Search

Biological communication system for neurological disorder patients is similar to the Brain Computer Interface in a way that it facilitates the connection to the outside world in real time. The interdisciplinary field of Electroencephalogram based message depiction is gaining importance as it assists the paralysed person to communicate. In the proposed method a novel approach of feature extraction is done by Empirical Mode Decomposition on non- stationary & non-linear kind of EEG signal. EMD helps in the effective time frequency analysis by disintegrating the EEG signal in the form of six Intrinsic Mode Functions with help of the frequency components. In all nine features are extracted from the decomposed IMFs so as to predict the states or messages of the patient. The above computed features are then served to the Deep Neural Network to perform the classification. The performance of suggested method is studied through applying it to the acquired database generated by the designed hardware as well as also in real time message depiction. The maximum classification accuracy 97% for the acquired database & 85% in real time are obtained respectively by comparative analysis. The command messages generated from the proposed system helps the person suffering from neurological disorder to establish the communication link with the outside world in an efficient way. Thus, the proposed novel method shows better performance in real time message depiction purpose as related to other existing methods. [ABSTRACT FROM AUTHOR]

Congenital melanocytic nevi (CMN) are pigmented lesions present at birth, varying widely in size and clinical impact. In rare instances, these nevi become visible during the first months of life, a phenomenon known as tardive melanocytic nevi (tardive CMN). Giant congenital melanocytic nevi (GCMN) are defined as nevi larger than 40 cm in projected adult size (PAS). Their association with the central nervous system (CNS) poses significant risks, including melanoma and neurocutaneous melanocytosis (NCM), where melanocytes infiltrate the CNS, potentially causing seizures, hydrocephalus, and, rarely, CNS melanoma. MRI is recommended for GCMN patients, particularly those with numerous satellite nevi or neurological symptoms, to detect CNS involvement. The Nevosurgery Network recommends MRI examinations in cases of GCMN (>40 cm PAS), the presence of over 20 concomitant nevi, and neurological symptoms requiring clarification. CMN can be associated with melanocyte accumulations and melanin deposits in the brain, spinal cord, and leptomeninges. [ABSTRACT FROM AUTHOR]

Background: The spinal cord is a crucial part of the vertebrate CNS, controlling movements and receiving and processing sensory information from the trunk and limbs. However, there is much we do not know about how this essential organ develops. Here, we describe expression of 21 transcription factors and one transcriptional regulator in zebrafish spinal cord. Results: We analyzed the expression of aurkb, foxb1a, foxb1b, her8a, homeza, ivns1abpb, mybl2b, myt1a, nr2f1b, onecut1, sall1a, sall3a, sall3b, sall4, sox2, sox19b, sp8b, tsc22d1, wdhd1, zfhx3b, znf804a, and znf1032 in wild‐type and MIB E3 ubiquitin protein ligase 1 zebrafish embryos. While all of these genes are broadly expressed in spinal cord, they have distinct expression patterns from one another. Some are predominantly expressed in progenitor domains, and others in subsets of post‐mitotic cells. Given the conservation of spinal cord development, and the transcription factors and transcriptional regulators that orchestrate it, we expect that these genes will have similar spinal cord expression patterns in other vertebrates, including mammals and humans. Conclusions: Our data identify 22 different transcriptional regulators that are strong candidates for playing different roles in spinal cord development. For several of these genes, this is the first published description of their spinal cord expression. Key Findings: We identify 22 distinct transcriptional regulators with broad expression in the developing spinal cord.We analyze their expression at key developmental stages in WT and MIB E3 ubiquitin protein ligase 1 mutant zebrafish embryos.Their expression patters are distinct from one another, some are predominanatly expressed in progenitor domains, and others in subsets of post‐mitotic cells.We expect that these genes will have similar spinal cord expression patterns in other vertebrates. [ABSTRACT FROM AUTHOR]

Amyotrophic lateral sclerosis (ALS) is a refractory neurodegenerative disease characterized by the degeneration and loss of motor neurons, typically resulting in death within five years of onset. There have been few effective treatments, making the development of robust therapies an urgent challenge. Genetic mutations have been identified as contributors to ALS, with mutations in superoxide dismutase 1 (SOD1), which neutralizes the harmful reactive oxygen species superoxide, accounting for approximately 2% of all ALS cases. To counteract the toxic gain of function caused by SOD1 mutations, therapeutic strategies aimed at suppressing SOD1 gene expression have shown promise. Antisense oligonucleotide (ASO) is an artificially synthesized, short, single-stranded DNA/RNA molecule that binds to target RNA to alter gene expression, representing a next-generation therapeutic approach. In 2023, tofersen became the first ASO drug approved by the FDA for ALS. Administered intrathecally, tofersen specifically binds to SOD1 mRNA, inhibiting the production of toxic SOD1 protein, thereby improving biomarkers of ALS. The long-term efficacy and safety of tofersen require further validation, and the development of more optimized treatment protocols is essential. A series of studies and therapeutic developments related to SOD1 mutations have advanced the understanding of ALS pathophysiology and significantly contributed to treatment strategies for central nervous system disorders. This review focuses on an overview of SOD1 mutations and the development process of tofersen, aiming to deepen the understanding of advancements in ALS research and discuss future challenges and directions for ASO therapy. [ABSTRACT FROM AUTHOR]

