YALE JOURNAL OF BIOLOGY AND MEDICINE耶鲁生物学与医学杂志
YALE JOURNAL OF BIOLOGY AND MEDICINE(英文缩写 YALE J BIOL MED),ISSN 0044-0086,eISSN 1551-4056,中文译名:耶鲁生物学与医学杂志 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 | 3.434 | Q2 |
| 2022 | 2.700 | Q2 |
| 2023 | 2.500 | Q2 |
| 2024 | 3.900 | Q1 |
| 2025 | 4.800 | Q1 |
YALE JOURNAL OF BIOLOGY AND MEDICINE 最新收录文献
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1. Chrysoeriol-Mediated Neuroprotection in Parkinson's Disease in Mice: Targeting Apoptosis, α-Synuclein Accumulation, and Functional Recovery.
1. 金圣草黄素对小鼠帕金森病的神经保护作用：靶向细胞凋亡、α-突触核蛋白积累与功能恢复PMID:日期:2026-03-31Parkinson's disease (PD) is a neurodegenerative disorder marked by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta, leading to significant motor dysfunction. Current treatments stabilize dopamine levels but fail to address underlying neuronal apoptosis, highlighting the need for novel approaches. Although chrysoeriol, a 3'-O-methoxy flavone and luteolin derivative, is well-documented for its anti-cancer, anti-diabetic, antioxidant, and anti-inflammatory properties, its neuroprotective potential in PD, particularly , remains largely unexplored. This study fills a critical gap by being the first to systematically assess chrysoeriol's neuroprotective effects in a PD mouse model. We evaluated the effects of 5 mg/kg chrysoeriol administered intraperitoneally (IP) for 14 days in an acute 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD model. Behavioral tests showed notable recovery, as chrysoeriol eliminated deficits in motor function, coordination, and balance, as assessed by the pole test, forced swim test, and tail suspension test. It also mitigated exploratory and locomotor deficits in the open field test, and the Y-maze test revealed improved spatial and learning memory. Hematoxylin and eosin staining indicated a significant reduction in neuronal damage across key brain regions. qPCR analysis showed reduced 1-methyl-4-phenylpyridinium (MPP+)-induced toxicity, downregulation of α-synuclein, and an improved Bcl-2/Bax ratio. These findings suggest chrysoeriol may protect against MPP+-induced apoptosis in mice, potentially via the PI3K/Akt signaling pathway, and reduces mitochondrial damage by downregulating α-synuclein.
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2. Musicality is Preserved in Neurodegeneration.
PMID:日期:2026-03-31Certain musical abilities can endure even as language, memory, and behavior decline in dementia, yet the neural basis of this resilience remains poorly understood. We draw on behavioral and neuroimaging evidence to explain why musicality is selectively preserved or impacted across Alzheimer's disease (AD) and the frontotemporal dementias (FTDs). Adopting a network-based perspective, we describe how musicality arises from interactions across large-scale brain systems that support perception, emotion, and memory. Evidence from case studies and neuroimaging work suggests that music engages lower-level auditory processing and higher-order networks across the brain, which may help explain the heterogeneous effects of neurodegeneration on musicality. Preserved and impaired musical abilities may reflect the selective vulnerability of distinct intrinsic connectivity networks. In early AD, relatively preserved salience and reward circuitry may sustain emotional responses to familiar music and facilitate autobiographical recall even as episodic memory declines. Degeneration of anterior temporal and salience network regions in the FTDs may disrupt the emotional and conceptual interpretation of music while leaving lower-level auditory systems relatively intact. Significant gaps remain in understanding how different components of musicality are affected in specific neurodegenerative diseases. Greater methodological standardization, larger cohorts, longitudinal study designs, and multimodal approaches will be critical for identifying how musicality is preserved or impacted across dementia syndromes. Addressing these questions may advance theoretical models of music perception in the human brain and guide the development of targeted music-based interventions that enhance emotion, memory, and quality of life for people living with dementia.
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3. Burden of Neurological Disorders in Resource-Limited Settings: Lessons from Pakistan for Global Neurology.
