Central Nervous Disorders Research Articles

Wearable Sensor‐Based Multi‐modal Fusion Network for Automated Gait Dysfunction Assessment in Children with Cerebral Palsy

Gait, fundamental to human movement, becomes compromised in cerebral palsy (CP), a childhood‐onset central nervous system motor disorder. Precise assessment of patients’ gait is crucial for tailored rehabilitation interventions. Currently, clinical scales assessing CP gait dysfunction mostly, while valuable, rely on subjective clinician observations. To enhance objectivity and efficiency in CP diagnosis and rehabilitation, there is a need for more objective assessment procedures. This study introduces a multi‐modal and multi‐scale feature fusion (MMFF) framework, a new framework for automating gait dysfunction assessment in children with CP. By utilizing surface electromyography and acceleration signals recorded during children's walking, MMFF generates a feature vector enriched with adaptively refined feature maps, cross‐mode correlations, and both local and global information. Validation of MMFF's effectiveness is evident through an accomplished classification accuracy of 99.13%. The mean values for precision, recall, and F1‐score in Gross Motor Function Classification System (GMFCS)‐1, GMFCS‐2, and GMFCS‐3, reaching 99.00%, 99.00%, and 98.33%, respectively, further reflect the accuracy of functional assessments at each level. This study underscores MMFF's potential as an objective, streamlined tool for clinicians, promising improved gait assessment and well‐informed rehabilitation strategies for children with CP.

The Interplay between Ferroptosis and Neuroinflammation in Central Neurological Disorders.

Central neurological disorders are significant contributors to morbidity, mortality, and long-term disability globally in modern society. These encompass neurodegenerative diseases, ischemic brain diseases, traumatic brain injury, epilepsy, depression, and more. The involved pathogenesis is notably intricate and diverse. Ferroptosis and neuroinflammation play pivotal roles in elucidating the causes of cognitive impairment stemming from these diseases. Given the concurrent occurrence of ferroptosis and neuroinflammation due to metabolic shifts such as iron and ROS, as well as their critical roles in central nervous disorders, the investigation into the co-regulatory mechanism of ferroptosis and neuroinflammation has emerged as a prominent area of research. This paper delves into the mechanisms of ferroptosis and neuroinflammation in central nervous disorders, along with their interrelationship. It specifically emphasizes the core molecules within the shared pathways governing ferroptosis and neuroinflammation, including SIRT1, Nrf2, NF-κB, Cox-2, iNOS/NO·, and how different immune cells and structures contribute to cognitive dysfunction through these mechanisms. Researchers' findings suggest that ferroptosis and neuroinflammation mutually promote each other and may represent key factors in the progression of central neurological disorders. A deeper comprehension of the common pathway between cellular ferroptosis and neuroinflammation holds promise for improving symptoms and prognosis related to central neurological disorders.

Cellular and molecular mechanisms involved in the analgesic effects of botulinum neurotoxin: A literature review.

Botulinum neurotoxins (BoNTs), derived from Clostridium botulinum, have been employed to treat a range of central and peripheral neurological disease. Some studies indicate that BoNT may be beneficial for pain conditions as well. It has been hypothesized that BoNTs may exert their analgesic effects by preventing the release of pain-related neurotransmitters and neuroinflammatory agents from sensory nerve endings, suppressing glial activation, and inhibiting the transmission of pain-related receptors to the neuronal cell membrane. In addition, there is evidence to suggest that the central analgesic effects of BoNTs are mediated through their retrograde axonal transport. The purpose of this review is to summarize the experimental evidence of the analgesic functions of BoNTs and discuss the cellular and molecular mechanisms by which they can act on pain conditions. Most of the studies reviewed in this article were conducted using BoNT/A. The PubMed database was searched from 1995 to December 2022 to identify relevant literature.