Background: Neurological conditions constitute approximately 10% of feline cases referred to veterinary clinics. Such cases often present manifestations of central nervous system (CNS) damage, including inflammatory lesions, neoplastic growth and structural and cellular transformations. Objectives: This study aimed at identifying histopathological changes in the CNS of cats that had succumbed to neurological symptoms. Methods: Microscopic evaluation of different sections within the CNS was conducted on 20 cats that had either died naturally or were euthanized due to neurological signs. After performing a necropsy, we examined the CNS tissues and conducted PCR testing to screen for possible viral infections, including feline infectious peritonitis (FIP), feline immunodeficiency virus (FIV) and feline leukemia virus (FeLV). Results: The majority of cases showed characteristic histopathologic lesions, notably mononuclear and suppurative meningoencephalitis, perivascular cuffing, disseminated intravascular coagulation (DIC), granulomatous meningoencephalitis, acute neuronal necrosis, liquefactive necrosis, epididymitis, thrombosis and demyelination. Among the 20 cats studied, 12 tested positive for FIP by PCR analysis, while 5 cats exhibited positive results for FIV. Also, FeLV PCR tests displayed positive results in 4 cats. No evidence of feline spongiform encephalopathy (FSE) was observed. Conclusion: This study is the first of its kind conducted in Iran. Based on the results, the most prevalent viral agents infecting cats' CNS were FIP, FIV and FeLV. The investigation revealed no evidence of FSE in cats with neurological signs. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Zhejiang University: Science B is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The enteric nervous system (ENS) is a fundamental component of the gastrointestinal system, composed of a vast network of neurons and glial cells. It operates autonomously but is interconnected with the central nervous system (CNS) through the vagus nerve. This communication, known as the gut–brain axis, influences the bidirectional communication between the brain and the gut. Background/Objectives: This study aimed to review neurological pathologies related to the ENS. Methods: To this end, a comprehensive literature search was conducted in the "PubMed" database. Articles available in "free format" were selected, applying the filters "Humans" and limiting the search to publications from the last ten years. Results: The ENS has been linked to various neurological diseases, from autism spectrum disorder to Parkinson's disease including neurological infection with the varicella zoster virus (VZV), even sharing pathologies with the CNS. This finding suggests that the ENS could serve as an early diagnostic marker or therapeutic target for neurological diseases. Gastrointestinal symptoms often precede CNS symptoms, and the ENS's accessibility aids in diagnosis and treatment. Parkinson's patients may show intestinal lesions up to twenty years before CNS symptoms, underscoring the potential for early diagnosis. However, challenges include developing standardized diagnostic protocols and the uneven distribution of dopaminergic neurons in the ENS. Continued research is needed to explore the ENS's potential in improving disease prognosis. Conclusions: The ENS is a promising area for early diagnosis and therapeutic development. Nevertheless, it is essential to continue research in this area, especially to gain a deeper understanding of its organization, function, and regenerative capacity. [ABSTRACT FROM AUTHOR]

Dengue illness, caused by the dengue viruses, continues to be a major global health concern, with increasing incidence and the emergence of severe manifestations such as neurological complications. An overview of the current understanding of dengue epidemiology, clinical manifestations, and research priorities is presented here. Dengue transmission has escalated in recent years, exacerbated by factors such as vector expansion, climate change, and socioeconomic challenges. The clinical spectrum of dengue ranges from mild febrile illness to severe manifestations, including hemorrhagic fever and neurological complications. Neurological manifestations of dengue, once considered rare, are now increasingly reported, encompassing encephalitis, myelitis, and Guillain–Barré Syndrome, among others. Diagnosis primarily relies on laboratory methods such as RT/PCR, NS1 antigen detection, and serological assays. Despite advancements in understanding the dengue pathogenesis, there remains a critical need for effective vaccines, antiviral drugs, improved surveillance methods, predictive models for disease severity, and long-term studies on post-Dengue sequelae. Integrated programs and holistic approaches to dengue control are essential for mitigating its impact. Addressing these research priorities will be pivotal in combating dengue and reducing its global burden. [ABSTRACT FROM AUTHOR]

Abstract Biological communication system for neurological disorder patients is similar to the Brain Computer Interface in a way that it facilitates the connection to the outside world in real time. The interdisciplinary field of Electroencephalogram based message depiction is gaining importance as it assists the paralysed person to communicate. In the proposed method a novel approach of feature extraction is done by Empirical Mode Decomposition on non- stationary & non-linear kind of EEG signal. EMD helps in the effective time frequency analysis by disintegrating the EEG signal in the form of six Intrinsic Mode Functions with help of the frequency components. In all nine features are extracted from the decomposed IMFs so as to predict the states or messages of the patient. The above computed features are then served to the Deep Neural Network to perform the classification. The performance of suggested method is studied through applying it to the acquired database generated by the designed hardware as well as also in real time message depiction. The maximum classification accuracy 97% for the acquired database & 85% in real time are obtained respectively by comparative analysis. The command messages generated from the proposed system helps the person suffering from neurological disorder to establish the communication link with the outside world in an efficient way. Thus, the proposed novel method shows better performance in real time message depiction purpose as related to other existing methods.

Introduction: Epilepsy is a long-standing brain disorder struck by a persistent propensity to have seizures that are not caused by any instant injury to the central nervous system. It also involves numerous consequences on cognition, the brain’s biology, psychology, and social aspects due to periodic seizures. Epilepsy can affect individuals of all ages and genders worldwide. In patients diagnosed with epilepsy based on clinical symptoms, EEG results, age over 60 months, and frequency of unprovoked seizures, the occurrence of seizures during a fever can be triggered. This is because changes in body temperature can impact the electrical activity of neurons and other cellular processes. This study aimed to investigate the effect of oral diazepam on the number of attacks of seizures in epilepsy patients during febrile illness. Methods: from 2020 to 2023, patients were collected during the consultations to private clinics, and outpatient (pediatric & neuro-medicine clinic). 430 patients were collected all those patients diagnosed as epilepsy according to clinical findings and EEG. All patients on antiepileptic drugs either monotherapy or 2 types of drugs aged more than 5 years. 96 patients involved in the study half of them given prophylactic oral diazepam and the 2nd group placebo. Results: The number of assaults per year during febrile illness is significantly reduced with therapy; there is no significant correlation was seen between treatment and age or sex. Conclusion: Oral diazepam can reduce the number of attacks of seizures in epilepsy patients during febrile illness.

Abstract Cerebral toxoplasmosis is a common opportunistic infectious disease in immunocompromised patients that usually involves the central nervous system. The clinical features and neuroimaging findings of cerebral toxoplasmosis are often similar to brain abscess and tuberculoma. We report a case of hepatitis C with cerebral toxoplasmosis, with the aim of enhancing understanding of the imaging manifestations of cerebral toxoplasmosis and thereby improving the differential diagnosis of brain space‐occupying lesions.

