Current Neuropharmacology当代神经药理学
Current Neuropharmacology(英文缩写 CURR NEUROPHARMACOL),ISSN 1570-159X,eISSN 1875-6190,中文译名:当代神经药理学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 7.708 | Q1 |
| 2022 | 5.300 | Q1 |
| 2023 | 4.800 | Q1 |
| 2024 | 5.300 | Q1 |
| 2025 | 6.100 | Q1 |
Current Neuropharmacology 最新收录文献
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1. Therapeutic Implications of Cell Death Pathways Across the Course of Amyotrophic Lateral Sclerosis.
1. 细胞死亡通路在肌萎缩侧索硬化病程中的治疗意义PMID:日期:2026-09-23Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by progressive motor neuron loss, resulting in paralysis and limited survival. Multiple regulated cell death pathways, including apoptosis, necroptosis, ferroptosis, pyroptosis, lysosomal cell death, autophagy-dependent cell death, NETosis, and other emerging cell death modalities, have been implicated in ALS, but their mechanistic interactions and relative contributions remain poorly understood. This knowledge gap has hindered the development of effective therapies. Better experimental models are needed to dissect these pathways. This review summarizes current knowledge on the roles of cell death pathways in ALS. A tiered framework (M1-M4) is applied to critically evaluate data from human postmortem tissue, patient-derived cells, and animal models, ranking studies according to their relevance to human disease. Potential crosstalk among these pathways is further examined. It is also proposed that the relative contribution of specific cell death pathways may shift with disease progression, although this hypothesis requires longitudinal validation. To integrate this dynamic perspective, cell death pathway activities are hypothetically aligned with the King's clinical staging system. This stage-informed framework is presented as a conceptual model intended to generate hypotheses rather than to serve as a validated clinical algorithm. The model distinguishes established therapies from preclinical and exploratory strategies. Future research should prioritize the development of human-relevant model systems, the identification of longitudinal biomarkers of cell death, and the implementation of rigorously designed combination trials. These efforts may ultimately enable more precise, stage-appropriate therapeutic strategies for ALS.
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2. GABA Signaling in Glioma: Paradoxes and Therapeutic Perspectives.
PMID:日期:2026-09-23Glioma is the most common primary malignant brain tumor in adults and is characterized by an extremely poor prognosis. A distinctive feature of glioma is its profound dependence on the unique brain microenvironment. Gamma-Aminobutyric Acid (GABA), the principal inhibitory neurotransmitter in the central nervous system, has been implicated in the regulation of glioma pathophysiology. However, evidence regarding its influence on tumor progression remains highly contradictory. Current findings indicate that GABA can exert either tumor-suppressive or tumor-promoting effects depending on multiple interconnected factors, including Isocitrate Dehydrogenase 1 (IDH1) mutation status, intracellular chloride ion concentration governed by Na+-K+-Cl- Cotransporter 1 (NKCC1) and K+-Cl- Cotransporter 2 (KCC2) transporters, heterogeneous GABAA and GABAB receptor expression patterns, and dynamic glioma-neuron synaptic interactions. Among these, the NKCC1/KCC2 balance emerges as a central molecular switch governing intracellular chloride homeostasis and, consequently, the functional polarity of GABAA receptor activation. This review provides a comprehensive overview of the complex and paradoxical roles of GABA signaling in glioma biology, with particular emphasis on dysregulated GABA synthesis and catabolism as well as divergent GABA receptor-mediated mechanisms. Furthermore, we discuss potential explanations for the conflicting findings reported in the literature and highlight promising therapeutic targets within the GABAergic system, including metabolic enzymes, chloride cotransporters, and specific receptor antagonists that may be exploited for clinical intervention.
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3. Therapeutic Targeting of IL-33 in Ischemia-Reperfusion Injury: Progress and Prospects.
