CNS & neurological disorders drug targets最新文献

{"title":"Cannabidiol from Conventional to Advanced Nanomedicines for the Management of Cancer-Associated Pain.","authors":"Abhishek Jain, Saba Qureshi, Km Rafiya, Irfan Ali, Mohd Shahrukh, Nazeer Hasan, Farhan Jalees Ahmad","doi":"10.2174/0118715273337554250311060327","DOIUrl":"https://doi.org/10.2174/0118715273337554250311060327","url":null,"abstract":"<p><p>Chemotherapy-induced pain is one of the major challenges that hamper the patient's quality of life. Several cases of insufficient pain management were reported globally, especially in the case of patients who do not respond well to conventional pain management regimes and opioid analgesics. Additionally, conventional pain management has several shortcomings, and evidence suggests that cannabidiol has the potential to overcome those shortcomings. Cannabidiol (CBD) is a non-psychoactive compound of the Cannabis plant that shows an effective outcome in chemotherapy- induced pain as well as in cancer treatment, as it possesses anti-inflammatory and analgesic properties. The mechanism of pain and its management by cannabidiol, with all possible evidence, is well summarised in the paper. This article concludes the types of pain experienced by cancer patients, the effectiveness of CBD in the management of pain, and challenges faced by patients after using Cannabidiol with various case studies. Later, antitumor efficacy studies of CBD were disclosed, and its various types of formulations and nano-formulations were summarized in the paper. Overall, the paper establishes the role of cannabidiol in Chemotherapy-induced pain.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143733729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erythropoietin for Seizures and Epilepsy: Neuroprotective Effects, Mechanisms, and Contradictory Risks.","authors":"Heba M Mahdy","doi":"10.2174/0118715273367111250307081826","DOIUrl":"https://doi.org/10.2174/0118715273367111250307081826","url":null,"abstract":"<p><strong>Background: </strong>Epilepsy is a widespread neurological disorder, particularly affecting children and the elderly, presenting complex and varied challenges in management. Recently, erythropoietin has gained significant attention due to its neuroprotective effects, which have been demonstrated experimentally in various neurological conditions, including epilepsy. This review aims to analyze current literature on the role of erythropoietin in seizures and epilepsy.</p><p><strong>Method: </strong>A comprehensive literature search was conducted through PubMed, Scopus, and Web of Science databases up to September 30, 2024. The search terms included \"Epilepsy AND Erythropoietin\", \"Seizures AND Erythropoietin,\" and \"Status Epilepticus AND Erythropoietin\", applied to titles, abstracts, and keywords.</p><p><strong>Results: </strong>The review highlights ongoing debates surrounding erythropoietin's effects on epilepsy. While erythropoietin shows potential in mitigating seizure-induced brain damage and modulating cellular processes such as anti-apoptotic and anti-inflammatory pathways, its clinical application is complicated by conflicting evidence. Some studies suggest that erythropoietin may trigger seizures, with factors such as dosage and individual patient characteristics potentially influencing this risk.</p><p><strong>Conclusion: </strong>Experimental studies suggest that erythropoietin offers neuroprotective benefits in epilepsy. However, its possible pro-convulsant effects-which might be linked to erythropoietin-induced hypertension, rapid increases in hematocrit levels, dosage, or individual patient characteristics-raise safety concerns. These risks complicate its clinical use, making it premature to endorse erythropoietin as a treatment fully. Future research should focus on non-erythropoietic derivatives that retain neuroprotective effects without stimulating red blood cell production, thereby reducing risks, such as hypertension and thrombosis. Well-designed clinical trials and further investigation into erythropoietin's mechanisms are essential to clarify its role and optimize its therapeutic potential in epilepsy.