Viral infection is frequently assayed by ongoing expression of viral genes. These assays fail to identify cells that have been exposed to the virus but limit or inhibit viral replication. To address this limitation, we used a dual-labeling vesicular stomatitis virus (DL-VSV), which has a deletion of the viral glycoprotein gene, to allow evaluation of primary infection outcomes. This virus encodes Cre, which can stably mark any cell with even a minimal level of viral gene expression. Additionally, the virus encodes GFP, which distinguishes cells with higher levels of viral gene expression, typically due to genome replication. Stereotactic injections of DL-VSV into the murine brain showed that different cell types had very different responses to the virus. Almost all neurons hosted high levels of viral gene expression, while glial cells varied in their responses. Astrocytes (Sox9+) were predominantly productively infected, while oligodendrocytes (Sox10+) were largely abortively infected. Microglial cells (Iba1+) were primarily uninfected. Furthermore, we monitored the early innate immune response to viral infection and identified unique patterns of interferon (IFN) induction. Shortly after infection, microglia were the main producers of IFNb, whereas later, oligodendrocytes were the main producers. IFNb+ cells were primarily abortively infected regardless of cell type. Last, we investigated whether IFN signaling had any impact on the outcome of primary infection and did not observe significant changes, suggesting that intrinsic factors are likely responsible for determining the outcome of primary infection. [ABSTRACT FROM AUTHOR]

The poliovirus (PV) enters the central nervous system (CNS) via the bloodstream, suggesting the existence of a mechanism to cross the blood–brain barrier. Here, we report that PV capsid proteins (VP1 and VP3) can penetrate cells, with VP3 being more invasive. Two independent parts of VP3 are responsible for this function. Both peptides can penetrate human umbilical cord vascular endothelial cells, and one peptide of VP3 could also penetrate peripheral blood mononuclear cells. In an in vitro blood–brain barrier model using rat‐derived astrocytes, pericytes, and endothelial cells, both peptides were observed to traverse from the blood side to the brain side at 6 h after administration. These results provide insights into the molecular mechanisms underlying PV invasion into the CNS. [ABSTRACT FROM AUTHOR]

Introduction: Epilepsy is a long-standing brain disorder struck by a persistent propensity to have seizures that are not caused by any instant injury to the central nervous system. It also involves numerous consequences on cognition, the brain’s biology, psychology, and social aspects due to periodic seizures. Epilepsy can affect individuals of all ages and genders worldwide. In patients diagnosed with epilepsy based on clinical symptoms, EEG results, age over 60 months, and frequency of unprovoked seizures, the occurrence of seizures during a fever can be triggered. This is because changes in body temperature can impact the electrical activity of neurons and other cellular processes. This study aimed to investigate the effect of oral diazepam on the number of attacks of seizures in epilepsy patients during febrile illness. Methods: from 2020 to 2023, patients were collected during the consultations to private clinics, and outpatient (pediatric & neuro-medicine clinic). 430 patients were collected all those patients diagnosed as epilepsy according to clinical findings and EEG. All patients on antiepileptic drugs either monotherapy or 2 types of drugs aged more than 5 years. 96 patients involved in the study half of them given prophylactic oral diazepam and the 2nd group placebo. Results: The number of assaults per year during febrile illness is significantly reduced with therapy; there is no significant correlation was seen between treatment and age or sex. Conclusion: Oral diazepam can reduce the number of attacks of seizures in epilepsy patients during febrile illness. [ABSTRACT FROM AUTHOR]

Objective To summarize the imaging findings of intracranial central nervous system (CNS) malformations children in the high-altitude plateau (Xigaze city). Methods We retrospectively reviewed the imaging data of the suspected patients having CNS malformations, which enrolled either by the clinic or by the ultrasound in the Shigatse People’s hospital from June, 2019 to June, 2023. All imaging data were interpreted by two experienced radiologists with consensus reading. Imaging characteristics were recorded roughly by primary/secondary, supra-/subtentorial malformation type and the corresponding clinical symptoms. Results A total of 36 children were included in this study, including 19 patients ≤ 1 year old (including 2 newborns), 7 patients between 1 and 3 years old, and 10 patients >3 years old. Seven cases underwent MRI examination, others having CT scan. Polygyria and pachygyria malformation were the most common type of congenital neurological malformations (7 cases, 31.8%), followed by cystic changes of the cerebral parenchyma (3 cases, 13.6%). Cerebral atrophy was the most common type of secondary CNS abnormalities group (8 cases, 57.1%), followed by communicative hydrocephalus (3 cases, 21.4%). Five patients in the congenital group and 4 patients in the secondary CNS group had the complex malformations. There were 8 dead cases (all in the ≤1-year-old group), 12 cases having neurological sequelae, 1 case with normal development and 15 cases with loss of follow-up. There were no significant differences between primary and secondary CNS group regarding the final outcome. Conclusion In this study, gyrus developmental malformation and encephalatrophy were the most common etiologies in infants’ CNS malformations. Reasonable use of imaging modalities will help depict the complicated CNS malformations and design individual treatment. [ABSTRACT FROM AUTHOR]

Transmembrane proteins known as hyperpolarization-activated cyclic nucleotide-gated (HCN) channels control the movement of Na+ and K+ ions across cellular membranes. HCN channels are known to be involved in crucial physiological functions in regulating neuronal excitability and rhythmicity, and pacemaker activity in the heart. Although HCN channels have been relatively well investigated in the brain, their distribution and function in the retina have received less attention, remaining their physiological roles to be comprehensively understood. Also, because recent studies reported HCN channels have been somewhat linked with the dysfunction of photoreceptors which are affected by retinal diseases, investigating HCN channels in the retina may offer valuable insights into disease mechanisms and potentially contribute to identifying novel therapeutic targets for retinal degenerative disorders. This paper endeavors to summarize the existing literature on the distribution and function of HCN channels reported in the vertebrate retinas of various species and discuss the potential implications for the treatment of retinal diseases. Then, we recapitulate current knowledge regarding the function and regulation of HCN channels, as well as their relevance to various neurological disorders. [ABSTRACT FROM AUTHOR]

