CNS & neurological disorders drug targets最新文献

{"title":"Serotonergic Dynamics in Autism Spectrum Disorder: Unraveling the Intricate Connection.","authors":"Abhishek Chander, Jeetesh Sharma, Shushank Mahajan, Sanchit Dhankhar, Samrat Chauhan, Monika Saini, Sanjana Mehta","doi":"10.2174/0118715273378214250213114328","DOIUrl":"https://doi.org/10.2174/0118715273378214250213114328","url":null,"abstract":"<p><p>Autism Spectrum Disorder (ASD) constitutes a group of neurodevelopmental disorders characterized by impairments in verbal and nonverbal communication skills, social interactions, and stereotypes of behavior, with an estimated frequency of 1.2% of children throughout the world. The lack of specific treatments or molecular biomarkers underscores the complexities of ASD as a nonunified clinical entity. Comorbid medical conditions are particularly associated with gastrointestinal issues that may suggest potential interactions between the brain and gut. This review suggests that serotonin plays a significant role in the enteric and central nervous systems in relation to ASD. The modulatory role of serotonin in the enteric nervous system is examined in relation to the pathophysiology of ASD in order to shed light on prospective biomarkers and therapeutic targets that could increase the precision of diagnosis and treatment.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143461233","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":"A Review on Nanotechnology based In Situ Gelling System as a Reliable Weapon for Targeting Alzheimer's Disease via Intranasal Route.","authors":"Priyanka Deorankar, Vahid Vikram Minglani, Bhupendra G Prajapati, Meenakshi B Patel","doi":"10.2174/0118715273335978250127070434","DOIUrl":"https://doi.org/10.2174/0118715273335978250127070434","url":null,"abstract":"<p><p>A recent World Health Organization report claims that along with the growing world population and emerging life prospects, the prevalence of neurological disorders is also increasing. Out of all neurological disorders, Alzheimer's disease is the most widespread and alarming concern. The disease poses significant therapeutic challenges due to the blood-brain barrier's restrictiveness and the lack of effective drug delivery systems. The olfactory and trigeminal nerves have direct access to the brain, therefore, intranasal drug delivery can be a promising route for the direct delivery of anti-Alzheimer's drugs. Despite this advantage, brain targeting is limited through this route due to mucociliary clearance. Thus, in situ, nanotechnology offers a transformative approach by leveraging the intranasal route to directly target the central nervous system. This comprehensive review discusses recent advancements, mechanisms, and applications of in situ nanotechnology in Alzheimer's disease therapeutics, highlighting its potential to enhance drug delivery efficiency, improve bioavailability, and mitigate the progression of this debilitating condition. The importance of intranasal drug delivery has been emphasized in this review, along with the clear benefits of in situ lipid- based nanotechnology for the efficient delivery of medication in targeting Alzheimer's disease.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143451187","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":"Clinical Markers and Diagnostics for Diagnosing Cerebral Infarction.","authors":"Thangavel Lakshmipriya, Subash C B Gopinath","doi":"10.2174/0118715273372575250212091813","DOIUrl":"https://doi.org/10.2174/0118715273372575250212091813","url":null,"abstract":"<p><p>Cerebral or brain infarction is a pathological process that restricts or blocks the supply of blood to the brain due to occlusion or narrowing of cerebral blood vessels. At present, computed tomography (CT) and magnetic resonance imaging (MRI) are commonly used to image cerebral infarction. Along with imaging, numerous non-invasive external brain monitoring tools are being developed that use a variety of technologies to act as sensors for neurological disorders, including stroke. This review briefly discussed the recent biomarkers for cerebral infarction and its diagnostic system through different biosensors.