Neuroimaging features of primary central nervous system post-transplantation lymphoproliferative disorder following hematopoietic stem cell transplant in patients with β-thalassemia: a case series and review of literature

PurposePrimary central nervous system post-transplantation lymphoproliferative disorder (PCNS-PTLD) is a rare but serious complication of hematopoietic stem cell transplantation (HSCT) in patients with severe β-thalassemia. This study aimed to assess the clinical presentation, pathological characteristics, neuroimaging findings, and treatment strategies in patients with β-thalassemia who developed PCNS-PTLD and to compare a case series from our transplant center to reported cases from literature.MethodsWe retrospectively reviewed our hospital database and identified four cases of pathologically confirmed PCNS-PTLD without a history of systemic PTLD in patients with severe β-thalassemia after HSCT. We also performed a relevant literature review on PCNS-PTLD.ResultsThe median time from transplantation to diagnosis of PCNS-PTLD was 5.5 months. Intracerebral lesions were usually multiple involving both supratentorial and infratentorial regions with homogeneous or rim enhancement. All patients had pathologically confirmed PCNS-PTLD with three patients having diffuse large B-cell lymphoma and the fourth patient having plasmacytic hyperplasia. There was low response to treatment with a median survival of 83 days.ConclusionPCNS-PTLD should be considered in the differential diagnosis of patients with β-thalassemia who had an intracranial lesion on neuroimaging after HSCT.Critical relevance statementThis case series with a comprehensive review of neuroimaging and clinical characteristics of children with primary central nervous system post-transplantation lymphoproliferative disorder should advance our understanding and improve management of this rare yet severe complication following transplant for β-thalassemia.Key points• We assessed clinical presentation, treatment strategies, and neuroimaging characteristics of PCNS-PTLD in patients with β-thalassemia after transplantation.• Patients with β-thalassemia may have post-transplantation lymphoproliferative disorder presenting as brain lesions on neuroimaging.• Neuroimaging findings of the brain lesions are helpful for prompt diagnosis and proper management.Graphical

Discovery of a New Compound, Erinacerin W, from the Mycelia of Hericium erinaceus, with Immunomodulatory and Neuroprotective Effects.

One new compound with an isoindolinone skeleton, along with erinacines A, C, and S, was isolated from the mycelia of Hericium erinaceus, an edible fungus with a long history of use in traditional Chinese medicine. Based on analysis of MS and NMR spectral data, the structure of the compound was identified as (2E,6E)-8-(2-(1-carboxy-3-methylbutyl)-4,6-dihydroxy-1-oxoisoindolin-5-yl)-2,6-dimethylocta-2,6-dienoic acid. In light of this discovery, we have given this compound the name erinacerin W. Using a co-culture in vitro LPS-activated BV2 microglia-induced SH-SY5Y neuroinflammation model, the results showed that erinacerin W demonstrated protection against the LPS-activated BV-2 cell-induced overexpression of IL-6, IL-1β, and TNF-α on SH-SY5Y cells. This finding may provide potential therapeutic approaches for central nervous disorders.

The neurosurgical outpatient clinic: comparison between accesses in public and private activities

BackgroundNeurosurgical clinic assesses presence and extent of pathologies of central and peripheral nervous system or disorders affecting the spine, to identify most effective treatment and possible recourse to surgery. The aim of the study is to evaluate the appropriateness of request for a neurosurgical consult both in private and in public outpatient clinics.Materials and methodsWe collected and analyzed all the reports of outpatient visits of public and private clinic over a period between January and December 2018.ResultsThere were 0.62% real urgent visits in the public sector and 1.19% in the private sector (p = 0.05). Peripheral pathologies represented 12.53% and 6.21% of pathologies evaluated in public and private sector respectively (p < 0.00001). In addition, 15.76% of visits in public lead to surgery, while they represented 11.45% in private (p = 0.0003).ConclusionsNo study is available comparing accesses of patients in neurosurgical outpatient clinics. In public clinic, visits are booked as urgent on the prescription of the general practitioner: in reality, only 5% of these visits were really confirmed as urgent by the specialist. Peripheral pathologies are more frequent in public clinic, while cranial pathologies are more frequent in private one. Patients with cranial pathologies prefer to choose their surgeon by accessing private clinic.