3. IL-33在缺血再灌注损伤中的治疗靶向：进展与展望PMID:日期:2026-09-23Ischemia-Reperfusion Injury (IRI) is a prototypical sterile inflammatory process that complicates solid-organ transplantation, reperfusion therapy for acute myocardial infarction, and revascularization procedures. Clinical management relies largely on supportive and procedural measures; no specific targeted therapy is available. Interleukin-33 (IL-33), a multifunctional member of the IL-1 cytokine family, is constitutively localized to the nucleus in several structural cell types and acts extracellularly as an alarmin after release. The IL-33/ST2 signaling axis has been implicated in multiple phases of IRI. This review describes the conserved core of the IL-33/ST2 signaling cascade. It also examines the regulatory mechanisms and functional heterogeneity of IL-33 across six major IRI-susceptible organ systems: the cardiovascular system, kidney, liver, lung, brain, and gastrointestinal tract. Available evidence suggests a recurrent but not universal pattern: IL-33 can amplify acute sterile inflammation in some organs and models, yet support inflammation resolution and tissue repair in other settings or at later stages. The effects of IL-33 depend on the organ involved, the cellular source of IL-33, the spatial distribution of ST2-expressing target cells, the local microenvironment, and the phase of injury and timing of intervention. This review summarizes recent preclinical advances in IL-33/ST2-targeted strategies and discusses the principal challenges to their clinical translation. These include limited human efficacy and safety data, the lack of clinically feasible intervention strategies, and the absence of validated companion biomarkers. The IL-33/ST2 axis may be an organ- and context-specific therapeutic target for IRI, but further validation is required before clinical application.
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4. The Interaction Between Gut Microbiota and Neuroinflammation in the Gut-Brain Axis of Autism Spectrum Disorder.
PMID:日期:2026-09-22Autism Spectrum Disorder (ASD) is characterized primarily by social deficits and repetitive behaviors, often accompanied by gastrointestinal dysfunction. Its etiology involves interactions among genetic, environmental, and biological factors. Current studies indicate that neuroinflammation and gut microbiota imbalance are key factors in the development of ASD. Neuroinflammation is characterized by elevated levels of pro-inflammatory factors and abnormal glial cell activation, whereas gut microbiota imbalance is evidenced by dysbiosis and compromised intestinal barrier function. The gut-brain axis regulates neuroinflammation and synaptic function through pathways such as short-chain fatty acids (SCFAs), tryptophan metabolism, γ-aminobutyric acid (GABA) metabolism, and the hypothalamic-pituitary-adrenal (HPA) axis. Although modulation of the microbiota, for example, fecal microbiota transplantation (FMT) and probiotics, could improve ASD symptoms by repairing the intestinal barrier and alleviating neuroinflammation, the molecular mechanisms underlying these effects remain to be elucidated. This article reviews the interaction between gut microbiota and neuroinflammation in ASD, aiming to provide insights for treatment and research.
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5. Therapeutic Strategies Targeting TREM2 for Alzheimer's Disease: Current Advances and Future Perspectives.
PMID:日期:2026-09-22Alzheimer's disease is a progressive neurodegenerative disorder characterized by cognitive decline and protein aggregation. The Triggering Receptor Expressed on Myeloid Cells 2 (TREM2) has been identified as a key regulator of pathogenesis. This review summarizes current understanding of the receptor's structure, ligands, signaling, roles in disease, and therapeutic targeting strategies. A structured narrative review was conducted using targeted searches of PubMed, Web of Science, and Scopus, supplemented by citation tracking and searches of ClinicalTrials.gov. TREM2 is a microglial immunoreceptor that recognizes apolipoprotein E and amyloid-β. Through the canonical DAP12-SYK axis, TREM2 regulates microglial phagocytosis, metabolism, and inflammatory responses. In Alzheimer's disease, it modulates amyloid-β clearance, tau hyperphosphorylation, and neuroinflammation in a stage-dependent manner. Loss-of-function variants increase disease risk. Therapeutic strategies include direct membrane-TREM2 agonistic antibodies, shedding-modifying antibody fragments, soluble TREM2-based approaches, gene-delivery platforms, small-molecule agonists, and indirect TREM2-associated natural-product modulators. These approaches differ in target-binding evidence, TREM2 dependence, disease-model relevance, safety, and clinical maturity. TREM2 functions within a context-dependent framework in which gene dosage, disease stage, pathological substrate, microglial state, and activation duration jointly determine protective or maladaptive outcomes. Therapeutic modalities differ in specificity, brain exposure, reversibility, and translational readiness, while target engagement alone does not guarantee clinical benefit. TREM2 remains a promising but context-sensitive therapeutic target. Successful translation will require controllable modulation, stage- and pathology-specific treatment windows, biomarkers of functional response, and patient stratification according to genotype, amyloid-β and tau burden, and microglial state.
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6. Crosstalk and Convergence in Alzheimer's Disease: Integrating Brain Injury, Neuroinflammation, and Precision Medicine for Next-Generation Therapeutics.