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434703","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":"Abnormality of Voltage-Gated Sodium Channels in Disease Development of the Nervous System. A Review Article.","authors":"Bakhtawar Khan, Muhammad Khalid Iqbal, Hamid Khan, Mustafa Kiyani, Shahid Bashir, Li Shao","doi":"10.2174/0118715273347470250126185122","DOIUrl":"https://doi.org/10.2174/0118715273347470250126185122","url":null,"abstract":"<p><p>Sodium channels are necessary for electrical activity in modules of the nervous system. When such channels fail to work properly, it may cause different neurological diseases. This review will discuss how particular mutation in these channels leads to different diseases. Positive alterations can lead to such diseases as epilepsy, or any muscle disorder due to over activation of neurons. Conversely, loss-of-function mutations may cause heart diseases and problems regarding motor and mental activity since neurons are not functioning well because of lost machinery. The review would discuss over familiar channelopathies such as genetic epilepsies, the familial hemiplegic migraine, and Para myotonia congenital and relatively new interrelations with the complex ailments including Alzheimer's, Parkinson's and multiple sclerosis. Thus, knowledge of these mechanisms is important in designing specific therapeutic approaches. There is a rationale for altering the sodium channel activity in the treatment of these neurological disorders by drugs or indeed genetic methods. Thus, the review is undertaken to provide clear distinctions and discuss the issues related to sodium channel mutations for the potential development of individualized medicine. The review also gives information on the function and general distribution of voltage-gated sodium channels (VGSCs), how their activity is controlled, and what their structure is like. The purpose therefore is to draw understanding over the apparently multifaceted functions exerted by VGSCs in the nervous system relative to several diseases. This knowledge is imperative in the attempt to produce treatments for these disabling disorders.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143392740","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":"Recent Trends in Physical Therapy Interventions and Neuromodulation Techniques to Improve Neurorehabilitation.","authors":"Patralika Nath, Barnana Roy, Soumya Saswati Panigrahi, Kamirul Islam, Asim Kumar Basak","doi":"10.2174/0118715273341882250114054733","DOIUrl":"https://doi.org/10.2174/0118715273341882250114054733","url":null,"abstract":"<p><p>Promoting neuroplasticity for better recovery and function restoration has lately become the focus of rehabilitation techniques for individuals with neurologic disorders. A rapidly expanding medical specialty, neuromodulation includes a broad variety of methods for activating particular neurological pathways, such as Transcranial magnetic stimulation (TMS), Transcranial direct current stimulation (tDCS), peripheral nerve stimulation, and SCS, among many others. Research on the use of neuromodulation in the context of spinal cord injury (SCI) is limited, in contrast to the abundance of literature on its potential benefits in chronic pain treatment. Combining exercise with non-invasive neuromodulation improves recovery outcomes for some patient groups, according to our research. While we mostly focus on the motor components of recovery, we do briefly mention the non-motor effects of these disorders. The difficulties of applying ideas in clinical practice and the gaps in the existing research are also brought to light. In order to better customize the individual neuroplastic responses associated with each disease, we identify research gaps and propose routes for future investigations. This review is useful for rehabilitation professionals and researchers since it focuses on neuroplastic exercise treatments for specific illnesses and diagnoses. Few studies have used long-term randomized-controlled trials, even though these approaches have great promise for enhancing overall functionality and impairment levels. If these novel modalities may be therapeutically employed to reduce pain, restore function, and improve the quality of life for individuals impacted, then more study is required to support them.