Psoriasis and risk of central neurological disorders in European populations: A mendelian randomization analysis

BackgroundPeople with psoriasis are at a higher risk for having central neurological problems, according to previous studies; however, it is unclear if there is a genetic link between the risk of developing psoriasis and developing central neurological disorders. In this study, the possible link between genetically predisposed psoriasis and the risk of common central nervous system disorders was comprehensively investigated. MethodsThere was no overlap in the participant populations between the psoriasis and central neurological disorders genome-wide association studies, which provide the genetic resources. Inverse variance weighting, often used as Mendelian randomization (MR) analysis, is the main method. To guarantee the accuracy of our findings, a number of sensitivity studies were carried out. ResultsMR analysis revealed that although psoriasis was reported to increase the risk of Parkinson's disease (OR = 4.42, 95%CI[-3.81～6.79], P = 0.58) and epilepsy (OR = 4.71, 95%CI[-2.20～5.30], P = 0.42) in this study, they did not reach statistical significance. At the same time, this study did not observe that psoriasis would increase the risk of multiple sclerosis (OR = 0.01, 95%CI [-12.61～3.83], P = 0.30) and migraine (OR = 0.99, 95%CI [0.94～1.05], P = 0.78), they also did not reach statistical significance. Under all sensitivity assessments, the results remained stable. ConclusionsPsoriasis does not appear to raise the risk of migraine, Parkinson's disease, multiple sclerosis, or epilepsy, according to our study.

Identification of potential crucial genes and therapeutic targets for epilepsy

BackgroundEpilepsy, a central neurological disorder, has a complex genetic architecture. There is some evidence suggesting that genetic factors play a role in both the occurrence of epilepsy and its treatment. However, the genetic determinants of epilepsy are largely unknown. This study aimed to identify potential therapeutic targets for epilepsy.MethodsDifferentially expressed genes (DEGs) were extracted from the expression profiles of GSE44031 and GSE1834. Gene co-expression analysis was used to confirm the regulatory relationship between newly discovered epilepsy candidate genes and known epilepsy genes. Expression quantitative trait loci analysis was conducted to determine if epilepsy risk single-nucleotide polymorphisms regulate DEGs’ expression in human brain tissue. Finally, protein–protein interaction analysis and drug–gene interaction analysis were performed to assess the role of DEGs in epilepsy treatment.ResultsThe study found that the protein tyrosine phosphatase receptor-type O gene (PTPRO) and the growth arrest and DNA damage inducible alpha gene (GADD45A) were significantly upregulated in epileptic rats compared to controls in both datasets. Gene co-expression analysis revealed that PTPRO was co-expressed with RBP4, NDN, PAK3, FOXG1, IDS, and IDS, and GADD45A was co-expressed with LRRK2 in human brain tissue. Expression quantitative trait loci analysis suggested that epilepsy risk single-nucleotide polymorphisms could be responsible for the altered PTPRO and GADD45A expression in human brain tissue. Moreover, the protein encoded by GADD45A had a direct interaction with approved antiepileptic drug targets, and GADD45A interacts with genistein and cisplatin.ConclusionsThe results of this study highlight PTPRO and GADD45A as potential genes for the diagnosis and treatment of epilepsy.

Disorders of Copper Metabolism in Children-A Problem too Rarely Recognized.

