REVIEWS IN THE NEUROSCIENCES神经科学评论
REVIEWS IN THE NEUROSCIENCES(英文缩写 REV NEUROSCIENCE),ISSN 0334-1763,eISSN 2191-0200,中文译名:神经科学评论 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：2025-09-27 至 2026-09-27，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 | 4.703 | Q2 |
| 2022 | 4.100 | Q2 |
| 2023 | 3.400 | Q2 |
| 2024 | 4.100 | Q1 |
| 2025 | 4.800 | Q1 |
REVIEWS IN THE NEUROSCIENCES 最新收录文献
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1. Central nervous system involvement of hantaviruses: clinical presentations, neuroimaging findings, and current implications.
PMID:日期:2026-09-09Because of their involvement in outbreaks, hantaviruses as emerging zoonotic diseases have been regarded a public health issue. Recent reports have identified CNS symptoms of hantavirus infection, although the data are still relatively sparse and inconsistent, especially for (ANDV) and to a lesser extent Puumala virus (PUUV). Reported neurological features include headache, dizziness, altered mental state, seizures, focal deficits, and peripheral neuropathy, possibly accompanied by ocular symptoms such as impaired vision and photophobia. The results of neuroimaging have been inconsistent and nonspecific, ranging from hemorrhagic or edematous changes to thalamic or brainstem abnormalities and splenial lesions. Evidence could suggest that endothelial dysfunction, capillary leak, inflammatory damage, and, in certain situations, potential intrathecal immunological responses or direct viral presence may all contribute to CNS involvement. However, most evidence stems from case reports or case series, and causative neuroinvasion may not have been fully demonstrated. Recent studies, especially the recent ANDV-associated outbreak, may emphasize the necessity for rigorous neurological examination. A better understanding of the neurological range of hantavirus infection may enhance detection, risk stratification, and supportive therapy.
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2. BDNF-related brain-liver communication in metabolic syndrome: implications for anxiety and depression.
PMID:日期:2026-08-27Metabolic syndrome is frequently accompanied by anxiety and depression, suggesting interactions between metabolic dysfunction and affective regulation. Brain-derived neurotrophic factor (BDNF) and its high-affinity receptor tropomyosin receptor kinase B (TrkB) are involved in energy balance, neuroplasticity, stress adaptation, and emotional processing, positioning BDNF-related signaling as a potential interface within brain-liver communication. Experimental evidence strongly supports central BDNF-TrkB signaling in the regulation of feeding and energy expenditure, while central BDNF-sensitive pathways can also influence hepatic glucose production. Conversely, obesity and metabolic dysfunction alter the systemic lipid, endocrine, inflammatory, vascular, and neural environment, which can impair hypothalamic and hippocampal BDNF-related signaling. These processes occur within a broader neuro-metabolic network involving the liver, adipose tissue, gut, skeletal muscle, immune system, and vasculature rather than through a liver-specific pathway. Chronic stress, anxiety, and depression further intersect with metabolic dysfunction through partly distinct neuroendocrine and neuroplastic mechanisms, including hypothalamic-pituitary-adrenal axis and glucocorticoid signaling. Glucagon-like peptide-1 signaling represents an additional interface between metabolic regulation and central neuroplasticity, although the contribution of BDNF to its hepatic and neurobehavioral effects remains incompletely defined. Key uncertainties include the functional significance of liver-associated and circulating BDNF, BDNF-defined autonomic pathways to the liver, genetic variation, and tissue-specific therapeutic targeting. Future studies integrating circuit- and tissue-specific manipulation, standardized BDNF measurements, both sexes, and longitudinal human phenotyping are needed to distinguish causal mechanisms from associative relationships.
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3. Noncoding RNAs in epilepsy: from molecular mechanisms to clinical translation.
