International Review of Neurobiology国际神经生物学评论
International Review of Neurobiology,ISSN 0074-7742,eISSN 2162-5514,中文译名:国际神经生物学评论 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：2025-10-01 至 2026-09-30，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 |
|---|---|---|
| 2020 | 3.230 | Q3 |
| 2021 | 4.280 | Q2 |
International Review of Neurobiology 最新收录文献
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1. Stress and medial prefrontal cortex: Sex-dependent effects in rodent models.
PMID:日期:2026-09-14Chronic stress significantly alters rodent medial prefrontal cortical (mPFC) structure and function, contributing to cognitive and affective dysfunction associated with stress-related psychiatric disorders. Although the effects of stress on the male mPFC have been extensively characterized, growing evidence demonstrates that females exhibit distinct behavioral, structural, and molecular responses to chronic stress. This review synthesizes current findings regarding sex differences in stress-induced plasticity within the adult mPFC, discussing the behavioral outcomes, activation, and neural plasticity of the region in response to stress exposure. Across stress paradigms, males generally exhibit earlier dendritic retraction, spine loss, and impairments in cognitive flexibility, whereas females often demonstrate delayed mPFC effects despite persistent affective behavioral deficits. Emerging evidence suggests that females may recruit compensatory inhibitory mechanisms, particularly through parvalbumin neuron activation, that transiently buffer pyramidal cells from stress-induced remodeling. In contrast, stress in males may influence mPFC structure and function via somatostatin interneuron signaling, glucocorticoid receptor-mediated pathways, and microglial-dependent synaptic remodeling. However, sex differences are strongly influenced by stress modality, duration, and intensity, which contributes to variability across studies. Despite this variability, patterns in the literature suggest that males and females recruit distinct mPFC mechanisms in response to stress. Improved understanding of sex-specific stress adaptations may inform the development of targeted interventions for stress-related psychiatric disorders.
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2. Parkinson's disease-Crucial advances and on-going challenges.
PMID:日期:2026-09-10Dramatic advances have been seen over the past 5 years in neurodegenerative disease medicine. In Parkinson's disease (PD), significant advances have been made in molecular biomarkers and imaging tools. These have led to improved diagnostic accuracy for clinical trial recruitment and stratification, as well as contributing fundamentally to biomarker-based disease frameworks that define PD by its biology. In combination, these advances may enable the tracking of disease progression and improved evaluation of disease-modifying therapies in the research setting. Biofluid-based biomarkers currently available in research settings have the potential to reach real-world settings as commercially viable diagnostic tests. These will provide physicians with the necessary tools required to diagnose PD early and accurately without relying solely on the presence of clinical symptoms. Moreover, with each trial that reports, greater insights are gained into those individuals likely to benefit from different therapeutic options for PD, particularly with monoclonal antibody immunotherapy strategies targeting α-synuclein, where disease-modifying signals have been reported in some trials. This review focuses on some of the groundbreaking advances and the immediate challenges faced by researchers, clinicians, and individuals with PD, as they collaborate to address the great-and ever-growing-clinical need in PD.
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3. Vulnerability in the womb: Charting the effects of prenatal cannabinoid exposure to mitigate developmental actions on dopamine metabolic capacities and circuits.
PMID:日期:2026-09-09Prenatal cannabis exposure (PCE) is increasingly recognized as a major public health concern as cannabis use during pregnancy continues to rise worldwide. While early studies focused on cannabinoid receptor-mediated alterations in neurotransmission, emerging evidence indicates that PCE induces long-lasting developmental reprogramming affecting neural circuits, metabolism, and endocrine regulation. In this roadmap, we propose a shift from viewing PCE as a discrete synaptic disturbance to considering it a disorder of developmental coordination. We discuss how prenatal cannabinoid exposure may alter mesolimbic dopamine circuit maturation through the interaction of neuronal excitability, mitochondrial bioenergetics, and stress-related hormonal signaling. Particular attention is given to mitochondrial-circuit coupling in dopaminergic neurons and the potential role of mitochondrial cannabinoid receptors (mtCB1) in shaping long-term neuronal function. We further highlight the contribution of astrocytes, microglia, and neuroimmune processes in determining vulnerability or resilience trajectories. We propose that PCE generates latent neurobiological vulnerabilities that may emerge during adolescence or later life when challenged by environmental or physiological stressors. This framework provides new opportunities for early intervention, and prevention, while also offering insights into how early-life metabolic and mitochondrial dysfunction may contribute to lifelong brain vulnerability, including increased susceptibility to age-related neurodegenerative disorders such as Alzheimer's disease.