Copper plays an important role in metabolic processes. Both deficiency and excess of this element have a negative effect and lead to pathological conditions. Copper is a cofactor of many enzymatic reactions. Its concentration depends on the delivery in the diet, the absorption in enterocytes, transport with the participation of ATP7A/ATP7B protein, and proper excretion. Copper homeostasis disorders lead to serious medical conditions such as Menkes disease (MD) and Wilson's disease (WD). A mutation in the ATP7A gene is the cause of Menkes disease, it prevents the supply of copper ions to enzymes dependent on them, such as dopamine β-hydroxylase and lysyl oxidase. This leads to progressive changes in the central nervous system and disorders of the connective tissue. In turn, Wilson's disease is an inherited autosomal recessive disease. It is caused by a mutation of the ATP7B gene encoding the ATP7B protein which means excess copper cannot be removed from the body, leading to the pathological accumulation of this element in the liver and brain. The clinical picture is dominated by the liver, neurological, and/or psychiatric symptoms. Early inclusion of zinc preparations and chelating drugs significantly improves the prognosis in this group of patients. The aim of the study is to analyse, based on the latest literature, the following factors: the etiopathogenesis, clinical picture, diagnostic tests, treatment, prognosis, and complications of disease entities associated with copper disturbances: Menkes disease and Wilson's disease. In addition, it is necessary for general practitioners, neurologists, and gastroenterologists to pay attention to these disease entities because they are recognized too late and too rarely, especially in the paediatric population.

The Role and Mechanism of Autoantibodies in Dysimmunity Related Neurological Diseases

Autoantibodies are antibodies produced by B cells capable of attacking their own tissues or organs after loss of immune tolerance. A large body of literature shows that autoantibodies play an important role in neurological diseases associated with immune abnormalities. Nowadays, neurological disorders are an important cause of disability and death in populations around the world, so it is important to study the role and mechanisms of autoantibodies in neurological disorders associated with immune abnormalities. The blood-brain barrier is biologically important for maintaining the normal physiological state of the central nervous system, and we have previously found that monoclonal autoantibodies of SLE origin can inhibit the expression of tight junction proteins in the blood-brain barrier. Our findings provide clues for the study of the role of autoantibodies in neurological disorders and greatly attract us to conduct a more in-depth and systematic review and synthesis. In this paper, we summarize the functions of autoantibodies in autoimmune and non-autoimmune diseases and focus on the roles and mechanisms of autoantibodies in immune-associated neurological disorders by taking central and peripheral neurological diseases as the entry points, which can provide new molecular targets and new theoretical basis for the specific diagnosis and targeted therapy of neurological diseases.

Characteristics of long-term complications in Langerhans cell histiocytosis

About 100 cases of Langerhans cell histiocytosis (LCH) occur annually in Japan. It predominantly occurs in infants, presenting as multisystem disease or multifocal bone involvement. However, LCH can also occur in adults aged 20 to 40. Single-system skin involvement is rare, with most cases presenting with multisystem disease, including bone lesions, which respond to chemotherapy. In adults, lung lesions that improve with smoking cessation are well-known, although multisystem disease is more common and requires aggressive therapeutic intervention similar to that in children. In some infant cases, progression of liver, spleen, and bone marrow lesions can be difficult to control and can become severe. However, targeted molecular therapies are now available as a lifesaving option. More than 30% of cases of multisystem LCH recur at least once, often leading to long-term complications. In particular, the emergence of central diabetes insipidus, anterior pituitary dysfunction, and central nervous system neurodegenerative disorders several years after the diagnosis of LCH is a unique feature not observed in other diseases. New therapeutic strategies are needed to counter these problems.

A case of primary central nervous system post-transplant lymphoproliferative disease 14 years after living donor liver transplantation

The patient was a 51-year-old man who had undergone living donor liver transplantation for type B cirrhosis at the age of 37 years, and had a history of immunosuppressive drug use. He had developed focal seizures starting from his right upper limb, and MRI showed a lesion in the subcortical white matter of his left parietal lobe. Sensory disturbance and paralysis progressed in his right upper and lower limbs, and his brain lesion rapidly enlarged. A brain biopsy revealed diffuse large B-cell lymphoma, and Epstein-Barr virus-encoded small RNA in situ hybridization was positive. The patient was diagnosed with primary central nervous system post-transplant lymphoproliferative disorder (PCNS-PTLD) with no lesions in other organs. There are few reports of PCNS-PTLD cases after living donor liver transplantation in Japan. Although rare, it is nevertheless important to consider this disease in patients receiving immunosuppressive drugs after organ transplantation who develop brain lesions, regardless of which organ was transplanted.