Brain metastasis, characterized by poor clinical outcomes, is a devastating disease. Despite significant mechanistic and therapeutic advances in recent years, pivotal improvements in clinical interventions have remained elusive. The heterogeneous nature of the primary tumor of origin, complications in drug delivery across the blood–brain barrier, and the distinct microenvironment collectively pose formidable clinical challenges in developing new treatments for patients with brain metastasis. Although current preclinical models have deepened our basic understanding of the disease, much of the existing research on brain metastasis has employed a reductionist approach. This approach, which often relies on either in vitro systems or in vivo injection models in young and treatment-naive mouse models, does not give sufficient consideration to the clinical context. Given the translational importance of brain metastasis research, we advocate for the design of preclinical experimental models that take into account these unique clinical challenges and align more closely with current clinical practices. We anticipate that aligning and simulating real-world patient conditions will facilitate the development of more translatable treatment regimens. This brief review outlines the most pressing clinical challenges, the current state of research in addressing them, and offers perspectives on innovative metastasis models and tools aimed at identifying novel strategies for more effective management of clinical brain metastasis. [ABSTRACT FROM AUTHOR]

Purpose of review: A review of existing and emerging therapies for the treatment of fungal infections of the CNS is presented, highlighting more recent studies. Newly authorized and emerging therapies and the data surrounding their use are also introduced. Recent findings: Early data suggests Ibrexafungerp, a newly released antifungal for the treatment of vulvovaginal candidiasis, does not have a significant role in the treatment of CNS infections. Combination therapy including therapy with terbinafine appears promising for difficult-to-treat fungal infections of the CNS. Antifungal treatment remains pathogen-specific but in resource-available areas, liposomal amphotericin B or triazole are the first line for CNS fungal infections. A one-time liposomal amphotericin B infusion followed by flucytosine and fluconazole can be considered for persons living with HIV in resource-poor areas. Summary: Pathogen-specific management is reviewed and the latest evidence surrounding treatment is discussed. [ABSTRACT FROM AUTHOR]

Central nervous system (CNS) injury or disease states are often difficult to treat due to the closed system of the dura mater/blood-brain barrier and the bony skull and vertebrae. The closed system results in at least partial containment of any pro-inflammatory molecules, pathogens, or toxic byproducts in the case of brain or spinal cord lesions, which can result in a destructive feedback loop. Cervical-approach access techniques (lateral C1-C2, suboccipital and lateral atlanto-occipital space punctures) are less-common methods of cerebrospinal fluid (CSF) sampling due to the relative ease and safety of lumbar spinal taps. However, with improved image-guidance, these cervical-level CSF access points are still useful when there are certain contraindications and difficulties when attempting to sample the CSF via the typical lumbar spinal approach. With the advent of microcatheters and minimally invasive techniques, combined with body fluid filtration technology, the question arises: could dual microcatheters be introduced for inflow and outflow of purified or artificial CSF to break the destructive feedback loop and thus diminish CNS damage?. We hypothesize that intrathecal spinal catheters could be placed in 2 positions (e.g., via a cervical route and the typical lumbar spinal route) to allow for both an input and output to more effectively filter or flush the CSF. This could have broad implications in the treatment of strokes, traumatic brain or spinal cord injury, infections, autoimmune diseases, and even malignancies within the CNS-in short, any disease with abnormalities detectable in the CSF.

Parkinson's disease (PD) is recognized as the second most common neurodegenerative disease worldwide. Even if PD etiopathogenesis is not yet fully understood, in recent years, it has been advanced that a chronic state of inflammation could play a decisive role in the development of this pathology, establishing the close link between PD and neuroinflammation. In the broad panorama of inflammation and its several signaling pathways, the C-C chemokine receptor type 1 (CCR1) could play a key pathogenic role in PD progression, and could constitute a valuable target for the development of innovative anti-PD therapies. In this study, we probed the neuroprotective properties of the CCR1 antagonist BX471 compound in a mouse model of MPTP-induced nigrostriatal degeneration. BX471 treatments were performed intraperitoneally at a dose of 3 mg/kg, 10 mg/kg, and 30 mg/kg, starting 24 h after the last injection of MPTP and continuing for 7 days. From our data, BX471 treatment strongly blocked CCR1 and, as a result, decreased PD features, also reducing the neuroinflammatory state by regulating glial activation, NF-κB pathway, proinflammatory enzymes, and cytokines overexpression. Moreover, we showed that BX471's antagonistic action on CCR1 reduced the infiltration of immune cells, including mast cells and lymphocyte T activation. In addition, biochemical analyses carried out on serum revealed a considerable increase in circulating levels of CCR1 following MPTP-induced PD. In light of these findings, CCR1 could represent a useful pathological marker of PD, and its targeting could be a worthy candidate for the future development of new immunotherapies against PD. [ABSTRACT FROM AUTHOR]

Human immunodeficiency virus type 1 (HIV-1) infection can result in HIV-associated neurocognitive disorder (HAND), a spectrum of disorders characterized by neurological impairment and chronic inflammation. Combined antiretroviral therapy (cART) has elicited a marked reduction in the number of individuals diagnosed with HAND. However, there is continual, low-level viral transcription due to the lack of a transcription inhibitor in cART regimens, which results in the accumulation of viral products within infected cells. To alleviate stress, infected cells can release accumulated products, such as TAR RNA, in extracellular vesicles (EVs), which can contribute to pathogenesis in neighboring cells. Here, we demonstrate that cART can contribute to autophagy deregulation in infected cells and increased EV release. The impact of EVs released from HIV-1 infected myeloid cells was found to contribute to CNS pathogenesis, potentially through EV-mediated TLR3 (Toll-like receptor 3) activation, suggesting the need for therapeutics to target this mechanism. Three HIV-1 TAR-binding compounds, 103FA, 111FA, and Ral HCl, were identified that recognize TAR RNA and reduce TLR activation. These data indicate that packaging of viral products into EVs, potentially exacerbated by antiretroviral therapeutics, may induce chronic inflammation of the CNS observed in cART-treated patients, and novel therapeutic strategies may be exploited to mitigate morbidity. [ABSTRACT FROM AUTHOR]

