Current Neuropharmacology最新文献

{"title":"Chlorogenic Acid: Characteristics, Neuroprotective Effects, and Potential Mechanisms.","authors":"Jingjing Zeng, Peiru Wang, Zhongyu Fan, Guoqing Wang, Ji Zhou, Feng Zhang","doi":"10.2174/011570159X459115260204170117","DOIUrl":"https://doi.org/10.2174/011570159X459115260204170117","url":null,"abstract":"<p><p>In this review, we explore recent evidence connecting chlorogenic acid (CGA) to neuropsychiatric disorders and critically discuss the biological mechanisms underlying these effects. CGA is a natural polyphenol that usually exists in fruits and vegetables. CGA has long been recommended for its broad pharmacological activities. Increasing evidence from animal studies has revealed that dietary CGA supplementation may confer protective effects on the nervous system. Here, we summarize multiple findings on CGA in animal models of neuropsychiatric disorders, including Parkinson's disease, Alzheimer's disease, stroke, depression, epilepsy, and other neuropsychiatric disorders. We place equal emphasis on chemical features, natural sources, bioavailability, and pharmacological properties of CGA; all of these can have a critical impact on CGA's intervention. Current experimental evidences suggest that the neuroprotective effects of CGA are driven by the convergence of several processes, including suppression of neuroinflammation, attenuation of oxidative stress, and context-dependent effects on synaptic and cellular homeostasis. In some models, CGA has also been associated with changes in autophagic activity and reduced accumulation of misfolded or aggregated proteins. Despite these advances, the field still lacks a coherent molecular framework that links CGA exposure to specific neural outcomes. Therefore, resolving this gap will be essential for the clinical application of CGA.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147670981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting Epigenetics in Ischemic Stroke: From Mechanisms to Therapeutics.","authors":"Xiao Lan, Xin Xie, ChangQing Deng","doi":"10.2174/011570159X462267260120104242","DOIUrl":"https://doi.org/10.2174/011570159X462267260120104242","url":null,"abstract":"<p><p>Ischemic stroke is the main cause of death and disability in human diseases worldwide. Due to the complexity of its pathophysiological mechanism, the treatment effect is not ideal. Epigenetics refers to the mechanisms of affecting gene function and expression by chemical modification or chromatin structure without changing the DNA sequence. The epigenetic network is mainly composed of various epigenetic modifying enzymes (such as DNA methyltransferase/demethylase, DNMT/tet, histone methyltransferase/demethylase, HMT/hdm, histone acetyltransferase/deacetylase hat/hdac) and non-coding RNAs with different functions. Epigenetic enzymes or non-coding RNAs can participate in the core pathophysiological processes after ischemic stroke, such as neuroinflammation, oxidative stress, and cell apoptosis, by regulating the activation or silencing of key gene transcription. Due to the regulatory role of epigenetic modifying enzymes and non-coding RNAs after ischemic stroke, targeted intervention of these epigenetic modifying enzymes and non-coding RNAs has been confirmed to improve the pathological process and neurological outcome after ischemia. Therefore, they are regarded as a series of therapeutic targets with great research and development potential. This study systematically reviewed the role and mechanism of DNA methylation, histone modification, and non-coding RNA in the pathological development of ischemic stroke, and discussed the research progress of related therapeutic drugs targeting these epigenetic modifying enzymes, in order to provide a theoretical basis and ideas for the development of new clinical diagnosis and treatment strategies for ischemic stroke.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147671062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Twelve-Week Follow-up Study of Obesity, Antioxidant Enzyme Activity, and Clinical Symptoms in First-Episode Schizophrenia Patients Treated with Risperidone.","authors":"Jing Yao, Cheng Zhu, Fei Wang, Meihong Xiu, Fengchun Wu, Xiangyang Zhang","doi":"10.2174/011570159X321613240902104936","DOIUrl":"https://doi.org/10.2174/011570159X321613240902104936","url":null,"abstract":"<p><strong>Objective: </strong>Overweight/obesity is highly prevalent in schizophrenia (Sch), which can perturb brain function and correlate with symptom severity. An impaired antioxidant defense system is involved in the pathophysiology of Sch and obesity. This longitudinal study aimed to investigate the impact of overweight/obesity on the antioxidant enzymes and the response to risperidone in patients with Sch.</p><p><strong>Methods: </strong>Two hundred and sixty-nine patients with Sch were recruited and received 12-week treatment with risperidone. Clinical symptoms, weight, and antioxidant enzyme were measured at baseline and week 12.</p><p><strong>Results: </strong>Non-obese patients with Sch showed decreased GSHPx activity after treatment with risperidone but no difference in obese patients. In obese patients, GSHPx activity was associated with an improvement in positive symptoms. Meanwhile, in non-obese patients, a reduction in GSHPx activity was correlated with an improvement in general psychology.