Creutzfeldt–Jakob Disease, a Diagnostic Challenge and Management in ICU: A Case Report

PPrion disease is a group of neurogenerative disorders caused by misfolding of prion proteins into abnormal proteins. It is presented with multiple central nervous system-related disorders such as decreased cognitive function, movement disorder, seizure, speech problems, dementia, visual blurring, and limb weakness. It is rapidly progressive and highly fatal with an annual incidence of about one per million all over the world. A 65-year-old lady presented in our hospital with all the above mix-up complaints in poor general condition. All workups relevant to the above scenario were done to find the diagnosis. All possible metabolic cause was ruled out; however, magnetic resonance imaging of the brain led to suspicion of Creutzfeldt–Jakob disease. Electroencephalogram was done further to make this diagnosis confirm. The patient responded to the general supportive treatment and discharge with stable and improved status. Key words: Creutzfeldt Jacob disease, Prion, Intensive care unit, Electroencephalogram, Dementia.

Acupuncture Treatment in a Mouse Model of Chronic Hypoxia-Induced Cognitive Dysfunction.

The treatment of central nervous disorders has consistently posed significant challenges to the medical field. Acupuncture, a non-pharmacological practice rooted in traditional Chinese medicine, entails the insertion of fine needles into precise points on the body and is commonly employed for the management of diverse conditions. Recently, acupuncture has emerged as a promising therapeutic intervention for a range of neurological diseases, including anxiety and respiratory disorders. However, the potential of acupuncture in treating cognitive dysfunction induced by chronic hypoxia has not yet been explored. This paper presents a comprehensive protocol for establishing a mouse model of chronic hypoxia-induced cognitive impairment, administering mild anesthesia, performing acupuncture treatment, and assessing behavioral changes and memory abilities using open field tests and water mazes. The step-by-step protocol provides detailed instructions on accurately locating and positioning acupoints and needles for cognitive improvement. By employing this protocol, researchers can conduct systematic studies to thoroughly evaluate the therapeutic potential of acupuncture for cognitive dysfunction.

Reliability and validity of the Lever Sign Test in suspected ligament and/or meniscus injuries of the knee: a comparison between an orthopaedist and a physical therapist

The purpose of this study was to investigate the intertester reliability and validity of the Lever Sign Test. Intertester reliability has received little attention in previous studies. In order to make comparisons with other studies, the intertester reliability and validity of the Lachman and Anterior Drawer Tests were also calculated. Patients between 18 and 50 years of age with suspected ligament and/or meniscus injuries were included. Exclusion criteria were suspected malignant, systemic, or central neurologic disease, acute cartilage injury, suspected fracture, or knowledge of the participant's knee findings. Testing was randomized and blinded by an experienced orthopaedic surgeon and a physical therapist. Cohen's kappa was calculated for intertester reliability. Sensitivity and specificity, positive and negative predictive value, and positive and negative likelihood ratio were calculated. MRI findings were used as the gold standard. Thirty-six patients were enrolled in the study, 27 male (75%) and 9 female (25%). The prevalence of anterior cruciate ligament lesions was 44.4%. Cohen's kappa (κ) was κ=0.6 (CI 95% [0.29, 0.91]) for the Lever Sign Test, κ=0.64 (CI 95% [0.35, 0.93]) for the Lachman test, and κ=0.63 (CI 95% [0.3, 0.95]) for the Anterior Drawer Test. The sensitivity of the Lever Sign Test was 0.53 and 0.40 for the orthopaedic surgeon and physical therapist, respectively, specificity was 0.89 and 0.79, the positive predictive value was 0.80 and 0.60, the negative predictive value was 0.70 and 0.62, the positive likelihood ratio was 4.80 and 1.90, respectively, and the negative likelihood ratio was 0.76 and 0.53. The estimated intertester reliability of the Lever Sign Test was good. The Lever Sign Test is suitable as a complement to the Lachman Test, which is considered the most valid test in the literature. The weaknesses and ambiguities of the operating mechanism of the Lever Sign Test should not be ignored and should be further explored.