Transmembrane proteins known as hyperpolarization-activated cyclic nucleotide-gated (HCN) channels control the movement of Na+ and K+ ions across cellular membranes. HCN channels are known to be involved in crucial physiological functions in regulating neuronal excitability and rhythmicity, and pacemaker activity in the heart. Although HCN channels have been relatively well investigated in the brain, their distribution and function in the retina have received less attention, remaining their physiological roles to be comprehensively understood. Also, because recent studies reported HCN channels have been somewhat linked with the dysfunction of photoreceptors which are affected by retinal diseases, investigating HCN channels in the retina may offer valuable insights into disease mechanisms and potentially contribute to identifying novel therapeutic targets for retinal degenerative disorders. This paper endeavors to summarize the existing literature on the distribution and function of HCN channels reported in the vertebrate retinas of various species and discuss the potential implications for the treatment of retinal diseases. Then, we recapitulate current knowledge regarding the function and regulation of HCN channels, as well as their relevance to various neurological disorders. [ABSTRACT FROM AUTHOR]

The article focuses on exploring genetic polymorphisms as potential contributors to severe postoperative pain. Topics include the use of pharmacogenetics in pain therapy to predict individual analgesic response, the impact of genetic variants on opioid metabolism, and the influence of genetic polymorphisms on the effectiveness of analgesics in specific patient populations, such as those with red hair.

The interaction between the central nervous system (CNS) and peripheral nervous system (PNS) governs various physiological functions, influences cognitive processes and emotional states. It is necessary to unravel the mechanisms governing the interaction between the brain and the body, enhancing our understanding of physical and mental well-being. Neuro-ergonomics-based human-computer interaction can be improved by comprehending the intricate interrelation between the CNS and PNS. Various studies have been explored using diverse methodologies to study CNS-PNS interaction in specific psychophysiological states, such as emotion, stress, or cognitive tasks. However, there is a need for a thorough, extensive, and systematic review covering diverse interaction forms, applications, and assessments. In this work, an attempt has been made to perform a systematic review that examines the interaction between the CNS and PNS across diverse psychophysiological states, focusing on varied physiological signals. For this, scientific repositories, namely Scopus, PubMed, Association for Computing Machinery, and Web of Science, are accessed. In total, 61 articles have been identified within the period of January 2008 to April 2023 for systematic review. The selected research articles are analyzed based on factors, namely subject information, stimulation modality, types of interactions between the brain and other organs, feature extraction techniques, classification methods, and statistical approaches. The evaluation of the existing literature indicates a scarcity of publicly available databases for CNS-PNS interaction and limited application of machine learning and deep learning-based advanced tools. Furthermore, this review underscores the urgent need for enhancements in several key areas including the development of a more refined psycho-physiological model, improved analysis techniques, and better electrode-surface interface technology. Additionally, there is a need for more research involving daily life activities, female-oriented studies, and privacy considerations. This review contributes to standardizing protocols, improves the diagnostic relevance of various instruments, and extracts more reliable biomarkers. The novelty of this study lies in guiding researchers to point out various issues and potential solutions for future research in the field of bio-signal-based CNS-PNS interaction.

The central nervous system (CNS) is a rare but serious site of tuberculosis spread that manifests in three forms: meningitis, spinal arachnoiditis, and CNS tuberculoma. CNS tuberculoma, or intracranial tuberculous granuloma, is a caseating or non-caseating granulomatous reaction within the brain parenchyma that may mimic a brain tumor. We present the case of a 10-year-old male patient with a travel history to Western Africa who presented to our institution after his fourth tonic-clonic seizure over 2 months. MRI of the brain revealed a solitary cortical/subcortical enhancing intracranial mass with intralesional hemorrhage and mineralization, pathologically proven to represent a CNS tuberculoma. While rare, this etiology should be considered with the appropriate travel history and for which prompt treatment may improve outcomes in the pediatric population.

Congenital melanocytic nevi (CMN) are pigmented lesions present at birth, varying widely in size and clinical impact. In rare instances, these nevi become visible during the first months of life, a phenomenon known as tardive melanocytic nevi (tardive CMN). Giant congenital melanocytic nevi (GCMN) are defined as nevi larger than 40 cm in projected adult size (PAS). Their association with the central nervous system (CNS) poses significant risks, including melanoma and neurocutaneous melanocytosis (NCM), where melanocytes infiltrate the CNS, potentially causing seizures, hydrocephalus, and, rarely, CNS melanoma. MRI is recommended for GCMN patients, particularly those with numerous satellite nevi or neurological symptoms, to detect CNS involvement. The Nevosurgery Network recommends MRI examinations in cases of GCMN (>40 cm PAS), the presence of over 20 concomitant nevi, and neurological symptoms requiring clarification. CMN can be associated with melanocyte accumulations and melanin deposits in the brain, spinal cord, and leptomeninges.

Neurologic disorders such as traumatic brain injury, multiple sclerosis, Alzheimer’s disease, and drug-resistant epilepsy have a high socioeconomic impact around the world. Current therapies for these disorders are often not effective. This creates a demand for the development of new therapeutic approaches to treat these disorders. Recent data suggest that autoreactive naturally occurring immunoglobulins produced by subsets of B cells, called B1 B cells, combined with complement, are actively involved in the processes of restoration of neuronal functions during pathological conditions and remyelination. The focus of this review is to discuss the possibility of creating specific therapeutic antibodies that can activate and fix complement to enhance neuronal survival and promote central nervous system repair after injuries associated with many types of neurodegenerative diseases.