PMID:日期:2026-09-22Alzheimer's Disease (AD) is a complex disorder whose underlying biology is not fully explained by traditional single-pathway models. For several decades, research has largely focused on the roles of amyloid-β and tau in the formation and deposition of plaques and neurofibrillary tangles associated with AD pathology and neurodegeneration. Despite this sustained focus, therapeutic strategies targeting amyloid-β and tau alone have shown limited success in altering the natural course of the disease. Accordingly, there is a clear need for an adaptive and integrative framework that better captures the heterogeneity and dynamic nature of disease progression over time. This review proposes conceptualizing Alzheimer's disease as a neural circuit disorder that emerges from sustained crosstalk among multiple interacting pathways, including brain injury, neuroinflammation, mitochondrial and metabolic dysfunction, neurovascular dysfunction (impaired supply chain), synaptic dysfunction, and individual vulnerability. Evidence is presented to illustrate (1) how the traumatic and chronic nature of brain injury predisposes the brain to persistent inflammation and neurodegeneration; (2) how astrocytic and microglial activation states contribute to synaptic dysfunction and neuronal damage; and (3) how pathological interactions among amyloid pathology, tau dysregulation, and immune signaling collectively exacerbate neuroinflammatory responses and accelerate disease progression in AD.
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7. Mapping Cell-Type-Specific Regulatory Variants in Vascular Dementia by Integrating Single-Cell Chromatin Accessibility and Gene Expression.
PMID:日期:2026-09-21Vascular dementia (VaD), the second most common form of dementia, is a growing burden in aging populations and lacks disease-modifying therapy. Although immunerelated regulatory mechanisms are increasingly implicated, the role of immune cell-specific chromatin accessibility variants remains poorly understood. Using 379 instruments across 377 chromatin accessibility peaks in 17 immune cell types, we performed Mendelian randomization against FinnGen GWAS data, with independent evaluation in the UK Biobank. Because most loci were instrumented by a single variant, formal heterogeneity and horizontal-pleiotropy testing was not feasible. Candidate effector genes were then investigated by regulatory annotation and Bayesian colocalization of single-cell eQTLs with the VaD GWAS. Four loci reached FDR < 0.05:a risk-increasing B cell/naïve B cell enhancer at chr7:24758459-24759192 (OR = 2.78 and 2.29) and the protective NK/cytotoxic NK cell loci at chr8:20109125-20109944 (OR = 0.63 and 0.62). In the UK Biobank, the B cell association was directionally concordant but, given the few cases, is supportive rather than confirmatory. Regulatory annotation and colocalization nominated GSDME as a candidate effector gene, with moderate evidence in immature B cells. These findings are consistent with peripheral immune regulation at cell type-specific regulatory elements; brain-resident populations were not examined. The nomination of GSDME generates the hypothesis of a B cell pyroptosis-related mechanism; this is an association-level, hypothesis- generating result rather than evidence of a causal or mediating role, and remains to be validated. Immune cell-type-specific chromatin accessibility variation-notably a B cell locus nominating GSDME as a candidate effector gene, alongside a protective NK signal-is associated with VaD risk, generating cell-resolved hypotheses. As most instruments were single variants, these results should be read as genetic associations rather than causal inference.
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8. Clinical Predictors of Lithium Response in Patients with Bipolar Disorder: Potential Predictive Role of Chronotype, Rumination and Traumatic Events.
8. 双相障碍患者锂盐反应的临床预测因素：晨昏类型、反刍思维与创伤事件的潜在预测作用PMID:日期:2026-09-21Bipolar Disorders (BD) are severe, recurrent, and well-characterized psychiatric conditions with lithium as the first-line approved treatment for BD. This study aims to evaluate lithium response using the ALDA scale and to identify reliable predictors in a cohort of patients with BD. In this cross-sectional observational study, one hundred and fourteen consecutively recruited patients with a primary diagnosis of BD type I or II were included between June 2022 and June 2025. Sociodemographic and clinical characteristics were collected through a semi-structured interview. Lithium response was retrospectively assessed using the ALDA scale. Psychometric instruments (CTQ, MEQ, MWQ, DDFS, RRS, BIS-11) were administered. Logistic regression analyses were performed to identify independent predictors of lithium response. Forty-one (36%) individuals were classified as lithium responders according to the ALDA Scale. Lithium responders were younger, engaged in physical activity more frequently, were more frequently diagnosed with BD type II, had a shorter illness duration, a Manic-Depressive-Interval (MDI) course, and showed fewer residual symptoms. Non-responders were associated with rapid cycling, psychotic symptoms, more hospitalizations, and illicit substance use. Childhood trauma, impulsivity, and rumination were more common among non-responders, while morning chronotype was more prevalent among responders. In the regression analysis, the MDI pattern, higher total scores for attentional impulsivity and rumination, and morning chronotype were all significantly associated with lithium responsiveness. On the other hand, the presence of psychotic symptoms, a history of ≥ 5 hospitalizations, comorbid substance use, and higher scores of emotional abuse were associated with a lower likelihood of response to lithium. Integrating the evaluation of trauma history, impulsive profiles, ruminative tendencies, and circadian features into clinical assessment may enhance the prediction of lithium response. Our findings support the development of personalized treatment strategies for BD.
