidine + Bupivacaine group. The Clonidine + Bupivacaine group showed higher incidences of bradycardia and hypotension than the other groups. The Bupivacaine + Buprenorphine group reported more side effects, including chest pain, cough, nausea and vomiting, than the other groups. Conclusion: This study found that spinal clonidine, in comparison to bupivacaine alone, gives better post-operative analgesia and sensory and motor blockage over a longer period of time.

The Regulation of Cerebral Lymphatic Drainage in the Transverse Sinus Region of the Mouse Brain.

Cerebral lymphatic drainage is an important pathway for metabolic waste clearance in the brain, which plays a crucial role in the progression of central nervous system diseases. Recent studies have shown that norepinephrine (NE) is involved in the regulation of cerebral lymphatic drainage function, but the modulation mechanism remains unknown. In this study, we confirmed that NE rapidly reduced glymphatic influx and enhanced meningeal lymphatic clearance. Moreover, the transverse sinus (TS) was the vital region of cerebral lymphatic drainage regulation by NE. Further analysis revealed that NE inhibition could simultaneously enhance glymphatic drainage and dorsal meningeal lymphatic drainage, mainly acting on the TS region. This study demonstrated that the cerebral lymphatic drainage system can be regulated by NE, with the TS region serving as the primary modulating site. The findings provide a potential regulatory target for the amelioration of neurological diseases associated with cerebral lymphatic drainage function.

Evaluation of the Frequency of (rs2227981 and rs2282055) Single Nucleotide Polymorphisms in Programmed Cell Death 1 and Its Ligand Genes of Iraqi Patients With Multiple Sclerosis

Abstract Multiple sclerosis (MS) is a central nervous system disease that causes demyelination and persistent inflammation and most of them among young adults. The current study aimed to assess gene polymorphism of PDCD1 and PDLCD1 genes and the frequency of two SNPs (rs2227981 and rs2282055). MS patients (n=100) were divided into two groups; newly diagnosed (42), and patients with ongoing treatments (58). These groups were compared to healthy subjects (n=55); the mean age ±SD was (30±8.46 years), (37±8.06years), and (31±8.73 years) for MS newly patients, patients with ongoing treatments, and healthy subjects, respectively. Studies for gene polymorphism of PDCD1 and PDLCD1 Genes and the Frequency of Two SNPs (rs2227981 and rs2282055) were measured by Real-time PCR by used HRM. The results of this study found that the genotypic frequencies of MS patient were 31% (n=31) normal AA and 48 % (n=48) heterozygous AG. Mutant homozygous was found in GG 21 % (n=21). In controls, the results demonstrate 69% (n=38) wild type AA, 27.27% (n=15) heterozygous AG and mutant homozygous GG 3.6% (n=2). The odds ratio for the GG genotype was 12.8 (0.2-5.9) with p=0.001 indicating that the homomutant genotype In PD1 gene polymorphism rs2227981 GG was a higher risk of MS than the wild-type PD1 gene polymorphism rs2227981 AA, The PD1 gene polymorphism rs2227981 AG genotype has the second risk of MS after PD1 gene polymorphism rs2227981GG with 3.92 fold high risk than the wild type AA (OR =3.92 (1.8-8.2) p=0.0003). The present study concludes that the population-based case-control study, which focused on the three PD-1 SNPs PD-1.3, PD-1.5, and PD-1.9, found that polymorphism variation might actually be a disease-modifying factor as opposed to an MS risk factor. There were substantially more PD-L1 gene SNP loci in MS patients compared to controls, and there were significantly more PD-L1 gene SNP loci in MS patients compared to controls. The pathogenesis of MS might be connected to PD-1 and PD-L1 SNPs. PD-L1 gene SNP locus rs2282055 and PD-1 gene SNP locus rs2227981 might be potential MS candidate polymorphism loci.

The Role of Estrogen in Brain MicroRNAs Regulation

Brain disorders are global health issues and cause mortality and morbidity. Experimental data have shown that the rate of cognitive impairments in the reproductive age is lower in women than men, which refers to the importance of sex hormones in the brain. Estrogen as a sex hormone has a protective effect on the central nervous system (1) diseases and its role is changed by aging. Estrogenic hormonal activity affects brain function through their specific estrogen receptors to promote the expression of target gene changes at the transcriptional level. miRNAs regulate gene expression via inhibiting translational processes and have been estimated to be involved in regulating almost 30% of all protein-coding genes in mammals. Our review highlights the present knowledge about the role of estrogen-sensitive miRNAs and their efficacy in regulating brain functions and disorders.