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4. Cannabinoids and therapeutic potential in neuropsychiatry.
PMID:日期:2026-09-07Cannabinoids have therapeutic utility in some specific areas of medicine, including as an anti-nausea adjunct for chemotherapy and as an anti-inflammatory agent, among others. However, as a therapeutic agent in neuropsychiatric conditions, the data is more limited. Cannabis itself is viewed as a recreational drug of abuse with no medical utility; however, the reality may be more complex when considering individual components of the plant. Cannabinoid components may have some benefit as therapeutic agents in neuropsychiatry, with cannabidiol most often purported to be a therapeutic agent for some seizure disorders. However, recent studies suggest that the cannabis plant is proving to be broader and more complicated in how it delivers potential therapeutic effects. It may be that a combination of components is more effective than any one component. This chapter reviews the medical usage of cannabinoids in neuropsychiatric illness, as reported in the literature, and proposes future approaches that may more effectively avail the attributes of this plant.
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5. Roadmap update: Sensory neurodegeneration in diabetes.
PMID:日期:2026-09-04Human diabetic polyneuropathy (DPN) is a pervasive disabling complication of both types 1 and 2 diabetes mellitus (DM). Here we build on our previous report in this journal, addressing the direct targeting of sensory neurons and the subsequent withdrawal of their distal axon terminals. Specific, albeit largely untested, translational therapeutic approaches are available to 'shore up' the sensory neuron and enable it to regrow its branches. This review provides updated information over several selected pathways our research team has been focused on. We review the evidence for sensory neuron targeting in DM including new human work, specific molecules within neuron perikarya (cell bodies) that foster sensory regeneration and newer ideas on how local nonsystemic targeting of growth cones might also promote regrowth. Our update presupposes important connections between the molecular machinery that supports intact neurons and the capacity of neurons to regrow, reversing DPN deficits. This review is limited in scope but may be a template to investigate the wide repertoire of proteins and noncoding RNAs that might be employed to eventually treat and reverse DPN.
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6. Imaging the glymphatic system in Huntington's disease: The benefits of a multimodal approach and clinical implications.
PMID:日期:2026-09-04The glymphatic system, the cerebrospinal fluid-based circulation and waste clearance system for the brain, is gaining increasing attention in Huntington's disease (HD) due to its potential role in neurodegeneration. Glymphatic dysfunction may contribute to progressive neuronal damage and key clinical features such as cognitive decline and sleep disturbances. This chapter explores the current neuroimaging techniques used to assess glymphatic function in HD, as well as emerging approaches applied in other neurodegenerative disorders, with an emphasis on magnetic resonance imaging and positron emission tomography. We discuss the biological specificity and methodological limitations of these imaging proxies, including the need for multimodal integration. Finally, we outline the clinical and translational implications of glymphatic imaging, including its potential use as a biomarker for early disease detection, longitudinal disease monitoring, and the development of targeted therapeutic strategies.
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7. Advances in nanomaterial-based biomarker detection for neurodegenerative diseases: Special focus on Alzheimer's and Parkinson's disease.
PMID:日期:2026-08-31Amyloid-β aggregation, tau hyperphosphorylation, and α-synuclein misfolding are pathological processes that occur decades before clinical onset in neurodegenerative diseases like Alzheimer's disease (AD) and Parkinson's disease (PD), but detection is still symptom based and technologically insufficient. Disease staging has been redefined by biomarker-centric frameworks, especially the AT(N) classification. However, low abundance, structurally heterogeneous biomarkers in complex biofluids are not resolved by current detection strategies because of limited sensitivity, matrix interference, and lack of conformational specificity. In this regard, nanomaterial enabled sensing platforms offer unique physicochemical properties: magnetic nanostructures enable background independent detection, carbon nanomaterials enable electrochemical signal amplification through improved charge transfer, and plasmonic nanostructures enable label-free optical detection via surface plasmon resonance. When combined, these systems allow for real-time analysis in physiologically relevant matrices, multiplexed detection, and femtomolar sensitivity. Despite advancements in analytical techniques, the practical application of these technologies is hindered by challenges such as biofouling, inconsistencies between batches, and a lack of adequate clinical validation. This review examines the potential of nanomaterial-based sensing strategies for developing clinically relevant neurodiagnostics, categorizes them systematically, and links them to biomarker profiles for AD and PD.