Brain tumors are a diverse collection of neoplasms affecting the brain with a high prevalence rate in people of all ages around the globe. In this pathological context, glioblastoma, a form of glioma that belongs to the IV-grade astrocytoma group, is the most common and most aggressive form of the primary brain tumors. Indeed, despite the best treatments available including surgery, radiotherapy or a pharmacological approach with Temozolomide, glioblastoma patients' mortality is still high, within a few months of diagnosis. Therefore, to increase the chances of these patients surviving, it is critical to keep finding novel treatment opportunities. In the past, efforts to treat glioblastoma have mostly concentrated on customized treatment plans that target specific mutations such as epidermal growth factor receptor (EGFR) mutations, Neurotrophic Tyrosine Receptor Kinase (NTRK) fusions, or multiple receptors using multi-kinase inhibitors like Sunitinib and Regorafenib, with varying degrees of success. Here, we focused on the receptor tyrosine kinase AXL that has been identified as a mediator for tumor progression and therapy resistance in various cancer types, including squamous cell tumors, small cell lung cancer, and breast cancer. Activated AXL leads to a significant increase in tumor proliferation, tumor cell migration, and angiogenesis in different in vitro and in vivo models of cancer since this receptor regulates interplay with apoptotic, angiogenic and inflammatory pathways. Based on these premises, in this review we mainly focused on the role of AXL in the course of glioblastoma, considering its primary biological mechanisms and as a possible target for the application of the most recent treatments. [ABSTRACT FROM AUTHOR]

Simple Summary: In the realm of neurology, advanced imaging tools play a crucial role as critical endpoints in clinical trials. While magnetic resonance imaging (MRI) serves as a primary diagnostic tool, it exhibits limitations in specific scenarios. Ongoing research in neuro-oncological imaging aims to address these limitations. Our review explores the latest advancements in imaging modalities for neuro-oncology, highlighting the accuracy and competence of each modality. These include PET tracers and radiolabeled amino acids, PET/MRI, radiomics, deep learning, MR perfusion imaging, MR fingerprinting, MR spectroscopy imaging, MR elastography, and intra-operative ultrasound techniques. The focus is on the potency of these modalities in diagnosis, cancer staging, prognosis, and post-treatment evaluation, ultimately enhancing accuracy and effectiveness in managing brain tumors. This study delineates the pivotal role of imaging within the field of neurology, emphasizing its significance in the diagnosis, prognostication, and evaluation of treatment responses for central nervous system (CNS) tumors. A comprehensive understanding of both the capabilities and limitations inherent in emerging imaging technologies is imperative for delivering a heightened level of personalized care to individuals with neuro-oncological conditions. Ongoing research in neuro-oncological imaging endeavors to rectify some limitations of radiological modalities, aiming to augment accuracy and efficacy in the management of brain tumors. This review is dedicated to the comparison and critical examination of the latest advancements in diverse imaging modalities employed in neuro-oncology. The objective is to investigate their respective impacts on diagnosis, cancer staging, prognosis, and post-treatment monitoring. By providing a comprehensive analysis of these modalities, this review aims to contribute to the collective knowledge in the field, fostering an informed approach to neuro-oncological care. In conclusion, the outlook for neuro-oncological imaging appears promising, and sustained exploration in this domain is anticipated to yield further breakthroughs, ultimately enhancing outcomes for individuals grappling with CNS tumors. [ABSTRACT FROM AUTHOR]

Extracellular vesicles (EVs) are membrane‐enclosed nanovesicles secreted by cells into the extracellular space and contain functional biomolecules, e.g. signaling receptors, bioactive lipids, nucleic acids, and proteins, which can serve as biomarkers. Neurons and glial cells secrete EVs, contributing to various physiological and pathological aspects of brain diseases. EVs confer their role in the bidirectional crosstalk between the central nervous system (CNS) and the periphery owing to their distinctive ability to cross the unique blood–brain barrier (BBB). Thus, EVs in the blood, cerebrospinal fluid (CSF), and urine can be intriguing biomarkers, enabling the minimally invasive diagnosis of CNS diseases. Although there has been an enormous interest in evaluating EVs as promising biomarkers, the lack of ultra‐sensitive approaches for isolating and detecting brain‐derived EVs (BDEVs) has hindered the development of efficient biomarkers. This review presents the recent salient findings of exosomal biomarkers, focusing on brain disorders. We summarize highly sensitive sensors for EV detection and state‐of‐the‐art methods for single EV detection. Finally, the prospect of developing advanced EV analysis approaches for the non‐invasive diagnosis of brain diseases is presented. [ABSTRACT FROM AUTHOR]

Stroke was the 2nd leading cause of death and a major cause of morbidity. Unfortunately, there are limited means to promote neurological recovery post-stroke, but research has unearthed potential targets for therapies to encourage post-stroke neurogenesis and neuroplasticity. The occurrence of neurogenesis in adult mammalian brains, including humans, was not widely accepted until the 1990s. Now, adult neurogenesis has been extensively studied in human and mouse neurogenic brain niches, of which the subventricular zone of the lateral ventricles and subgranular zone of the dentate gyrus are best studied. Numerous other niches are under investigation for neurogenic potential. This review offers a basic overview to stroke in the clinical setting, a focused summary of recent and foundational research literature on cortical neurogenesis and post-stroke brain plasticity, and insights regarding how the meninges and choroid plexus have emerged as key players in neurogenesis and neuroplasticity in the context of focal cerebral ischemia disrupting the anterior circulation. The choroid plexus and meninges are vital as they are integral sites for neuroimmune interactions, glymphatic perfusion, and niche signaling pertinent to neural stem cells and neurogenesis. Modulating neuroimmune interactions with a focus on astrocyte activity, potentially through manipulation of the choroid plexus and meningeal niches, may reduce the exacerbation of stroke by inflammatory mediators and create an environment conducive to neurorecovery. Furthermore, addressing impaired glymphatic perfusion after ischemic stroke likely supports a neurogenic environment by clearing out inflammatory mediators, neurotoxic metabolites, and other accumulated waste. The meninges and choroid plexus also contribute more directly to promoting neurogenesis: the meninges are thought to harbor neural stem cells and are a niche amenable to neural stem/progenitor cell migration. Additionally, the choroid plexus has secretory functions that directly influences stem cells through signaling mechanisms and growth factor actions. More research to better understand the functions of the meninges and choroid plexus may lead to novel approaches for stimulating neuronal recovery after ischemic stroke. [ABSTRACT FROM AUTHOR]