Integrating large-scale single-cell RNA sequencing in central nervous system disease using self-supervised contrastive learning

The central nervous system (CNS) comprises a diverse range of brain cell types with distinct functions and gene expression profiles. Although single-cell RNA sequencing (scRNA-seq) provides new insights into the brain cell atlases, integrating large-scale CNS scRNA-seq data still encounters challenges due to the complexity and heterogeneity among CNS cell types/subtypes. In this study, we introduce a self-supervised contrastive learning method, called scCM, for integrating large-scale CNS scRNA-seq data. scCM brings functionally related cells close together while simultaneously pushing apart dissimilar cells by comparing the variations of gene expression, effectively revealing the heterogeneous relationships within the CNS cell types/subtypes. The effectiveness of scCM is evaluated on 20 CNS datasets covering 4 species and 10 CNS diseases. Leveraging these strengths, we successfully integrate the collected human CNS datasets into a large-scale reference to annotate cell types and subtypes in neural tissues. Results demonstrate that scCM provides an accurate annotation, along with rich spatial information of cell state. In summary, scCM is a robust and promising method for integrating large-scale CNS scRNA-seq data, enabling researchers to gain insights into the cellular and molecular mechanisms underlying CNS functions and diseases.

Discovery of tetrahydro γ-carboline based novel glucose uptake agent for the treatment of diabetes and Alzheimer’s diseases

The emergence of diabetes mellitus (DM), one of the prevalent metabolic disorders, has increased at alarming rates around the globe in the past few decades. The early discovery of insulin paved the way for the broadened non-invasive anti-hyperglycemic drug therapies to manage and treat diabetes. Recently, insulin resistance in brain tissues has been considered a new hallmark of disease progression, leading to neurodegeneration. Tetrahydro γ-carbolines are privileged scaffolds with various activities against obesity, cancer, and central nervous system (CNS) diseases. The failure of Latrepirdine in clinical phase trials as anti-AD, prompted us to explore further the γ-Carboline derivatives with anti-diabetic activity. To address this, we have leveraged our expertise in drug design to develop tetrahydro γ-carboline derivatives and studied their effect on glucose uptake. All the compounds exhibited low cytotoxicity towards the mammalian cell line 3T3-L1. Next, we screened the 10 derivatives to identify the novel anti-diabetic activities using a fluorescent glucose analog 2-NBDG (2-(N-(7-nitrobenz-2-oxa-1, 3-diazol-4-yl)-2-deoxy-D-glucose) based on a glucose-uptake assay in differentiated 3T3-L1 adipocytes. Compound 11a has significantly increased glucose uptake at 100 µM compared to rH-Insulin. The dose optimization (1 nM-100 nM) of lead compounds for 2-NBDG-glucose uptake clearly indicated that 11a is superior compared to Insulin. The 11a is the close analog of Latrepirdine, an anti-histamine drug, reported for Alzheimer disease (AD). Further, to understand its anti-AD potential we carried out in silico docking studies with its probable targets, Acetylcholinesterase (AChE), 5-hydroxytryptamine (5HT6) receptor, Butyrylcholinesterase (BChE), and N-methyl-D-aspartate (NMDA) receptor. The docking studies revealed that 11a had stronger binding to these targets than Latrepirdine, correlating with the glucose uptake assay. Thus, 11a is a potential lead disease-modifying agent and could be considered for the management and treatment of type 2 DM and AD.

Metformin and the PI3K/AKT signaling pathway: implications for cancer, cardiovascular, and central nervous system diseases.

Recent findings have brought our understanding of diseases at the molecular level, highlighting upstream intracellular pathways as potential therapeutic targets. The PI3K/AKT pathway, a key regulator of cellular responses to environmental changes, is frequently altered in various diseases, making it a promising target for intervention. Metformin is the most known anti-diabetic agent that is known due to its effects on cancer, inflammatory-related diseases, oxidative stress, and other human diseases. It is clearly understood that metformin modulates the activity of the PI3K/AKT pathway leading to a wide variety of outcomes. This interaction has been well-studied in various diseases. Therefore, this review aims to examine PI3K/AKT-modulating properties of metformin in cancer, cardiovascular, and central nervous system diseases. Our findings indicate that metformin is effective in treating cancer and CNS diseases, and plays a role in both the prevention and treatment of cardiovascular diseases. These insights support the potential of metformin in comprehensive strategies for disease management.