PMID:日期:2026-03-31Neurological disorders (NDs) are a leading global cause of disability and mortality, with their burden falling disproportionately on low- and middle-income countries (LMICs). Pakistan exemplifies the systemic challenges faced in resource-limited settings, including delayed diagnosis, limited specialist access, and fragmented care pathways. Despite this, comprehensive spectrum-based data remain scarce. This study was aimed to quantify the burden and characterize the spectrum of NDs presenting to a major Pakistani tertiary-care center and to identify associated predictors and geographic disparities. A hospital-based cross-sectional study was conducted from May 2023 to January 2024, enrolling 537 consecutive patients with confirmed NDs. Descriptive statistics and logistic regression models were employed. Neurodevelopmental disorders were most frequent (31%), followed by neurovascular (20%), epilepsy (14%), autoimmune neurological disorders (12%), neurodegenerative (8%), neuroinfectious (7%), and neuromuscular disorders (6%). Logistic regression revealed strong age- and sex-dependent patterns, including markedly higher odds of neurodegenerative disorders in males and increased odds of neurovascular disorders with older age. Geographic analyses demonstrated a high burden of autoimmune and neuromuscular disorders among patients traveling >100 km, particularly from Khyber Pakhtunkhwa (KPK) and Azad Jammu Kashmir (AJK), highlighting significant access inequities. This study provides comprehensive clinical snapshot of NDs in Pakistan, revealing distinct epidemiological patterns shaped by socioeconomic disparities, geographic inequities, and genetic factors, such as consanguinity. The findings underscore the urgent need for strengthened neurological services, decentralization of specialized care, improved diagnostic capacity, early-interventions, and national surveillance systems. Lessons from Pakistan mirror broader challenges across LMICs and highlight the global imperative to invest in equitable neurological healthcare.
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4. Comparative Analysis of Prenatal Stress Models: Placental and Neurodevelopmental Outcomes in Mice.
4. 产前应激模型的比较分析：小鼠胎盘与神经发育结局PMID:日期:2026-03-31[中文摘要] 产前应激会影响子代发育。胎盘作为重要的母胎中介，易受产前应激影响，其生物学特性会影响胎儿神经发育，尤其是腹侧前脑。腹侧前脑发育中断与神经发育障碍（NDDs）相关，如孤独症谱系障碍（ASD）和注意缺陷/多动障碍（ADHD）。目前，多种小鼠模型被用于研究这些关联。然而，每种模型可能在胎盘和神经发育结局中诱导独特效应，而这些效应鲜有研究。为探讨这一问题，妊娠小鼠从胚胎第12天（E12）开始，每日3次暴露于三种应激模型之一：重复束缚应激（RS）、慢性不可预测应激（CUS）或重复足底电击应激（FS）。在E14或E18时，收集胎盘和胚胎脑，并进行qPCR和脑立体学测量。胎盘免疫和腹侧前脑GABA能基因表达在E14时受影响更大，许多变化到E18时已不明显，提示存在急性失调状态。不同模型既有独特效应，也有重叠效应。E18分析提示随时间推移对应激产生适应，表现为胎盘免疫因子变化总体受到抑制或缺失，脑内偏离减少，以及胎盘与脑之间的相关性，尤其在雌性中。慢性不可预测应激在E18时显示的变化最多。这些发现提示，尽管每种模型具有独特效应，但随着应激暴露进展，胎盘免疫功能可能促进脑GABA能系统的正常化，尤其在雌性中。进一步理解胎盘-脑轴可能有助于阐明增加和降低神经发育障碍风险的机制。
[英文摘要] Prenatal stress affects offspring development. The placenta, an important maternal-fetal mediator, is susceptible to prenatal stress, and its biology affects fetal neurodevelopment, particularly ventral forebrain. Ventral forebrain developmental disruption is linked to neurodevelopmental disorders (NDDs) such as autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD). Currently, multiple mouse models are used to study these links. However, each model may induce unique effects in both placental and neurodevelopmental outcomes, which are rarely studied. To explore this, pregnant mice were exposed 3 times daily to one of three stress models: repeated restraint stress (RS), chronic unpredictable stress (CUS), or repeated footshock stress (FS) beginning at embryonic day (E)12. At E14 or E18, placenta and embryonic brain were collected, and qPCR and brain stereological measurements were performed. Placental immune and ventral forebrain GABAergic gene expression was impacted more at E14, with many changes not apparent by E18, suggesting an acute dysregulated state. Different models had both unique and overlapping effects. E18 analyses suggested adaptation to stress over time, with overall suppression or lack of placental immune factor changes, fewer deviations in the brain, and correlations between placenta and brain, particularly in females. Chronic unpredictable stress showed the most changes at E18. These findings suggest that, while each model has unique effects, as stress exposure progresses, placental immune functioning may promote the normalization of brain GABAergic systems, particularly in females. Further understanding the placenta-brain axis may be valuable in delineating mechanisms that increase and decrease risk of neurodevelopmental disorders.
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5. Computational Investigation of Flavonoid-Associated Molecular Pathways in Astrogliosis Modulation.