Brain diseases have become one of the leading roots of mortality and disability worldwide, contributing a significant part of the disease burden on healthcare systems. The blood-brain barrier (BBB) is a primary physical and biological obstacle that allows only small molecules to pass through it. Its selective permeability is a significant challenge in delivering therapeutics into the brain for treating brain dysfunction. It is estimated that only 2% of the new central nervous system (CNS) therapeutic compounds can cross the BBB and achieve their therapeutic targets. Scientists are exploring various approaches to develop effective cargo delivery vehicles to promote better therapeutics targeting the brain with minimal off-target side effects. Despite different synthetic carriers, one of the natural brain cargo delivery systems, "exosomes," are now employed to transport drugs through the BBB. Exosomes are naturally occurring small extracellular vesicles (EVs) with unique advantages as a therapeutic delivery system for treating brain disorders. They have beneficial innate aspects of biocompatibility, higher stability, ability to cross BBB, low cytotoxicity, low immunogenicity, homing potential, targeted delivery, and reducing off-site target effects. In this review, we will discuss the limitations of synthetic carriers and the utilization of naturally occurring exosomes as brain-targeted cargo delivery vehicles and highlight the methods for modifying exosome surfaces and drug loading into exosomes. We will also enlist neurodegenerative disorders targeted with genetically modified exosomes for their treatment. [ABSTRACT FROM AUTHOR]

Background: Acute lymphoblastic leukemia (ALL) is prone to metastasize to the central nervous system (CNS), which is an important cause of poor treatment outcomes and unfavorable prognosis. However, the pathogenesis of CNS metastasis of ALL cells has not been fully illuminated. Recent reports have shed some light on the correlation between neural mechanisms and ALL CNS metastasis. These progressions prompt us to study the relationship between ALL central nervous system metastasis and neuronal development, exploring potential biomarkers and therapeutic targets of CNS metastasis. Materials and methods: ALL central nervous system metastasis- and neuronal development-related differentially expressed genes (DEGs) were identified by analyzing gene expression datasets GSE60926 and GSE13715. Target prediction and network analysis methods were applied to assess protein-protein interaction networks. Gene Ontology (GO) terms and pathway enrichment for DEGs were assessed. Co-expressed differentially expressed genes (co-DEGs) coupled with corresponding predicted microRNAs (miRNAs) were studied as well. Reverse transcription-polymerase chain reaction (RT-PCR) and flow cytometry were employed for the validation of key co-DEGs in primary ALL cells. Furthermore, ALL cells were treated with a vascular endothelial growth factor (VEGF) inhibitor to block neuronal development and assess changes in the co-DEGs. Results: We identified 216, 208, and 204 DEGs in ALL CNS metastasis specimens and neuronal development samples (GSE60926 and GSE13715). CD2, CD3G, CD3D, and LCK may be implicated in ALL CNS metastasis. LAMB1, MATN3, IGFBP3, LGALS1, and NEUROD1 may be associated with neuronal development. Specifically, four co-DEGs (LGALS1, TMEM71, SHISA2, and S100A11) may link ALL central nervous system metastasis and neuronal development process. The miRNAs for each co-DEG could be potential biomarkers or therapeutic targets for ALL central nervous system metastasis, especially hsa-miR-22-3p, hsa-miR-548t-5p, and hsa-miR-6134. Additionally, four co-DEGs (LGALS1, TMEM71, SHISA2, and S100A11) were validated in CNS-infiltrated ALL cells. The VEGF inhibitor demonstrated a suppressive effect on mRNA and protein expression of key co-DEGs. Conclusion: The bioinformatic survey and key gene validation suggest a possible correlation between ALL CNS metastasis and the neuronal development process. Simulating the neuronal development process might be a possible strategy for CNS metastasis in ALL. LGALS1, TMEM71, SHISA2, and S100A11 genes are promising and novel biomarkers and targets in ALL CNS metastasis. [ABSTRACT FROM AUTHOR]

[Display omitted] • Orm1 is overexpressed in both T-cell and non-T-cell-induced demyelination. • EAE: Cortex and SC display glial, synaptic, dendritic, and inflammatory changes. • Cuprizone: Cortex, but not SC, exhibits glial, synaptic, dendritic changes. • EAE: Mitochondrial dysfunction only in the spinal cord. • C3 is upregulated in the CNS of EAE, and downregulated in the cortex of cuprizone. Multiple sclerosis (MS) is a complex autoimmune and neurodegenerative disorder that affects the central nervous system (CNS). It is characterized by a heterogeneous disease course involving demyelination and inflammation. In this study, we utilized two distinct animal models, cuprizone (CPZ)-induced demyelination and experimental autoimmune encephalomyelitis (EAE), to replicate various aspects of the disease. We aimed to investigate the differential CNS responses by examining the proteomic profiles of EAE mice during the peak disease (15 days post-induction) and cuprizone-fed mice during the acute phase (38 days). Specifically, we focused on two different regions of the CNS: the dorsal cortex (Cx) and the entire spinal cord (SC). Our findings revealed varied glial, synaptic, dendritic, mitochondrial, and inflammatory responses within these regions for each model. Notably, we identified a single protein, Orosomucoid-1 (Orm1), also known as Alpha-1-acid glycoprotein 1 (AGP1), that consistently exhibited alterations in both models and regions. This study provides insights into the similarities and differences in the responses of these regions in two distinct demyelinating models. [ABSTRACT FROM AUTHOR]

The rapid growth and proliferation within healthcare of Virtual Reality (VR) technology's make it a promising platform for treating central nervous system (CNS)-related ailments. From neurorehabilitation to pain management and even cognitive enhancement, there are numerous benefits that VR offers this portion of medicine. Nevertheless, multiple risks among motion sickness and eye strain, exist with utilizing this new tech for CNS treatments. Beyond immediate physical harm concerns like these - researching the long-term impact on this area remains paramount regarding future implementation. The utilization of VR technology in the field of CNS presents considerable promise, the same its potential risks necessitate a meticulous analysis and resolution before its extensive acceptance across clinical settings. [ABSTRACT FROM AUTHOR]