</p><p><strong>Conclusion: </strong>This study suggests that obesity at the onset influences the improvement in the clinical symptoms after treatment with risperidone in patients with Sch, which is related to its modulations on GSHPx.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147670967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Mechanisms of Dopaminergic Neuron Degeneration in Parkinson's disease: A Comprehensive Review.","authors":"M D Abubakar, Shahnaz Alom, Farak Ali, Sheikh Rezzak Ali, Krishnendu Adhikary, S Sarika, Prakash Kumar Gupta, Eswara Rao Puppala, Krishna Murti, Sachchida Nand Rai, Nitesh Kumar","doi":"10.2174/011570159X446831260303200516","DOIUrl":"https://doi.org/10.2174/011570159X446831260303200516","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a neurological condition that starts with the degeneration of neurons. Neurons play a crucial role in producing dopamine (DA), a type of neurotransmitter that primarily regulates bodily functions such as motor control, posture, motivation, reward, pleasure, cognition, and memory. Other variables that contribute to the disorder include the buildup of Lewy bodies and Lewy neurites, which are composed of increased α-synuclein (α-syn). Depletion of DA in the striatal area and the death of DA-producing neurons are often considered the basis for the mo-tor impairments seen in PD. In addition, both genetic and environmental factors may play a role in PD etiology; specifically, genetic variations and exposure to toxins may contribute to the development of brain lesions. The article aims to outline the current state of knowledge on the dopaminergic pathway and how PD affects DA homeostasis. Various molecular mechanisms are involved in the pathogenesis of PD, including α-syn aggregation, lysosomal and chaperone-mediated autophagy, mitochondrial dysfunction, and abnormal regulation of calcium homeostasis. Intrinsic and extrinsic caspase-mediated apoptosis, autophagic cell death, and ferroptosis are also involved in neurodegen-eration that often leads to PD. The occurrence of PD can be controlled by the inclusion of antioxi-dants, such as mitoquinone, which inhibit mitochondrial oxidative damage, as well as modulation of autophagy, proteostasis, gene therapy, and its editing, and stem cell regeneration. Diverse mechanistic pathogenesis and genetic variations make PD a complicated disease to tackle. Potential treatment approaches, such as modulating autophagy-lysosomal pathways and protecting mitochon-dria, may be better understood with deeper insight into these mechanisms. We conclude by highlighting current and upcoming gene and cell therapies.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147671120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic Potentials of Pyrazole Analogues as Anti-neurodegenerative Agents.","authors":"Fahimeh Mohamadpour, Farzaneh Mohamadpour","doi":"10.2174/011570159X470473260325064647","DOIUrl":"https://doi.org/10.2174/011570159X470473260325064647","url":null,"abstract":"<p><p>Neurodegenerative Diseases (NDs) are disorders that cause nerve cells to gradually deteriorate or die. Progressive malfunction and neuronal loss from certain brain areas are hallmarks of neurodegenerative diseases. In various parts of the brain, this results in dementia, cognitive impairment, and a slowdown in motor function. Because pyrazole scaffolds play a significant role in the brain by enhancing cognitive processes, they have drawn a lot of interest for the treatment of neurodegeneration. Pyrazole-containing substances have recently been effectively produced as strong inhibitors of many biological targets implicated in various neurodegenerative disorders. In the present review, initially, we provide an overview of the chemistry of pyrazoles, methods for creating pyrazole derivatives, and the pharmaceutical properties of pyrazole derivatives. We show that, thanks to recent developments in synthetic medicinal chemistry, this class of molecules may be easily synthesized and targeted for novel drug discovery. In particular, the present review focuses on the neuroprotective properties of pyrazole scaffolds, given pyrazoles' importance in medicinal chemistry as neuroprotective agents. We have made an effort to examine several facets of the therapeutic potential of pyrazole analogues as anti-neurodegenerative agents in this review. The purpose of this study is to help medicinal chemists and neuroscientists who are investigating and using pyrazoles in neurodegenerative research projects, as well as to expedite future research initiatives in neurodegenerative disease. Future studies and fresh ideas in the search for logical designs to create more promising pyrazoles are anticipated to benefit from this review.