PMID:日期:2026-08-26Epilepsy comprises a heterogeneous group of brain disorders in which recurrent seizures arise from dynamic interactions among neuronal hyperexcitability, glial activation, neuroinflammation, vascular dysfunction, and maladaptive circuit remodeling. Despite advances in genetics, neuroimaging, and molecular profiling, clinically useful biomarkers remain limited, and disease-modifying therapies are still lacking. Noncoding RNAs (ncRNAs) have emerged as an important regulatory layer in epilepsy biology. MicroRNAs, long noncoding RNAs, circular RNAs, transfer RNA fragments, and other ncRNA species influence epileptogenesis through post-transcriptional repression, chromatin-associated regulation, competing endogenous RNA networks, stress-responsive translational control, and extracellular vesicle-mediated intercellular communication. These mechanisms converge on central pathological processes, including neuroinflammation, synaptic and ion-channel remodeling, neuronal injury, aberrant neurogenesis, blood-brain barrier dysfunction, and antiseizure drug resistance. Beyond brain tissue, circulating ncRNAs detectable in plasma, serum, cerebrospinal fluid, and extracellular vesicles have attracted increasing interest as minimally invasive biomarkers. Their relative stability in biofluids and potential ability to reflect disease-relevant cell-to-cell signaling support their translational relevance. However, clinical translation remains limited by substantial interstudy heterogeneity related to epilepsy subtype, sampling window, biospecimen handling, RNA isolation method, profiling platform, and normalization strategy. Preclinical studies targeting selected ncRNAs, particularly microRNAs, further support the possibility of RNA-based disease modification, although major challenges remain in target prioritization, CNS-directed delivery, and long-term safety. This Review integrates current knowledge of ncRNA biology in epilepsy with emerging biomarker and therapeutic evidence and outlines key steps required for clinical translation.
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4. Air pollution and the risk of schizophrenia: current evidence, mechanisms, and future directions.
4. 空气污染与精神分裂症风险：当前证据、机制和未来方向PMID:日期:2026-08-24Schizophrenia (SCZ) is a complex, polygenic neurodevelopmental disorder influenced by interactions between genetic vulnerability and environmental exposures. While research has historically prioritized genetic factors, air pollution has emerged as a potentially modifiable environmental factor associated with the onset, progression, and relapse of the disorder. This review synthesizes current clinical, epidemiological, and preclinical evidence to clarify the relationship between various air pollutants and SCZ. Epidemiological data, including large-scale cohort studies such as the UK Biobank, demonstrate dose-dependent associations between long-term exposure to particulate matter (PM., PM) and gaseous pollutants (NO, SO, CO) and increased SCZ risk. Notably, individuals with high polygenic risk scores (PRS) may exhibit heightened vulnerability, with hazard ratios reaching up to 7.38 when combined with high pollution exposure. Mechanistically, air pollutants may influence SCZ-related biology through direct neurotoxicity via olfactory translocation, neuroinflammatory signaling, oxidative stress, disruption of neuroplasticity (including brain-derived neurotrophic factor (BDNF) suppression), and dysregulation of the gut-brain axis. However, most mechanistic evidence is preclinical, and the translational gap to human disease remains substantial. Despite these insights, challenges remain regarding causal inference, biomarker validation, and geographical representation in research. Moving forward, large-scale longitudinal cohorts and the integration of exposomics with genomics are essential to refine risk stratification. At present, the evidence supports cautious consideration of air pollution as an environmental factor associated with schizophrenia, rather than as a proven causal determinant.
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5. Psychiatric and behavioral disorders in Parkinson's disease: co-pathogenic mechanisms of tau, Aβ, and α-synuclein proteins (narrative review).
5. 帕金森病的精神和行为障碍：tau、Aβ和α-突触核蛋白的共同致病机制（叙述性综述）PMID:日期:2026-08-24Parkinson's disease (PD) is a common neurodegenerative disorder affecting middle-aged and elderly individuals. Its clinical manifestations include both motor and non-motor symptoms. Traditionally, Lewy bodies (LBs), which are formed by misfolded α-synuclein (α-syn), have been regarded as the core pathological hallmark. It is believed that the selective damage to dopaminergic neurons in the nigrostriatal system by LBs constitutes the primary mechanism underlying motor symptoms. However, approximately 30-80 % of PD patients also experience psychiatric and behavioral disturbances, such as anxiety, depression, cognitive impairment, and sleep disorders. The pathological mechanisms underlying these symptoms cannot be fully explained by α-syn alone. Recent biomarker studies have confirmed that hyperphosphorylated tau protein forms neurofibrillary tangles (NFTs) and amyloid β-protein (Aβ) plaques can coexist with α-syn in the brains of PD patients, especially in advanced stages. These coexisting pathologies show significant positive correlations with cognitive impairment and sleep disorders, suggesting that the neuropsychiatric symptoms in PD may result from the synergistic effects of multiple protein pathologies involving α-syn, tau, and Aβ. This review synthesizes these findings to propose an integrated "synergistic co-pathogenic network" of α-syn, tau, and Aβ, thereby providing a novel theoretical framework for developing precise, multi-target therapeutic strategies against PD-related neuropsychiatric disorders.