Penerapan pijat kaki Terhadap Peningkatan Kekuatan Otot Pada Pasien Stroke

Background Stroke is a central nervous system function disorder in the form of blockage of brain blood vessels or rupture of blood vessels in the brain, symptoms that appear in hemiparesis disease, namely a decrease in muscle strength, one of the independent nursing interventions in dealing with decreased muscle strength by giving foot massage. Research Methods: This study uses a descriptive method with a case study approach. Sample: 1 stroke patient who experienced a decrease in muscle strength. Results: the study found that stroke patients experienced complaints of weakness on the right side of the body, muscle strength on the right 1. Nursing diagnoses were: physical mobility barriers, ineffective cerebral tissue perfusion, and damage to skin integrity. Mobilization support nursing interventions, Improved cerebral perfusion, skin integrity care. Nursing implementation was carried out for 6 days. Evaluation after applying foot massage nursing problems that arise in patients can be resolved. Conclusion: the application of foot massage can increase muscle strength there is a change in the value of muscle strength in stroke patients from a value of 1 to a value of 4 on day 6. Suggestion: it is hoped that it can provide independent nursing interventions as a companion to pharmacological therapy to overcome nursing problems that exist in non hemorrhagic stroke patients.

Alterations in Rat Hippocampal Glutamatergic System Properties after Prolonged Febrile Seizures

Febrile seizures during early childhood may result in central nervous system developmental disorders. However, the specific mechanisms behind the impact of febrile seizures on the developing brain are not well understood. To address this gap in knowledge, we employed a hyperthermic model of febrile seizures in 10-day-old rats and tracked their development over two months. Our objective was to determine the degree to which the properties of the hippocampal glutamatergic system are modified. We analyzed whether pyramidal glutamatergic neurons in the hippocampus die after febrile seizures. Our findings indicate that there is a reduction in the number of neurons in various regions of the hippocampus in the first two days after seizures. The CA1 field showed the greatest susceptibility, and the reduction in the number of neurons in post-FS rats in this area appeared to be long-lasting. Electrophysiological studies indicate that febrile seizures cause a reduction in glutamatergic transmission, leading to decreased local field potential amplitude. This impairment could be attributable to diminished glutamate release probability as evidenced by decreases in the frequency of miniature excitatory postsynaptic currents and increases in the paired-pulse ratio of synaptic responses. We also found higher threshold current causing hind limb extension in the maximal electroshock seizure threshold test of rats 2 months after febrile seizures compared to the control animals. Our research suggests that febrile seizures can impair glutamatergic transmission, which may protect against future seizures.

Functional near-infrared spectroscopy in non-invasive neuromodulation.

Non-invasive cerebral neuromodulation technologies are essential for the reorganization of cerebral neural networks, which have been widely applied in the field of central neurological diseases, such as stroke, Parkinson's disease, and mental disorders. Although significant advances have been made in neuromodulation technologies, the identification of optimal neurostimulation parameters including the cortical target, duration, and inhibition or excitation pattern is still limited due to the lack of guidance for neural circuits. Moreover, the neural mechanism underlying neuromodulation for improved behavioral performance remains poorly understood. Recently, advancements in neuroimaging have provided insight into neuromodulation techniques. Functional near-infrared spectroscopy, as a novel non-invasive optical brain imaging method, can detect brain activity by measuring cerebral hemodynamics with the advantages of portability, high motion tolerance, and anti-electromagnetic interference. Coupling functional near-infrared spectroscopy with neuromodulation technologies offers an opportunity to monitor the cortical response, provide real-time feedback, and establish a closed-loop strategy integrating evaluation, feedback, and intervention for neurostimulation, which provides a theoretical basis for development of individualized precise neurorehabilitation. We aimed to summarize the advantages of functional near-infrared spectroscopy and provide an overview of the current research on functional near-infrared spectroscopy in transcranial magnetic stimulation, transcranial electrical stimulation, neurofeedback, and brain-computer interfaces. Furthermore, the future perspectives and directions for the application of functional near-infrared spectroscopy in neuromodulation are summarized. In conclusion, functional near-infrared spectroscopy combined with neuromodulation may promote the optimization of central neural reorganization to achieve better functional recovery from central nervous system diseases.