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147627490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-alzheimer Drugs Development and Small Molecules: Mechanistic Understanding of the 5HT₄ and 5-HT₆ Receptor.","authors":"Meenakshi Dhanawat, Garima Malik, Kashish Wilson, Bharat Bhushan","doi":"10.2174/011570159X428162260224193303","DOIUrl":"https://doi.org/10.2174/011570159X428162260224193303","url":null,"abstract":"<p><p>Alzheimer's disease (AD) affects millions worldwide, yet currently approved therapies provide only symptomatic relief without altering disease progression. Increasing evidence shows that serotonergic dysfunction contributes to cognitive decline in AD, particularly through altera-tions in the 5-HT₄ and 5-HT₆ receptor pathways. Modulation of these receptors influences acetyl-choline release, APP processing, amyloid burden, and synaptic plasticity. This review summarizes the mechanistic roles of 5-HT₄ and 5-HT₆ receptors in AD pathology, highlights key structure-activity relationship (SAR) trends in ligand development, and evaluates clinical outcomes of recep-tor-targeted therapies. Recent work supports 5-HT₄ agonists and 5-HT₆ antagonists as promising candidates for cognitive enhancement and disease modification. However, challenges in target en-gagement, receptor selectivity, and clinical translation underscore the need for more refined drug-design strategies.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147618566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From Bench to Bedside: Understanding General Anesthetics' Impact on PTSD.","authors":"Ke Li, Guo Meimei, Wei Wei, Xiang Li, Mian Peng","doi":"10.2174/011570159X402072251103071408","DOIUrl":"https://doi.org/10.2174/011570159X402072251103071408","url":null,"abstract":"<p><p>Post-traumatic stress disorder (PTSD) is a multifaceted mental health disorder arising from exposure to traumatic events, characterized by persistent and distressing symptoms. Recent years have seen growing recognition of anesthesia's dual role in PTSD. While countless patients receive anesthetics during traumatic medical care, their long-term psychological impacts remain unclear, raising urgent clinical questions. This review provides an in-depth analysis of both clinical and animal studies examining the effects of commonly used inhaled and intravenous anesthetics, such as sevoflurane/isoflurane, benzodiazepines (BZDs), ketamine, propofol, and dexmedetomidine (Dex), on PTSD. These studies reveal a complex interplay between these anesthetic agents and PTSD, highlighting their potential to either alleviate or exacerbate symptoms depending on various factors such as dosage, timing, and individual susceptibility. Additionally, this review synthesizes the current understanding of the underlying neurobiological mechanisms through which these anesthetics affect fear memory and neuroplasticity, offering valuable insights into their potential applications and limitations in managing PTSD.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147607986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DHCR24 Emerges as a Promising Target in Enhancing Cognitive Function.","authors":"Zhang Lu, Tang Fei, Jiang Yuequan, Yao Chenguo, Wang Zhiqiang","doi":"10.2174/011570159X421264260206063501","DOIUrl":"https://doi.org/10.2174/011570159X421264260206063501","url":null,"abstract":"<p><strong>Introduction: </strong>Against the backdrop of an aging global population, cognitive decline poses significant challenges to individuals' quality of life. Currently, therapeutic interventions for cognitive impairment, particularly in neurological disorders such as Alzheimer's Disease (AD), remain limited. DHCR24 (3β-dehydrocholesterol-Δ24-reductase), a cholesterol synthase, has been shown to exert neuroprotective effects in AD by mitigating oxidative stress. This study aims to delineate the specific molecular mechanisms through which DHCR24 influences cognitive learning function.</p><p><strong>Methods: </strong>A total of twenty mice were randomly assigned to either an experimental group or a control group. DHCR24 expression was pharmacologically downregulated, and synaptic plasticity was examined using slice patch-clamp recordings. Additionally, Barnes-Maze testing was performed to evaluate the role of DHCR24 in learning and memory functions. The influence of DHCR24 on endogenous neural stem cell differentiation was further analyzed by fluorescence immunohistochemistry.</p><p><strong>Results: </strong>The findings of this study demonstrated that U18666A effectively suppressed DHCR24 expression. This downregulation was associated with the inhibition of endogenous neural stem cell differentiation and a reduction in the expression of the synaptic AMPA receptor subunit GluA2. Consistent with these molecular changes, patch-clamp recordings revealed a corresponding attenuation of AMPA receptor-mediated synaptic plasticity. Behavioral assessments further corroborated that pharmacological inhibition of DHCR24 resulted in significant cognitive impairment in mice.</p><p><strong>Discussion: </strong>This study implicates DHCR24 as a key factor capable of modulating cognitive function, thereby offering a novel direction and potential intervention target for research on Alzheimer's disease and neurodegeneration.</p><p><strong>Conclusion: </strong>DHCR24 represents a promising novel target for cognitive enhancement.