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6. The glymphatic system and hydrocephalus: emerging insights into pathophysiological mechanisms.
6. 淋巴系统和脑积水：对病理生理机制的新认识PMID:日期:2026-08-24Hydrocephalus is a complex neurological disorder traditionally thought to result from excessive cerebrospinal fluid (CSF) production, obstruction of CSF outflow, or impaired absorption. However, these classical theories have limitations in explaining key phenomena observed in certain clinical subtypes, such as normal pressure hydrocephalus. Recent advances in neuro-fluid dynamics have introduced the concept of the glymphatic system, a functional network in the brain that facilitates the exchange of CSF and interstitial fluid (ISF) along perivascular pathways and mediates the clearance of metabolic waste. This new perspective offers a fresh lens for understanding CSF circulation and fluid homeostasis. This review aims to reexamine the pathogenesis of hydrocephalus from the perspective of glymphatic dysfunction and, by integrating anatomical, physiological, and imaging evidence, explore its theoretical implications and clinical relevance.
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7. Glycolysis as a central pathological axis in neurodegenerative diseases.
PMID:日期:2026-08-24Glycolysis is increasingly recognized as a pathological backbone in neurodegenerative diseases rather than merely an accompanying epiphenomenon. This article first delineates the division of metabolic labor among neurons, astrocytes, microglia, and oligodendrocytes in the brain, with particular emphasis on cell type-specific glycolytic flux, lactate shuttling, and an integrated brain-periphery framework of energy metabolism. It then systematically compares alterations in glucose uptake, glycolytic intermediates, and lactate metabolism across Alzheimer disease (AD), Parkinson disease (PD), amyotrophic lateral sclerosis (ALS), Wilson disease (WD), Huntington's disease (HD), and multiple sclerosis (MS), highlighting pronounced heterogeneity across cell types, disease stages, and brain regions. These metabolic disturbances encompass not only global cerebral hypometabolism and an energy crisis, but also compensatory hyperglycolysis and inflammation-associated metabolic reprogramming in astrocytes and microglia, and extend further to systemic metabolic phenotypes involving peripheral blood cells, muscle, and liver. The article summarizes recent methodological advances for characterizing glycolytic reprogramming, including fluorodeoxyglucose positron emission tomography (FDG-PET), hyperpolarized carbon-13 magnetic resonance spectroscopy(ˆ13C-MRS), metabolomics, single-cell and spatial transcriptomics, genetically encoded metabolic sensors, and Seahorse assays. In addition, potential therapeutic strategies are discussed, focusing on targets such as 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3(PFKFB3), the astrocyte-neuron lactate shuttle (ANLS), microglial glycolysis and lactylation, as well as systemic metabolic modulation and nanodelivery approaches. Finally, key challenges are highlighted, including unclear causal relationships, biphasic and cell type-specific effects, insufficient brain-periphery integration, and the lack of standardized metrics, underscoring the need for longitudinal, multimodal, and stage-specific strategies to reposition glycolysis as a targetable therapeutic dimension in neurodegenerative diseases.
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8. The microbiota-gut-brain axis as a driver of secondary brain injury after aneurysmal subarachnoid hemorrhage: from bidirectional vicious cycle to therapeutic opportunities.