Matrine protects against experimental autoimmune encephalomyelitis through modulating microglial ferroptosis

Multiple sclerosis (MS) is an inflammatory demyelination neurodegenerative disease of the central nervous system (CNS). Ferroptosis has been implicated in a range of brain disorders, and iron-loaded microglia are frequently found in affected brain regions. However, the molecular mechanisms linking ferroptosis with MS have not been well-defined. The present study seeks to bridge this gap and investigate the impact of matrine (MAT), a herbal medicine with immunomodulatory capacities, on the regulation of oxidative stress and ferroptosis in the CNS of mice with experimental autoimmune encephalomyelitis (EAE), an animal model of MS. CNS of EAE mice contained elevated levels of ferroptosis-related molecules, e.g., MDA, LPCAT3 and PTGS2, but decreased expression of antioxidant molecules, including GSH and SOD, GPX4 and SLC7A11. This pathogenic process was reversed by MAT treatment, together with significant reduction of disease severity and CNS inflammatory demyelination. Furthermore, the expression of PTGS2 and LOX was largely increased in microglia of EAE mice, accompanied with increased production of IL-6 and TNF-α, indicating a proinflammatory phenotype of microglia that undergo oxidative stress/ferroptosis, and their expression was significantly reduced after MAT treatment. Together, our results indicate that ferroptosis/inflammation plays an important role in the pathogenesis of CNS autoimmunity, and inhibiting ferroptosis-induced microglial activation/inflammation could be a novel mechanism underlying the therapeutic effects of MAT on CNS inflammatory demyelination in EAE.

Utilizing Multifaceted Approaches to Target Drug Delivery in the Brain: From Nanoparticles to Biological Therapies.

The blood-brain barrier (BBB) poses an important obstacle to treating neurological disorders because it limits the entry of therapeutic agents into the central nervous system (CNS). Surmounting this barrier is crucial for delivering drugs effectively and targeting precise areas of the brain affected by conditions like Parkinson's disease, Alzheimer's disease, and brain tumors. This review examines the diverse strategies employed to enhance brain targeting, including nanotechnology, viral vectors, and biological therapies. Nanoparticles, liposomes, and dendrimers offer promising approaches for encapsulating drugs and facilitating their transport across the BBB. Viral vectors, such as adeno-associated viruses, demonstrate high transfection efficiency for gene therapy applications in CNS diseases. Biological therapies, including stem cell transplantation and neuromodulation techniques, can potentially restore normal cellular function and treat genetic disorders. Challenges such as BBB permeability, safety concerns, and regulatory considerations are discussed, along with future perspectives on precision medicine, noninvasive delivery methods, and biomarker discovery. By addressing these challenges and embracing innovative approaches, the field of brain drug targeting aims to transfer the way that neurological illness is treated and improve patient outcomes.

Chiral Azepines: In silico Potential in Cancer and Neurodegenerative Diseases, a Chemical Analysis

Background: Chiral azepines are synthesized with remarkable diastereoselectivity, but their biological activity has not been investigated. However, benzazepines have demonstrated notable effects, particularly on the central nervous system (CNS) and infections. This characteristic attracts the interest of bioinformatic investigations in this new family, as their structural similarity can confirm their potential based on their kinship or discovering new options for biological potential. Objective: Possible interaction targets of previously synthesized chiral azepines are investigated. This study involves examining the interaction between these targets, conducting molecular docking analysis, ADME (administration, distribution, metabolism, excretion), and toxicology prediction to assess biological potential. Methods: Modeling 3D-optimized structural, virtual screening, molecular docking, ADME, and toxicological studies were performed. Results: Structural analysis demonstrated potential against neurodegenerative diseases and cancer. In Molecular docking against cancer, pathways dependent on MAP2K1 and COX-2 exhibited energetically superior inhibitors than reference drugs, namely azepines 1, 3, and 6. Additionally, azepines 1 and 8 exhibited selective impacts against GSK3 and HMG-CoA-Reductase, respectively. Azepine 6 demonstrated an effect on CNS vs. GSK3 and HMG-CoA-Reductase, as well as potential against Alzheimer's disease; however, with a lower energy level with subunit 33 GABA-receptor. ADMETx investigations indicated satisfactory results for azepines. However, the opening of the cycle results in adverse effects and increased bioaccumulation, indicating the importance of preserving the integrity of azepine to propose its biological effect. Conclusion: Chiral azepines exhibit significant biological potential, particularly azepine 6 with a methyl substituent, which demonstrates multitarget potential. In addition, p-nitro phenyl substituent makes it highly selective towards CNS diseases. These findings indicate a strong relationship between biological activity and the stability of chiral azepines.