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143416321","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":"Barbigerone against Lipopolysaccharide-Induced Memory Deficit in Rodents via Alteration of Inflammatory and Oxidative Stress Pathway: In vivo and Molecular Dynamics Simulations Study.","authors":"Muhammad Shahid Nadeem, Jalaluddin Azam Khan, Fahad A Al-Abbasi, May M Alqurashi, Azizah Salim Bawadood, Sami I Alzarea, Nadeem Sayyed, Gaurav Gupta, Imran Kazmi","doi":"10.2174/0118715273332347250122112850","DOIUrl":"https://doi.org/10.2174/0118715273332347250122112850","url":null,"abstract":"<p><strong>Background: </strong>Memory loss and cognitive decline are prominent symptoms of various neurodegenerative diseases, impacting daily activities and posing a significant burden on healthcare systems. The study aimed to explore the effect of barbigerone against LPS-induced memory impairment in rats and may offer novel therapeutics for neurodegenerative diseases.</p><p><strong>Methods: </strong>A total of 30 male Wistar rats were utilized and subsequently divided into five distinct experimental groups: group I received saline water as a control, group II- received LPS, group III - received LPS, and barbigerone (10 mg/kg/p.o.), group IV- received LPS and a higher dose of barbigerone (20 mg/kg/p.o.), and group V -barbigerone alone (20 mg/kg/p.o.). Behavioural test was performed through the Morris water maze and Y-maze test. Biochemical markers such as oxidative, proinflammatory, apoptotic, and further molecular docking and simulations elucidate the mechanisms of barbigerone effects.</p><p><strong>Results: </strong>Barbigerone significantly improved the learning capacity of rats in both the MWM and Ymaze tests, indicating enhanced memory and reduced latency times. Furthermore, barbigerone exhibited beneficial effects on oxidative stress and inflammation markers, suggesting its potential to protect against neuronal damage and promote cognitive function. Based on molecular docking, barbigerone showed a greater binding affinity with different intermolecular interactions; among them, NF-KB (ISVC) had the most potent interaction. Molecular dynamics simulations were performed to assess the stability and convergence of complexes formed by Barbigerone with 1NME_ Barbigerone, 1SVC_Barbigerone, and 4AQ3 4AQ3_Barbigerone.</p><p><strong>Conclusion: </strong>These findings demonstrate that barbigerone possesses neuronal protective effects against LPS-induced memory deficits in rats by restoring endogenous antioxidant and pro-inflammatory cytokines.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143392743","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":"Sweroside Modulates Oxidative Stress and Neuroplasticity-Related Gene Expression in Scopolamine-Treated Zebrafish.","authors":"Ion Brinza, Bogdan Alexandru Stache, Marius Mihasan, Dragos Lucian Gorgan, Mohamed A El Raey, Walaa El-Kashak, Omayma A Eldahshan, Lucian Hritcu","doi":"10.2174/0118715273345712250119200430","DOIUrl":"https://doi.org/10.2174/0118715273345712250119200430","url":null,"abstract":"<p><strong>Background: </strong>A major issue with neurodegenerative diseases is cholinergic depletion, the development of oxidative stress, and the reduction in the ability to control the expression of genes involved in the regulation of neurogenesis. The most widespread neurodegenerative disease is Alzheimer's disease (AD). Current treatments are not able to improve the symptoms of the disease. Thus, selecting or creating a safe and effective drug is very important.</p><p><strong>Objective: </strong>In this context, the potential of sweroside (Swe) to regulate acetylcholinesterase (AChE) activity, malondialdehyde (MDA) level, and bdnf, npy, egr1, nfr2a, and creb1 gene expression in the scopolamine (Sco)-induced zebrafish model of cognitive impairment was investigated.</p><p><strong>Methods: </strong>Swe was administered daily for 16 days chronically to zebrafish at concentrations of 1 μg/L, 3 μg/L, and 5 μg/L whereas Sco (100 μM) was given to zebrafish for 30 min.</p><p><strong>Results: </strong>Exposure to Swe decreased AChE activity and MDA level along with upregulating of gene expression in the brain of the Sco-induced zebrafish model.</p><p><strong>Conclusion: </strong>Overall, our findings suggested that Swe has a positive role in the cholinergic system activity and brain antioxidant status and showed for the first time that it can restore the downregulated expression of bdnf, npy, egr1, nfr2a, and creb1 genes in the brain of the Sco-induced zebrafish model.