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143733664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidative Stress and the Role of Immune Cells in Alzheimer's Disease: Therapeutic Implications and Future Perspectives.","authors":"Nidhi Puranik, Minseok Song","doi":"10.2174/0118715273355336250226055826","DOIUrl":"https://doi.org/10.2174/0118715273355336250226055826","url":null,"abstract":"<p><p>The most common neurodegenerative illness and leading cause of death in the world is Alzheimer's disease (AD), which is extremely expensive to treat. None of the AD treatments that are currently in the market with approval have any effect on disease progression. However, numerous clinical studies aimed at reducing amyloid beta (Aβ) plaque development, boosting Aβ clearance, or reducing neurofibrillary tangle (NFT) failed or had conflicting results. As oxidative stress (OS), mitochondrial dysfunction, and chronic neuroinflammation are implicated in numerous interconnected vicious cascades, research has revealed new therapeutic targets, including enhancing mitochondrial bioenergetics and quality control, reducing oxidative stress, or modulating neuroinflammatory pathways. This review examines the role of oxidative stress (OS), mitochondrial dysfunction, neuroinflammation, and the interplay between peripheral and central immune systems in the pathogenesis of AD. We highlight how OS and immune dysregulation drive chronic neuroinflammation, exacerbating AD progression. Immune cells and inflammatory molecules emerge as critical players in disease pathology. Overall, this review concludes that targeting OS and immune system crosstalk represents promising therapeutic strategies for mitigating AD progression, providing a foundation for future interventions.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143671990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lithium Chloride Rescues Dopaminergic Neurons in a Parkinson's Disease Rat Model Challenged with Rotenone.","authors":"Eman Allam, Sary Khalil Abdel Ghafar, Manal Hussein, Ahmed Al-Emam, Khaled Radad","doi":"10.2174/0118715273365449250224090655","DOIUrl":"https://doi.org/10.2174/0118715273365449250224090655","url":null,"abstract":"<p><strong>Introduction: </strong>Parkinson's disease, the second most common neurodegenerative disease, is still lacking an effective treatment that can stop dopaminergic cell loss in substantia nigra and alter disease progression.</p><p><strong>Objective: </strong>The present study aimed to investigate the neuroprotective efficacy of lithium chloride in a rotenone-induced rat model of Parkinson's disease.</p><p><strong>Methods: </strong>Forty male Sprague Dawley rats were assigned into 4 groups: control, rotenone-, rotenone and lithium chloride- and lithium chloride-treated groups. Rotenone (2 mg/kg b.w.) and lithium chloride (60 mg/kg b.w.) were, respectively, administered subcutaneously and orally five times a week for 5 weeks. At the end of each treatment, the neuroprotective efficacy of lithium chloride against rotenone-induced derangements was evaluated by some behavioral tests, biochemical analysis, gel electrophoresis, histopathology, and immunohistochemistry.</p><p><strong>Results: </strong>Rotenone significantly resulted in neurobehavioral deficits, gastrointestinal dysfunction, decreased activities of catalase and superoxide dismutase, depleted glutathione, and increased levels of malondialdehyde. It also caused DNA fragmentation and loss of dopaminergic neurons in substantia nigra and decreased striatal tyrosine hydroxylase staining intensity. Concomitant treatment of rats with rotenone and lithium chloride significantly improved behavioral impairment and markedly alleviated gastrointestinal dysfunction. It also increased catalase activity and decreased malondialdehyde levels, indicating antioxidant effects. Moreover, it decreased DNA fragmentation, rescued dopaminergic neurons, and increased tyrosine hydroxylase immunoreactivity in the striatum compared to the rotenone-treated group.</p><p><strong>Conclusion: </strong>Lithium chloride rescued dopaminergic neurons in a rotenone model of PD, possibly through the improvement of behavioral deficits, decreasing oxidative stress, and reducing DNA damage.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143671987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of Known Flavonoids of Ficus carica L. as Aldose Reductase Inhibitors in Sciatic Nerve of Diabetic Neuropathy-induced Rats through Bioinformatics and Proteomics Analysis.","authors":"Dureshahwar Khan, Hemant D Une, Mubashir Mohammed, Jaiprakash N Sangshetti, Sanjay N Harke, Manoj Damale, Jitendra B Naik","doi":"10.2174/0118715273322121250124065659","DOIUrl":"https://doi.org/10.2174/0118715273322121250124065659","url":null,"abstract":"<p><strong>Introduction: </strong>The polyol pathway is responsible for the metabolism of almost one-third of the total glucose in people with chronic diabetes. Moreover, it causes complications in organs that rely on aldose reductase (AR) as an enzyme. The purpose of this research was to examine the in vitro and in vivo effects of a flavonoid-rich ethyl acetate fraction of a methanolic extract of Ficus carica Lam. leaves (FCEA) on the aldose reductase gene AKR1B1. The complicated relation of AR for target confirmation and analysis of the flavonoids of FCEA, quercetin, kaempferol, and chrysin was explored by building a flavonoid-protein complex network utilizing GeneCards®, String, and Cytoscape Networking.