PMID:日期:2026-08-24Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating stroke subtype with high morbidity and mortality, significantly contributed to by secondary brain injuries such as early brain injury and delayed cerebral ischemia. Despite advances in acute management, effective neuroprotective strategies remain an unmet need. The microbiota-gut-brain axis (MGBA), a pivotal bidirectional communication network, has recently emerged as a critical modulator of pathophysiology in acute brain injuries. However, its precise role and therapeutic potential in aSAH are not systematically defined. This review synthesizes clinical and preclinical evidence to move beyond correlation and delineate the spatiotemporal dynamics and the mechanisms that may underlie of MGBA dysregulation post-aSAH. We conceptualize a self-amplifying "brain-gut-brain" vicious cycle: the initial brain injury may disrupt intestinal barrier integrity and microbiota ecology via neuroendocrine and inflammatory pathways; in turn, gut-derived signals (e.g., altered microbial metabolites, endotoxin translocation) may propagate systemic inflammation and exacerbate neuroinflammation, blood-brain barrier disruption, and cerebral ischemia. We dissect this cycle by detailing the key molecular bridges (tryptophan metabolites, short-chain fatty acids, bile acids), signaling pathways (e.g., TLR4/NF-κB, NLRP3 inflammasome), and central effectors involved. Furthermore, we provide a critical, stratified evaluation of MGBA-targeting therapeutic strategies - including probiotics, prebiotics, fecal microbiota transplantation, and metabolite supplementation - assessing their mechanistic rationale, level of evidence, and translational challenges. Finally, we outline future directions emphasizing the need for defining therapeutic windows, establishing causal proof, and integrating MGBA modulation into multimodal neurocritical care. Harnessing the MGBA presents a novel and promising paradigm for developing adjunctive neuroprotective therapies to improve outcomes after aSAH.
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9. From peripheral neurotoxicity to central dysfunction: linking neuropathic pain and cognition in chemotherapy-induced peripheral neuropathy.
PMID:日期:2026-08-24Chemotherapy-induced peripheral neurotoxicity (CIPN) represents a significant clinical burden, affecting 70-80 % of patients during treatment and persisting chronically in 20-30 % of survivors. While peripheral nerve injury is the primary pathological hallmark, emerging evidence demonstrates that central nervous system (CNS) dysregulation plays a crucial role in pain chronification and associated cognitive impairment. This review synthesizes recent findings on cortical and subcortical alterations that drive neuropathic pain processing in CIPN, examining dysregulated glutamatergic and GABAergic neurotransmission, altered voltage-gated ion channel expression, and central sensitization across key pain-modulatory brain regions including the prefrontal cortex, anterior cingulate cortex, somatosensory cortices, and periaqueductal gray. We address chemotherapy-induced cognitive impairment ("chemobrain") as a manifestation of shared neuroinflammatory mechanisms linking peripheral nerve injury to CNS pathology. In fact, peripheral neuropathy-triggered neuroinflammation, characterized by microglial activation and cytokine dysregulation, compromises the blood-brain barrier and impairs hippocampal-dependent memory, synaptic plasticity, and adult neurogenesis. The paper integrates findings from both animal models and human patients and discusses how animal models of CIPN reveal central nervous system engagement beyond peripheral pathology. This review emphasizes CIPN as a disorder profoundly affecting central pain modulation and cognition, requiring integrated therapeutic strategies addressing both peripheral and central nervous system pathology.
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10. Glymphatic-meningeal lymphatic dysfunction drives remote organ injury after aneurysmal subarachnoid hemorrhage: a unified neuroimmune framework and time-stratified therapeutic roadmap.
PMID:日期:2026-08-06Aneurysmal subarachnoid hemorrhage (aSAH) confers substantial mortality and morbidity driven not only by primary brain injury but also by systemic remote organ complications across the pulmonary, cardiac, renal and gastrointestinal systems. Despite growing recognition of neuroimmune crosstalk in this process, a cohesive, systems-level model connecting intracranial hemorrhage to multi-organ dysfunction remains absent from the literature. Here, we propose a unified neuroimmune framework centered on a long-underappreciated mechanism: glymphatic and meningeal lymphatic drainage dysfunction is hypothesized to act as the upstream initiating event that forces brain-derived damage-associated molecular patterns, inflammatory cytokines and activated immune cells to spill into the systemic circulation. We systematically map three mechanistically distinct, mutually amplifying transmission pathways: the classical neuroendocrine-immune axis, the recently identified meningeal lymphatic-deep cervical lymph node immune drainage axis, and circulating humoral effectors exemplified by neutrophil extracellular traps. Most notably, we integrate these pathways with a temporally stratified immune continuum spanning early hyperinflammatory SIRS, stroke-induced immunodepression, and chronic low-grade inflammation - an integrative temporal architecture that has eluded prior single-organ or single-pathway studies. Grounded in this framework, we put forward a tiered, phase-specific neuroimmunomodulatory strategy that simultaneously addresses central inflammatory origins, systemic signal propagation, and end-organ tissue damage. By reframing remote organ injury as a time-dependent immune process rather than a collection of isolated organ complications, this work provides a mechanistic and translational roadmap for time-stratified clinical trials and redefines the investigative direction for multi-organ management in aSAH.