5. 黄酮类化合物相关分子通路调控星形胶质细胞增生症的计算研究PMID:日期:2026-03-31[中文摘要] 星形胶质细胞增生症的特征是脑内星形胶质细胞数量因损伤、创伤、感染、缺血、卒中、自身免疫反应或神经退行性疾病而异常增加。胶质纤维酸性蛋白（GFAP）是星形胶质细胞发育和星形胶质细胞增生症的标志物。黄酮类化合物在星形胶质细胞增生症中的抗神经炎症作用尚不明确。本计算分析首次研究了黄酮类化合物与参与GFAP表达的转录因子之间的潜在相互作用。使用AutoDock Vina，将60种已知具有抗炎特性的黄酮类化合物与26种参与GFAP表达的蛋白进行分子对接。使用ProtoxII服务器预测黄酮类化合物的毒性，并分别使用DruLiTo和pkCSM软件评估药物相似性和药代动力学特性。使用BIOVIA Discovery Studio软件评估黄酮类化合物与靶蛋白之间的相互作用。在所研究的黄酮类化合物中，biochanin A、bavachin、apigenin、epicatechin、wogonin、kaempferol、hispidulin、genistein、farrerol、diosmetin和daidzein表现出药物相似特性、无毒性、良好的药代动力学特性，并且对Janus激酶1（JAK1）、Janus激酶2（JAK2）、IκB激酶（I-κKB）、丝氨酸/苏氨酸激酶（AKT）和组蛋白乙酰转移酶（P300）具有更好的对接评分。本研究表明，黄酮类化合物与JAK1、JAK2、I-κKB、AKT和P300之间的预测性关联可能通过核因子κB（NF-κB）和Janus激酶/信号转导及转录激活因子（JAK/STAT）通路影响GFAP表达和星形胶质细胞增生症过程。黄酮类化合物与预测结合伴侣之间的相互作用已基于既往研究得到确认。这些预测性关联对于制定营养指南以及改进针对星形胶质细胞增生症驱动的神经系统疾病的基于黄酮类化合物的治疗策略极具价值。本研究为进一步研究和研究提供了见解。
[英文摘要] Astrogliosis is characterized by an abnormal increase in the number of astrocytes in the brain due to damage, trauma, infection, ischemia, stroke, autoimmune responses, or neurodegenerative disorders. Glial Fibrillary Acidic Protein (GFAP) is a marker for astrocyte development and astrogliosis. Flavonoids have unclear anti-neuroinflammatory effects in astrogliosis. This computational analysis was the first to investigate the potential interaction between flavonoids and the transcription factors involved in GFAP expression. Using AutoDock Vina, 60 flavonoids with known anti-inflammatory properties were docked to 26 proteins involved in GFAP expression. Toxicities of the flavonoids were predicted using the ProtoxII server, and drug-likeness and pharmacokinetic properties were assessed using the DruLiTo and pkCSM software, respectively. BIOVIA Discovery Studio software was used to evaluate the interactions between flavonoids and target proteins. Among the studied flavonoids, biochanin A, bavachin, apigenin, epicatechin, wogonin, kaempferol, hispidulin, genistein, farrerol, diosmetin, and daidzein displayed drug-like properties, no toxicity, favorable pharmacokinetic properties, and better docking scores for Janus Kinase 1 (JAK1), Janus Kinase 2 (JAK2), I Kappa B Kinase (I-κKB), Serine/Threonine Kinase (AKT), and Histone Acetyltransferase (P300). This study revealed that predictive associations between flavonoids and JAK1, JAK2, I-κKB, AKT, and P300 might affect both GFAP expression and the astrogliosis process via the Nuclear Factor Kappa-Light-Chain-Enhancer of Activated B Cells (NF-κB) and Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) pathway. The interactions between flavonoid(s) and predicted binding partner(s) were confirmed based on previous studies. These predictive associations are extremely valuable for developing nutritional guidelines and for improving flavonoid-based therapeutic strategies for neurological disorders driven by astrogliosis. This research provides insight for further and research.