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8. From risk detection to brain health action: The CheckPD-CheckBRAIN pathway across the missing middle in Parkinson's disease.
PMID:日期:2026-08-27Brain health has entered an implementation era, yet practical pathways for translating risk detection into meaningful action remain underdeveloped, particularly in low- and middle-income settings. Parkinson's disease (PD) offers a useful tracer condition for this challenge because it is common, progressive, clinically recognisable, functionally disabling, and highly sensitive to health-system capacity across awareness, referral, diagnosis, treatment, rehabilitation, caregiver support, and longitudinal monitoring. This review uses Thailand's CheckPD™ programme as an applied anchor for examining how digital PD screening can move beyond case-finding toward broader brain health implementation. CheckPD provides a population-facing digital screening and risk-stratification layer for PD and prodromal signals, but screening alone is insufficient. Without interpretation, risk communication, triage, referral completion, prevention advice, rehabilitation linkage, and follow-up, earlier detection may create earlier labelling rather than earlier benefit. We define this transition zone as the "missing middle." To address this gap, we propose CheckBRAIN™ as a post-screening brain health action framework organised around three domains: prevention pathways, resilience-building, and longitudinal brain health monitoring. Across primary prevention, CheckBRAIN promotes modifiable brain health and non-communicable disease risk reduction; across secondary prevention, it monitors risk trajectories, new prodromal symptoms, and conversion to clinical disease; and across tertiary prevention, it aims to preserve function, delay milestones, reduce complications, and support caregivers in established PD. By integrating prodromal PD risk science, digital screening, implementation science, resilience concepts, and global brain health strategy, the CheckPD-CheckBRAIN pathway offers a practical model for moving from early detection of neurodegeneration toward earlier, accessible, and actionable brain health care.
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9. Roadmap for functional neurological disorders: Shared circuitry and future directions.
PMID:日期:2026-08-26Functional Neurological Disorders, or FND, have become accepted in the vernacular of medicine. Although in the past, they were considered less valid than other conditions, now they are present among the differential diagnoses of most illnesses in neurology and psychiatry. Diagnostic approaches have markedly changed as phenotypic profiles become more consistent. Treatment strategies include pharmacologic and non-pharmacologic techniques and have a burgeoning presence in medical literature. Above all, conceptualization of FND has advanced to a sophisticated perspective that incorporates neural circuitry and roles of default mode systems as well as salience networks in the brain. The progress made has been groundbreaking and represents a blossoming field, which will require that clinicians update their acumen accordingly.
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10. Running out the clock: Circadian rhythm dysfunction in cognitive disease.
10. 耗尽时钟：认知疾病中的昼夜节律功能障碍PMID:日期:2026-08-25Lifespan is increasing such that within a few decades approximately twenty percent of the world's population is expected to be greater than sixty years of age. In concert with global aging of the population, neurodegenerative disorders have become the leading cause of disability with dementia now the seventh leading cause of death worldwide. Despite multi-faceted treatment approaches for disorders of cognition that include Alzheimer's disease and multiple sclerosis, present therapies ultimately cannot halt disease progression and eventually cognitive impairment continues unabated. Furthermore, co-morbidities, such as metabolic disorders with diabetes mellitus, also lack strategies to prevent disease progression. Given these clinical challenges for cognitive loss, innovative avenues of investigation that involve mammalian chronobiology with circadian rhythm clock genes and related pathways of aging, cellular senescence, oxidative stress, metabolic dysfunction, sleep fragmentation, apolipoprotein E, programmed cell death, silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae), nicotinamide adenine dinucleotide, the gut microbiota, and glucagon-like peptide-1 receptor agonism may offer exceptional promise for forging new strategies for cognitive disease treatment. These pathways are intimately linked to circadian rhythm processes, are complex in generating biological outcomes, can broadly influence clinical translation of both short- and long-term considerations for cognitive disease care, and necessitate dissection of their precise regulatory mechanisms with the benefit from early diagnostic platforms as well as artificial intelligence and machine learning applications to foster translation of these pathways into effective clinical treatments.