The Spectrum of Neurological Complications after Bariatric Surgery – Review of the Literature

Bariatric surgery represents one of the most efficient treatments addressing obesity and its associated complications with an increasing trend. Even if the medical benefits for patients are huge, due to weight loss and despite technical improvements in bariatric procedures, it is still associated with diverse types of complications. Most of the complications appear due to nutrient deficiency, as absorption is compromised after surgical anatomy modification. Neurological complications after bariatric surgery are very diverse with an occurrence within days to years after surgery, most frequently in patients with gastrointestinal or surgical complications. Any segment of the nervous system can be affected with distinct types of manifestations ranging from peripheral axonal neuropathy, nerve palsy secondary to compartment syndrome, encephalopathy, and myelopathy, to psychiatric and demyelinating central nervous system diseases. Identifying patients at risk and systematic screening for nutrient deficiency with proper supplementation is essential for preventing neurological complications and lifelong sequelae. In this paper, we present the spectrum of neurological complications reported after bariatric surgery.

Clinical spectrum of demyelinating disease of central nervous system and frequency of anti AQP4 and anti MOG among them: one-year single-center retrospective study

Background: Inflammatory demyelinating diseases of the central nervous system (CNS) are autoimmune conditions leading to significant neurological disability in adults. Recent classifications include myelin oligodendrocyte glycoprotein antibody associated disease (MOGAD) and neuromyelitis optica spectrum disorder (NMOSD) which pose diagnostic challenges due to overlapping clinical and radiological features. This study aimed to assess the clinical spectrum among adults and children diagnosed with CNS demyelinating diseases and to find the proportion of MOG and/or aquaporin-4 (AQP4) autoantibodies amongst them. Methods: This single-center, retrospective study examined 20 patients diagnosed with CNS demyelinating disorders between March, 2023 and February, 2024. Data pertaining to demographics, disease types, CSF analysis, MRI findings, treatment modalities, and serological profiles for anti-AQP4 and anti-MOG antibodies were collected from hospital records and evaluated. Results: Among 20 patients [median age, 34 years (IQR, 18.75); males (n=10) and females (n=10)], acute transverse myelitis (TM) was the most common demyelinating disorder at onset (60%) followed by optic neuritis (ON) (20%). CSF analysis found elevated protein levels in 53% and pleocytosis in 33% of patients. MRI findings revealed longitudinal extensive involvement in 52% of patients, predominantly affecting the cervical and dorsal spine. Serological testing identified 15% positive for anti-AQP4 and 10% for anti-MOG antibodies. MOG+ patients were significantly younger than AQP4+ patients (mean age 16.5 vs. 36.66 years, p=0.016). Both MOG+ patients were male, with 50% presenting with acute TM and 50% with acute disseminated encephalomyelitis. Among AQP4+ patients, the male-to-female ratio was 1:2, with 66.66% presenting with acute TM and 33.33% with ON. Conclusion: CNS demyelinating disorders primarily affect younger individuals, with TM as the most common initial disorder and extensive spinal involvement in cervical and dorsal regions. Serological testing identified three patients with anti-AQP4 and two with anti-MOG antibodies, providing valuable insights into the clinical spectrum of these disorders through cell-based assays.

Lymphotropic polyomavirus and Merkel cell polyomavirus in patients infected with HIV or hepatitis B or C virus

BackgroundLPV and MCV emerge as recent additions to the Polyomaviridae family, capable of inducing important infections. Studies have suggested the presence of LPV in human populations, with potential involvement in central nervous system (CNS) diseases. Additionally, MCV, closely related to LPV, has been implicated in Merkel cell carcinoma (MCC). This study aimed to explore the prevalence of LPV and MCV in individuals with compromised immunity due to chronic viral infections. Methods340 specimens, including HIV PCR-positive, HBV PCR-positive, HCV PCR-positive, and HIV/HBV/HCV negative sera, underwent screening via PCR technique to identify LPV and MCV genomes. Subsequently, sequencing was employed to validate the viral identity. ResultsOut of all specimens, MCV DNA was detected in 8.52 % of participants, with a significantly higher prevalence in HIV-positive individuals (26.4 %). LPV was detected in only one HIV-positive patient. No co-detection of MCV and LPV was observed. Phylogenetic analysis confirmed the genetic similarity of the detected MCV strains to known references, while the LPV sequence showed 99 % identity to the published sequences of LPV-K38. ConclusionThis research provides insights into the prevalence of LPV and MCV in individuals with chronic viral infections. The study highlights the potential association between MCV and immunocompromised states, emphasizing the need for comprehensive investigations to understand the epidemiology, transmission routes, and clinical implications of these polyomaviruses in human populations.