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9. Roles of the Neuregulin 1/ErbB4 Signaling Pathway in the Pathogenesis of Autism Spectrum Disorder.
PMID:日期:2026-09-21Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder that first manifests in the early stages of childhood. The exact underlying mechanism of ASD remains unknown, and its etiology is rather complex. Neuronal migration, cognitive development, and continuous neural plasticity are strongly influenced by the Neuregulin 1 (NRG1)/ErbB4 signaling pathway. Hence, the pathogenesis of ASD may be closely connected to dysfunction of the NRG1/ErbB4 pathway. According to our current review, either the activation or inhibition of this pathway can lead to the development of ASD, and GABAergic system dysfunction can result in ASD-like behaviors. Moreover, NRG1 binds to ErbB to promote GABA release, and abnormal NRG1 activity affects GABAergic neuron development and function, thus impairing cognition and social interactions. Additionally, the activity of the PI3K/AKT/mTOR pathway differs in various brain regions, and its activation or inhibition can lead to the development of ASD. By activating ErbB CTY-1, NRG1 promotes the development of neurodevelopmental disorders through further activation of the PI3K/AKT/mTOR pathway. Therefore, the NRG1/ErbB4 pathway can regulate GABAergic system functions and affect the activity of the PI3K/AKT/mTOR pathway, thereby resulting in abnormal social interactions and cognitive impairment. Targeting dysfunctions of the GABAergic system, the PI3K/AKT/mTOR pathway, and the NRG1/ErbB4 pathway are currently promising strategies for the treatment of ASD. Candidate agents that modulate these pathways have been shown to be effective in preclinical animal models. However, the limitations of these models and the considerable etiologic and phenotypic heterogeneity among patients with ASD continue to hinder their clinical translation. This article reviews evidence suggesting that the pathogenesis of ASD is closely associated with the NRG1/ErbB4 signaling pathway, the GABAergic system, and the PI3K/AKT/mTOR pathway. This article also analyzes the main obstacles to pharmacological interventions and provides a theoretical basis for understanding the pathogenesis of ASD and for identifying potential targets for future therapeutic strategies.
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10. Role of the Dorsal Striatum in Cognitive Functions and Related Disorders with Cognitive Impairment.
10. 背侧纹状体在认知功能及伴认知障碍的相关疾病中的作用PMID:日期:2026-09-17The dorsal striatum, recognized as a primary input nucleus of the basal ganglia, has traditionally been viewed as a crucial center for motor control. However, emerging evidence over the past five decades has sparked a paradigm shift, underscoring its vital role in a wide array of higher-order cognitive functions such as procedural learning, habit formation, working memory, executive function, and inhibitory control. This expanded understanding is grounded in the dorsal striatum's intricate architecture, which includes GABAergic Medium Spiny Neurons (MSNs) that form both the direct and indirect pathways, a diverse array of interneurons, and a compartmental organization characterized by striosomes and matrix. Furthermore, the dorsal striatum plays a pivotal role within the cortico-basal ganglia-thalamo-cortical loops and is influenced by the midbrain dopaminergic system. Dysfunction of the dorsal striatum, marked by neurotransmitter imbalances-such as dopaminergic depletion in Parkinson's Disease (PD) and cholinergic deficits in Alzheimer's Disease (AD)-along with synaptic plasticity impairments and the aggregation of pathological proteins (e.g., α-synuclein in PD and amyloid-β/tau in AD), is closely associated with cognitive decline in major neurodegenerative disorders. This review aims to provide a systematic overview of the structural and functional foundations of the dorsal striatum in cognitive regulation. It delineates the pathological mechanisms that contribute to cognitive impairments observed in PD and AD and addresses current challenges as well as future research directions. The goal is to establish a comprehensive framework that positions the dorsal striatum as a shared therapeutic target for cognitive dysfunction across various diseases, thereby offering valuable insights for the development of early diagnostic biomarkers and innovative intervention strategies.