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147590541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brivaracetam in Refractory Epilepsy: Mechanism, Tolerability, and Clinical Positioning.","authors":"Yen Yun Kung, Woon-Man Kung","doi":"10.2174/011570159X443312260218050229","DOIUrl":"https://doi.org/10.2174/011570159X443312260218050229","url":null,"abstract":"<p><p>Epilepsy is a common neurological disorder and has a considerable global impact. Established treatment options remain limited, as current antiseizure medications (ASMs) often do not adequately reduce the frequency of seizures. The standard of care for individuals with epilepsy using existing ASMs often fails to meet both the expectations of clinicians and patients. We observed that many ASMs are linked with a wide range of Adverse Events (AEs). Typically, multiple ASMs are administered to treat refractory epilepsy, but combination therapies can create unfavorable Drug-Drug Interactions (DDIs). An ideal ASM should meet several key criteria: it should effectively treat multiple types of epilepsy, induce minimal AEs to ensure good tolerability and long-term safety, be able to avoid clinically significant DDIs that require dose adjustments, and improve the quality of life of individuals living with epilepsy. Brivaracetam (BRV) is a selective, high-affinity ASM that specifically targets the synaptic vesicle protein 2A ligand. It exhibits greater drug permeability, selectivity, and binding affinity when compared with its structural predecessor, levetiracetam, which leads to more efficient brain penetration. Owing to a faster onset of action, BRV shows better anticonvulsant activity. Reported AEs associated with BRV are generally minor, nonspecific, transient, and manageable. BRV does not affect cytochromes P450 or P-glycoprotein. As a result, it minimizes the likelihood of DDIs that may occur between multiple ASMs or when ASMs are co-administered with pharmacological classes such as antipsychotics, anticoagulants, and antibiotics. When BRV is administered along with other drugs, consider carefully to prevent poten-tial DDIs. BRV is considered a supplemental therapy for refractory focal seizures, as suggested by most experts. Recent studies have demonstrated that BRV monotherapy can offer advantages such as good tolerability, high retention rates, safety, and improved seizure control. This narrative review aimed to synthesize the current preclinical and clinical evidence. We hope to provide a detailed overview of BRV, including its pharmacological properties, safety profile, and therapeutic relevance in the management of refractory epilepsy.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147607874","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Drug-Induced Reactivation of VZV and HSV1-2 in Adult Patients with Multiple Sclerosis Receiving Disease-modifying Therapies: A Systematic Review and Meta-analysis.","authors":"Drieda Zaçe, Lorenzo Vittorio Rindi, Francesca Napoli, Alessandra Imeneo, Gabriele Brugnoni, Enrico Perugini, Silvia Bartolomeo, Albiana Cekrezi, Camilla Aguglia, Loredana Sarmati, Girolama A Marfia, Doriana Landi, Marco Iannetta","doi":"10.2174/011570159X419181260129091748","DOIUrl":"https://doi.org/10.2174/011570159X419181260129091748","url":null,"abstract":"<p><strong>Introduction: </strong>Multiple Sclerosis (MS) patients treated with Disease Modifying Therapies (DMTs) are at risk of Herpes Simplex (HSV) and Varicella-Zoster (VZV) reactivation. This meta-analysis consolidates existing data on HSV and VZV reactivation in MS patients treated with DMTs to improve clinical strategies, including infectious disease screening, serological monitoring, and vaccination for MS patients on DMTs. We aimed to meta-analyze the incidence rates of clinically relevant VZV and HSV-1/2 reactivation in adults with multiple sclerosis treated with the included drugs, in comparison with unexposed patients.</p><p><strong>Methods: </strong>This systematic review and meta-analysis followed PRISMA and PICOST guidelines. Literature from 1996 to March 2024 was searched across five databases. Independent reviewers screened and extracted data, resolving conflicts with expert input. Risk of bias was assessed using ROB2 and the Newcastle-Ottawa Scale. Random-effects meta-analyses were conducted, reporting pooled incidence and heterogeneity, as well as risk ratios, where possible.</p><p><strong>Results: </strong>Seventy-eight studies were included in the review, with HSV/VZV reactivation most commonly reported for alemtuzumab (22), cladribine (11), and fingolimod (10). Meta-analyses showed that Fingolimod had HSV and VZV reactivation rates of 1.77 and 0.55 cases/100 persons, respectively, over mean follow-ups of 28.1 and 29.1 months, respectively. Alemtuzumab was associated with higher rates: 6.28 for HSV (4 studies) and 4.89 for VZV (11 studies) over 42 and 38.9 months, respectively. Meta-analysis of seven studies on natalizumab found a VZV reactivation rate of 0.29/100 person-years over 33.2 months, while five studies on rituximab reported a rate of 1.19/100 person-years over 33.0 months. Meta-analyses of placebo arms showed HSV reactivation at 1.10/100 persons and VZV reactivation at 0.50/100 persons over mean follow-up durations of 45.8 and 49 months, respectively.</p><p><strong>Discussion: </strong>This study may serve as a practical resource for clinicians to assess the risk of severe, disseminated, or fatal reactivations, especially in patients with additional risk factors, supporting more personalized infectious disease monitoring and prevention strategies.</p><p><strong>Conclusions: </strong>This study provides a comparative framework for evaluating herpetic reactivation rates during MS treatment with DMTs.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147607877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}