</p><p><strong>Method: </strong>The examination of ADMET was carried out after docking on the active sites of AR. By the binding and scoring abilities, the analysis was carried out. The ADMET characteristics demonstrated that these flavonoids had excellent solubility, absorption, and oral bioavailability, and the results demonstrate that they have potential. An additional in-vivo investigation was conducted on rats using a model induced by streptozotocin (STZ). Hence, upon induction, the rats' sciatic nerves were removed and prepared for an RT-PCR analysis of the AKR1B1 gene.</p><p><strong>Result: </strong>Compared to the diabetic normal group and the metformin group, rats treated with FCEA had lower levels of messenger RNA and AKR1B1 gene expression.</p><p><strong>Conclusion: </strong>This proves that FCEA has effectively blocked AR. It is highly likely to suggest FCEA as a potent aldose reductase inhibitor, as it considerably reduces the mRNA level of AKR1B1 gene expression in the sciatic nerve of sick rats, according to a combined bioinformatics prediction and RT-PCR analysis.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143607556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dopamine Depletion in Parkinson's Disease and Therapeutic Options.","authors":"Hussaini Adam, Subash C B Gopinath, Tijjani Adam, Evan T Salim, Makram A Fakhri","doi":"10.2174/0118715273366223250302092948","DOIUrl":"https://doi.org/10.2174/0118715273366223250302092948","url":null,"abstract":"","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143588420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chlorogenic Acid as a Neuroprotective Agent: Enhancing Plasticity and Promoting Brain Health and Functional Reserve.","authors":"Elizabeth Hernández-Echeagaray, Rubén Vázquez-Roque, Julio Cesar Morales-Medina, Francisco M Torres-Cruz, Elibeth Monroy, Gulmaro Galindo-Paredes, Gabriel Gutiérrez-Ospina, Gonzalo Flores","doi":"10.2174/0118715273339375250116042441","DOIUrl":"https://doi.org/10.2174/0118715273339375250116042441","url":null,"abstract":"<p><strong>Introduction: </strong>Functional reserve, the process that warrants the brain to have resources to maintain key functions and processes when facing neurodegeneration, may be strengthened in nominally healthy subjects by measures that prompt neural plasticity throughout life.</p><p><strong>Method: </strong>In this work, we administered Chlorogenic Acid (CGA) to evaluate its ability to promote functional morphological plasticity in the frontal cortical-striatal circuit of healthy mice, a pathway exposed constantly to oxidative challenges, excitotoxicity, and neuroinflammation. The magnitude of neural plasticity was estimated by assessing spontaneous motor behavior (open field), the relative magnitude of neuronal activation (number of c-Fos positive neurons), dendritic remodeling (Golgi- Cox impregnation), the availability of Brain-Derived Neurotrophic Factor (BDNF) (semiquantitative Western blotting), and lipid peroxidation (TBARS assay) in CGA- or vehicle-administered C57BL/6 male mice.</p><p><strong>Results: </strong>CGA administration increased c-Fos in the Dorsal striatum (Ds), changed the availability of BDNF and Pro-BDNF in the Frontal Cortex (FC) and DS, induced dendritic remodeling in FC and DS neurons, and reduced FC and DS lipid peroxidation without affecting motor performance or the availability of TrkB receptor isoforms.</p><p><strong>Conclusion: </strong>Our findings suggest that CGA increases functional reserve by promoting neuronal plasticity in healthy male mice. Future research should determine whether these additional resources indeed protect against neurodegeneration.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fluoride-induced Neurodevelopmental Toxicity- AMPK as a Possible Target.","authors":"Tejas Ahuja, Farmiza Begum, Fathima Beegum, Gautam Kumar, Nitesh Kumar, Rekha R Shenoy","doi":"10.2174/0118715273300345250206084817","DOIUrl":"https://doi.org/10.2174/0118715273300345250206084817","url":null,"abstract":"<p><p>Inorganic fluoride is widely used in dental practices to treat problems like dental caries and prevent bone-related issues. Exposure to excess amounts of fluoride both through drinking water or other sources impairs vital functions of the body and can prove to be toxic, especially for the central nervous system. Sodium fluoride (NaF) crosses the blood-brain barrier