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6. {"_":"Regulation and Interaction Among SOCS1 and SOCS3 by MicroRNAs in Multiple Sclerosis: A Review and Analysis.","i":["In Silico"]}
PMID:日期:2026-03-31Multiple sclerosis (MS) is a chronic demyelinating disease and a leading cause of disability in young adults. Its pathophysiology involves complex genetic and immunological mechanisms, among which the suppressors of cytokine signaling (SOCS) proteins play a critical role. These intracellular regulators control cytokine-mediated JAK/STAT signaling, thereby modulating immune activation. In particular, SOCS1 and SOCS3 inhibit key cytokines such as IL-2, IL-12, IL-6, and IL-23, preventing excessive Th1/Th17 responses and neuroinflammation. Dysregulation of SOCS expression or function can favor persistent immune activation and contribute to central nervous system demyelination. MicroRNAs (miRNAs), small non-coding RNAs that repress gene expression post-transcriptionally, have emerged as important modulators of immune regulation. Several miRNAs target SOCS transcripts, influencing their expression and, consequently, cytokine signaling. Altered miRNA profiles have been reported in autoimmune and neurodegenerative diseases, highlighting their potential relevance in MS pathogenesis and as biomarkers. This review summarizes current evidence on SOCS1 and SOCS3 in MS and examines their regulation by miRNAs. In addition, we present a hypothesis-generating analysis identifying candidate miRNAs with predicted interactions with SOCS genes. These computational findings are intended to support and prioritize potential regulatory relationships rather than provide direct experimental validation. Collectively, this integrative approach may offer new insights into disease biology and help guide future experimental studies aimed at identifying biomarkers or therapeutic targets in MS.
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7. {"_":"Homozygous Mutation in Intellectual Disability and Atypical Parkinsonism.","i":["PTRHD1"]}
7. {"_":"智力障碍与非典型帕金森综合征中的纯合突变。","i":["PTRHD1"]}PMID:日期:2026-03-31Five different homozygous mutations, two of them in more than one family, have been reported as responsible for intellectual disability (ID) and parkinsonism. In all 10 families, onset of ID was early childhood, and in parkinsonism, later childhood to the fourth decade. We report on a family with four siblings presenting with mild to moderate ID and mildly ataxic gait without spasticity or hemiparesis that is not consistent with parkinsonism. The signs of parkinsonism such as bradykinesia, tremor, slow to response, dementia, and gait problems appeared in the fourth decade. There was no muscle rigidity and postural instability, but there were unusual features of exotropia, pectus excavatum, and prominent clavicles. Linkage analysis using SNP genotyping followed by exome sequencing led to the discovery of c.155G>A (p.Cys52Tyr), already reported in an Iranian sibling pair. Our findings reveal that not all mutations manifest with muscle rigidity and postural instability and confirm that gait problems may not be evident until towards the end of the fourth decade. Early onset behavioral problems in presented patients include attention deficit, hyperactivity, aggressive behavior and seclusion, apraxia of speech, stuttering, and somniloquy. Gait ataxia, exotropia, pectus excavatum, and prominent clavicles further widen the clinical phenotype. is expressed in many organs, and we found widespread expression in the adult brain. The association of dysfunction with both cognitive and motor phenotypes highlights the potential role of the protein in neurodevelopment and neurodegeneration.
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8. The Bidirectional Regulatory Role of Neuroimmune Interaction in Neurodevelopment and Neurodegenerative Diseases.
8. 神经免疫相互作用在神经发育和神经退行性疾病中的双向调控作用PMID:日期:2026-03-31Neurological disorders pose a major public health challenge worldwide, with neuroimmune interaction emerging as a core regulatory mechanism underlying their pathogenesis. This review highlights the progression from static association to dynamic mechanisms between neuroimmune interaction and neurological diseases, filling the research gap in immune function changes during development and aging. We propose a triple regulatory logic framework, including multicellular crosstalk network, context-dependent signaling pathway switching, and host microenvironmental state, which clarifies the bidirectional regulatory patterns of neuroimmune interaction in physiological neurodevelopment and pathological neurodegeneration. Specifically, the neuroimmune system maintains central nervous system (CNS) homeostasis through four core processes during development, while its dysfunction drives chronic neuroinflammation and neurodegeneration via cascading pathological mechanisms. We further discuss clinical translation bottlenecks and targeted intervention strategies based on this framework, providing a theoretical basis for constructing a stage-specific neuroimmune interaction and regulation theory. This review offers new insights into the pathogenesis of neurological diseases and potential therapeutic targets for clinical practice.
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9. Neurodegeneration and Homelessness: A Bidirectional Relationship Shaping Health and Vulnerability.