In the present study, we compared the astrocyte-transducing potential of the relatively novel engineered AAV PHP.eB serotype and the well-examined conventional AAV5 serotype. We generated the AAV-based genetic constructs with membrane-bound fluorescent markers under the control of the astroglial promoter GfaABC1D to target astrocytes in vivo, either via local injection into the hippocampus (AAV5, AAV PHP.eB) or via systemic injection in the retro-orbital venous sinus (AAV PHP.eB). We collected new data on the transduction properties of locally injected PHP.eB and AAV5 viruses. A morphological examination and immunostainings of mouse brain slices revealed a dose-dependent shift of cellular tropism for locally injected PHP.eB from astroglial to astroglial-neuronal as the concentration increased. When the high doses of PHP.eB viruses were administered systemically, we observed strong astrocyte transduction throughout the brain, as confirmed by the morphological examination and GFAP immunostaining. AAV5 exhibited consistent astrocytic expression in all tested concentrations. The obtained results suggest that AAV5 is more suitable for astrocyte targeting in routine stereotaxic viral injection experiments. The widely used engineered PHP.eB capsid was originally designed for the transduction of both neurons and glia. Dual cellular tropism of PHP.eB viruses, observed using different doses and different delivery protocols (local vs. systemic), suggests that the usage of AAV5 is more reliable for astrocyte labeling and that intrahippocampal injection is more suitable than systemic injection for the preferential labeling of hippocampal astroglia. [ABSTRACT FROM AUTHOR]

Exosomes, membrane‐enclosed vesicles, are secreted by all types of cells. Exosomes can transport various molecules, including proteins, lipids, functional mRNAs, and microRNAs, and can be circulated to various recipient cells, leading to the production of local paracrine or distal systemic effects. Numerous studies have proved that exosomes can pass through the blood—brain barrier, thus, enabling the transfer of peripheral substances into the central nervous system (CNS). Consequently, exosomes may be a vital factor in the exchange of information between the periphery and CNS. This review will discuss the structure, biogenesis, and functional characterization of exosomes and summarize the role of peripheral exosomes deriving from tissues like the lung, gut, skeletal muscle, and various stem cell types in communicating with the CNS and influencing the brain's function. Then, we further discuss the potential therapeutic effects of exosomes in brain diseases and the clinical opportunities and challenges. Gaining a clearer insight into the communication between the CNS and the external areas of the body will help us to ascertain the role of the peripheral elements in the maintenance of brain health and illness and will facilitate the design of minimally invasive techniques for diagnosing and treating brain diseases. [ABSTRACT FROM AUTHOR]

Abstract In recent years, the role of nobiletin in neuronal disorders has received extensive attention. However, the study of nobiletin in the peripheral nervous system is limited. Nobiletin, as a compound with high fat solubility, high bioavailability and low toxicity, has been extensively studied. Accumulating scientific evidence has shown that nobiletin has a variety of biological functions in the nervous system, such as inhibiting the expression of inflammatory factors, reducing the neurotoxic response, improving the antioxidant capacity, promoting the survival of nerve cells, promoting axon growth, reducing blood‒brain barrier permeability, reducing brain oedema, promoting cAMP response element binding protein expression, improving memory, and promoting mild depolarization of nerve cell mitochondria to improve antioxidative stress capacity. Accumulating studies have shown that nobiletin also protects enteric nervous system, spinal cord and sciatic nerve. To explore the new therapeutic potential of nobiletin in the nervous system, recent and relevant research progress is reviewed in this article. This will provide a new research idea for nobiletin in the nervous system.

In the present study, we compared the astrocyte-transducing potential of the relatively novel engineered AAV PHP.eB serotype and the well-examined conventional AAV5 serotype. We generated the AAV-based genetic constructs with membrane-bound fluorescent markers under the control of the astroglial promoter GfaABC1D to target astrocytes in vivo, either via local injection into the hippocampus (AAV5, AAV PHP.eB) or via systemic injection in the retro-orbital venous sinus (AAV PHP.eB). We collected new data on the transduction properties of locally injected PHP.eB and AAV5 viruses. A morphological examination and immunostainings of mouse brain slices revealed a dose-dependent shift of cellular tropism for locally injected PHP.eB from astroglial to astroglial-neuronal as the concentration increased. When the high doses of PHP.eB viruses were administered systemically, we observed strong astrocyte transduction throughout the brain, as confirmed by the morphological examination and GFAP immunostaining. AAV5 exhibited consistent astrocytic expression in all tested concentrations. The obtained results suggest that AAV5 is more suitable for astrocyte targeting in routine stereotaxic viral injection experiments. The widely used engineered PHP.eB capsid was originally designed for the transduction of both neurons and glia. Dual cellular tropism of PHP.eB viruses, observed using different doses and different delivery protocols (local vs. systemic), suggests that the usage of AAV5 is more reliable for astrocyte labeling and that intrahippocampal injection is more suitable than systemic injection for the preferential labeling of hippocampal astroglia.

Neuroprosthetics are devices that are used when there has been an interruption in brain signals that produce and complete a series of intended movements, resulting in various forms of paralysis and physical disabilities. These synaptic connections can be replicated by electric pulses coming from the device. It can also be used on amputees with prosthetic limbs, connecting the piece that is placed on the motor cortex to a computer, which decodes the brain's input and converts the message to the prosthetic limb, thus creating the intended movement. The current main obstacles in optimizing neuroprosthetic abilities include needing better understanding the software of brain function, improving sensory features of neuroprosthetics, privacy and accountability controversy, and safety concerns. Overall, neuroprosthetics have the ability to allow affected individuals to regain their physical independence, and there is an enhanced progress in supporting wider ranges of movements.

Dengue illness, caused by the dengue viruses, continues to be a major global health concern, with increasing incidence and the emergence of severe manifestations such as neurological complications. An overview of the current understanding of dengue epidemiology, clinical manifestations, and research priorities is presented here. Dengue transmission has escalated in recent years, exacerbated by factors such as vector expansion, climate change, and socioeconomic challenges. The clinical spectrum of dengue ranges from mild febrile illness to severe manifestations, including hemorrhagic fever and neurological complications. Neurological manifestations of dengue, once considered rare, are now increasingly reported, encompassing encephalitis, myelitis, and Guillain–Barré Syndrome, among others. Diagnosis primarily relies on laboratory methods such as RT/PCR, NS1 antigen detection, and serological assays. Despite advancements in understanding the dengue pathogenesis, there remains a critical need for effective vaccines, antiviral drugs, improved surveillance methods, predictive models for disease severity, and long-term studies on post-Dengue sequelae. Integrated programs and holistic approaches to dengue control are essential for mitigating its impact. Addressing these research priorities will be pivotal in combating dengue and reducing its global burden.