in early developmental stages and causes impairments related to learning and memory, anxiety, decreased locomotor ability, and in some cases, depression-like behaviour, especially in children. Major mechanisms involved in this toxicity include reduction in levels of nicotinic and muscarinic receptors, autophagy, and apoptosis in neurons, decreased glucose consumption, inhibition of enzymes involved in the generation of energy and transmission of the synapse, mitochondrial dysfunction, and increased oxidative stress leading to inflammation and neuronal cell death. Out of all these, an increase in oxidative stress was reported to be one of the main mechanisms of fluoride-induced neurotoxicity. Based on these inferences, various natural compounds having antioxidant properties, like curcumin, aloe vera, quercetin, epigallocatechin gallate, etc. have been studied for their protective role in sodium fluoride-induced neurotoxicity. Involvement of other pathways like Nrf2/Keap pathways, SIRT3, etc., have warranted a need for further detailed study to identify other potential therapeutic targets like AMPK to prevent/treat fluoride-induced neurotoxicity. The present review captures fluoride, its role in neurodevelopment, and mechanisms & pathways involved by which fluoride can hurt neurodevelopment & how AMPK can be a possible therapeutic target.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143495050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic Predisposition and Severity of Eating Disorders- A Review.","authors":"Md Harun Rashid, Neha Deora, Shashidhar Ravindra Kolur, Suttur S Malini, Priyankar Sen","doi":"10.2174/0118715273372810250214054917","DOIUrl":"https://doi.org/10.2174/0118715273372810250214054917","url":null,"abstract":"<p><p>Eating disorders (EDs) are multifaceted psychiatric conditions with significant genetic, psychological, and environmental components. This review provides a comprehensive analysis of the genetic underpinnings and key molecular pathways contributing to anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED). Genetic studies, particularly genome-wide association studies (GWAS), have identified key loci associated with ED susceptibility, with heritability estimates for these disorders ranging between 48% and 74%. Among the critical genes explored, the Agouti-related protein (AGRP), ghrelin (GHRL), and brain-derived neurotrophic factor (BDNF) pathways emerge as pivotal regulators of appetite control, energy balance, and reward systems, offering insights into ED etiology. These pathways are modulated by environmental factors and often dysregulated in individuals with EDs, linking abnormal eating behaviors to disturbances in neurobiological functions. EDs also show a strong association with comorbid psychiatric disorders, such as depression and anxiety, and pose significant physical health risks, including cardiovascular disease and metabolic disturbances. Exploring the intricate genetic and neurobiological mechanisms underlying eating disorders (EDs) paves the way for more effective prevention, early detection, and tailored treatment strategies. This review highlights the potential of utilizing genetic insights to enhance diagnostic and intervention strategies, ultimately leading to better outcomes for individuals impacted by eating disorders.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143484731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Internet of Medical Things (IoMT) for Alzheimer Patient's Outcome.","authors":"Thangavel Lakshmipriya, Subash C B Gopinath","doi":"10.2174/0118715273371149250218081425","DOIUrl":"https://doi.org/10.2174/0118715273371149250218081425","url":null,"abstract":"<p><p>The Internet of Medical Things (IoMT) is a network system that connects devices with medical and healthcare for the ultimate aim of collecting, transmitting, and analyzing the acquired data in the presence of the internet. A wide range of equipment and monitoring systems have been generated with IoMT, and they permit real-time monitoring, sharing the data, analysis, patient care, and for efficient operation. At the advanced level, it is highly facilitated with remote patient digital monitoring and telemedicine. IoMT has a significant potential to enhance the care of Alzheimer's disease patients to overcome issues with a progressive neurological condition, memory loss, cognition, and behavior. This study aims to bring the potential of the Internet of Things (IoT) to be implemented in the Internet of Medical Things (IoMT), with a special focus on Alzheimer's disease patients.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143484732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}