9. 神经退行性变与无家可归：塑造健康与脆弱性的双向关系PMID:日期:2026-03-31[中文摘要] 神经退行性变与无家可归之间存在着深刻的相互关联。无家可归期间经历的许多结构性、环境性和人际层面的状况——例如不稳定的医疗保健、被迫流离失所、慢性压力和创伤——可通过多种途径导致认知加速衰退。相关的神经认知损害也可能增加无家可归的脆弱性。记忆、执行功能、注意力和冲动控制方面的缺陷可使人难以维持就业、管理财务、利用社会服务以及维系支持性关系。这些途径共同形成了一个强化模式：神经退行性变可增加失去住房的风险，而无家可归又可加剧驱动神经退行性变的生物学和社会心理应激因素。尽管越来越多的证据表明，无家可归者中神经退行性疾病的负担相当沉重，但这些疾病常常未被充分认识和诊断。碎片化的医疗保健以及症状与精神疾病或物质使用障碍的重叠可阻碍及时识别。漏诊或延迟诊断对个人和系统均产生重大影响。当神经退行性变在未被识别或治疗的情况下进展时，个体可能经历可预防的功能衰退、难以维持人际关系，以及反复且往往可避免地出入医院、收容所和监禁场所。若未获得诊断，个体还可能错失获取残疾福利、支持性住房选择以及可显著改善健康和生活质量的个性化照护规划的机会。以创伤知情、减少伤害为导向的新兴模式——例如移动外展服务、收容所内诊所和“住房优先”项目——为改善神经认知变化的识别和支持长期神经健康提供了有前景的策略。理解并解决神经退行性变与无家可归之间的双向关系，对于减少痛苦、促进稳定以及提供既有效又维护尊严的照护至关重要。
[英文摘要] Neurodegeneration and homelessness are deeply interconnected. Many structural, environmental, and interpersonal conditions experienced during homelessness-for example, inconsistent healthcare, forced displacement, chronic stress, and trauma-can contribute to accelerated cognitive decline through multiple pathways. Related neurocognitive impairment can also increase vulnerability to homelessness. Deficits in memory, executive functioning, attention, and impulse control can make it difficult to maintain employment, manage finances, navigate social services, and sustain supportive relationships. Together, these pathways create a reinforcing pattern: neurodegeneration can increase risk of losing housing, and homelessness can intensify the biologic and psychosocial stressors that drive neurodegeneration. Despite growing evidence suggesting a substantial burden of neurodegenerative conditions among people experiencing homelessness, these conditions are frequently underrecognized and underdiagnosed. Fragmented healthcare and symptom overlap with psychiatric conditions or substance use can hinder timely detection. Missed or delayed diagnosis has significant individual and systemic impacts. As neurodegeneration progresses without recognition or treatment, individuals may experience preventable functional decline, difficulty maintaining relationships, and repeated, often avoidable encounters with hospitals, shelters, and carceral settings. Without diagnosis, individuals may also miss opportunities to access disability benefits, supportive housing options, and personalized care planning that could significantly improve health and quality of life. Emerging models grounded in trauma-informed, harm reduction-oriented approaches-such as mobile outreach, shelter-based clinics, and Housing First programs-offer promising strategies to improve recognition of neurocognitive changes and support long-term neurologic health. Understanding and addressing the bidirectional relationship between neurodegeneration and homelessness is essential for reducing suffering, promoting stability, and delivering care that is both effective and dignity-affirming.
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10. Gonadotropins Across the Lifespan: Their role in the Neurodevelopment-Neurodegeneration Continuum.
10. 促性腺激素在生命周期中的作用：其在神经发育-神经退行性变连续体中的作用PMID:日期:2026-03-31Gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), mediate critical reproductive functions via the hypothalamus-pituitary-gonadal axis. Their levels fluctuate across the lifespan, particularly during puberty and menopause, and across the menstrual cycle. In addition to peripheral expression, gonadotropin receptors are widely expressed in the brain, notably in memory-associated regions such as the hippocampus and cortex. Alterations in FSH and LH during reproductive transitions correlate with structural and functional brain changes. Puberty disorders, including central precocious puberty (CPP) and congenital hypogonadotropic hypogonadism (CHH), show altered gray and white matter and functional connectivity in the default mode network (DMN), which supports memory and is disrupted early in Alzheimer's disease (AD). Although preclinical evidence implicates gonadotropins in amyloid and tau pathology, studies of attention and memory have yielded inconsistent results. However, reproductive disorders such as primary ovarian insufficiency (POI) and polycystic ovary syndrome (PCOS) are associated with deficits in cognitive performance, altered DMN dynamics, and increased AD risk. Menopause, characterized by marked gonadotropin elevation, is also accompanied by alterations in brain structure, connectivity, amyloid and tau deposition, and cognition, with associations with FSH and LH that are underexplored. This review synthesizes a broad range of basic and clinical evidence across reproductive transitions and disorders, highlighting shared and distinct mechanisms by which gonadotropins influence brain development, aging, and AD risk, and suggesting directions for future research.