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143401018","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":"User-Centered Design of Neuroprosthetics: Advancements and Limitations.","authors":"Yara Badr, Nour AlSawaftah, Ghaleb Husseini","doi":"10.2174/0118715273335487250102093150","DOIUrl":"https://doi.org/10.2174/0118715273335487250102093150","url":null,"abstract":"<p><p>Neurological conditions resulting from severe spinal cord injuries, brain injuries, and other traumatic incidents often lead to the loss of essential bodily functions, including sensory and motor capabilities. Traditional prosthetic devices, though standard, have limitations in delivering the required dexterity and functionality. The advent of neuroprosthetics marks a paradigm shift, aiming to bridge the gap between prosthetic devices and the human nervous system. This review paper explores the evolution of neuroprosthetics, categorizing devices into sensory and motor neuroprosthetics and emphasizing their significance in addressing specific challenges. The discussion section delves into long-term challenges in clinical practice, encompassing device durability, ethical considerations, and issues of accessibility and affordability. Furthermore, the paper proposes potential solutions with a specific focus on enhancing sensory experiences and the importance of user-friendly interfaces. In conclusion, this paper offers a comprehensive overview of the current state of neuroprosthetics, outlining future research and development directions to guide advancements in the field.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143060950","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":"Epigenetic Threads of Neurodegeneration: TFAM's Intricate Role in Mitochondrial Transcription.","authors":"Aishwarya Bharathi H M, Prabitha Prabhakaran, Logesh Rajan, Narasimha M Beeraka, Bijo Mathew, Prashantha Kumar Br","doi":"10.2174/0118715273334342250108043032","DOIUrl":"https://doi.org/10.2174/0118715273334342250108043032","url":null,"abstract":"<p><p>There is a myriad of activities that involve mitochondria that are crucial for maintaining cellular equilibrium and genetic stability. In the pathophysiology of neurodegenerative illnesses, mitochondrial transcription influences mitochondrial equilibrium, which in turn affects their biogenesis and integrity. Among the crucial proteins for keeping the genome in optimal repair is mitochondrial transcription factor A, more commonly termed TFAM. TFAM's non-specific DNA binding activity demonstrates its involvement in the control of mitochondrial DNA (mtDNA) transcription. The role of TFAM in controlling packing, stability, and replication when assessing the quantity of the mitochondrial genome is well recognised. Despite mounting evidence linking lower mtDNA copy numbers to various age-related diseases, the correlation between TFAM abundance and neurodegenerative disease remains insufficient. This review delves into the link between neurodegeneration and mitochondrial dysfunction caused by oxidative stress. Additionally, the article will go into detail about how TFAM controls mitochondrial transcription, which is responsible for encoding key components of the oxidative phosphorylation (OXPHOS) system.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143048884","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":"Beyond Dopamine: Novel Therapeutic Pathways for Parkinson's Disease Through Receptor Signaling.","authors":"Rashmi Bhushan, Falguni Goel, Shamsher Singh","doi":"10.2174/0118715273325667241212041540","DOIUrl":"https://doi.org/10.2174/0118715273325667241212041540","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a progressive neurological condition characterized by both dopaminergic and non-dopaminergic brain cell loss. Patients with Parkinson's disease have tremors as a result of both motor and non-motor symptoms developing. Idiopathic Parkinson's disease (idiopathic PD) prevalence is increasing in people over 60. The medication L-dopa, which is now on the market, merely relieves symptoms and has several negative effects. In this article, we highlight the therapeutic potential of glucagon-like peptide-1, adenosine A2A, and cannabinoid receptors as attractive targets for enhancing neuroprotection and reducing a variety of motor and non-motor symptoms. Recent research has widened knowledge of new therapeutic targets and detailed cellular mechanisms, providing invaluable insights into the essential roles of cannabinoid receptors, adenosine A2A receptors, and glucagon-like peptide-1 receptors in PD pathogenesis and unique opportunities for drug development for mankind globally.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143034038","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}