Low-dose adropin stimulates inflammasome activation of macrophage via mitochondrial ROS involved in colorectal cancer progression

Adropin is encoded by the energy homeostasis-associated (ENHO) gene and widely present in liver, pancreas, heart, kidney, brain, and vascular tissues. Abnormal adropin is associated with metabolic, inflammatory, immune, and central nervous disorders. Whether adropin is involved in the development of colorectal cancer (CRC) is still unclear. Here, decreased adropin expression of tumor-nest cells in advanced-stage CRC was demonstrated. Adropin expressed by carcinoma cells was negatively correlated with macrophage infiltration in the matrix of CRC tissues. However, tumor macrophages enhanced adropin expression and were positively correlated with tumor invasion and metastasis. ENHO gene transfection into colon cancer (MC38) cells inhibited tumor growth in vivo, accompanying the increase of M1 macrophages. Treatment with low-dose adropin (< 100 ng/mL) on macrophages ex vivo directly increased mitochondrial reactive oxygen species for inflammasome activation. Furthermore, ENHO−/− mice had less M1 macrophages in vivo, and ENHO−/− macrophages were inert to be induced into the M1 subset ex vivo. Finally, low-dose adropin promoted glucose utilization, and high-dose adropin enhanced the expression of CPT1α in macrophages. Therefore, variations of adropin level in carcinoma cells or macrophages in tumor tissues are differently involved in CRC progression. Low-dose adropin stimulates the antitumor activity of macrophages, but high-dose adropin facilitates the pro-tumor activity of macrophages. Increasing or decreasing the adropin level can inhibit tumor progression at different CRC stages.

Erythrina velutina Willd.: A review of its traditional uses, phytochemistry, pharmacology, and toxicology

Ethnopharmacological relevanceErythrina velutina Willd., commonly known as “mulungu” in Brazil, is a leguminous tree with various traditional medicinal uses. These uses include treating insomnia, central nervous system disorders, convulsions, nervous cough, and inflammation. Aim of the reviewThis review aims to comprehensively summarize the ethnomedicinal uses, chemical constituents, pharmacology, and toxicology of E. velutina to explore its potential as a source for new therapeutic agents. Materials and methodsInformation was collected from scientific databases, dissertations, and books. Chemical structures were generated using ChemDraw. To ensure the accuracy of the plant names, “World Flora Online” (www.worldfloraonline.org) was consulted for the accepted names of plants. ResultsE. velutina is indigenous to Brazil, Peru, Ecuador, Colombia, Venezuela, and Hispaniola. Approximately 244 compounds, mainly alkaloids and flavonoids, have been isolated from it. The plant and its extracts have exhibited various bioactivities, such as anti-inflammatory, anxiolytic, anticonvulsant, neuroprotective, analgesic, antimicrobial, and antioxidant effects, validating some of its traditional medicinal uses. Erythrina velutina shows promising therapeutic potential for conditions like convulsion, central nervous disorders, anxiety, insomnia, and inflammation, primarily due to its alkaloid and flavonoid content. ConclusionThe traditional medicinal uses of the plant, combined with modern scientific research, underscore its pharmacological potential. This makes it a significant candidate for drug development. Further research should focus on conducting toxicological studies, clinical trials, and mechanistic investigations. These efforts will enable a comprehensive exploration of its pharmacological properties and potential applications in drug development.