GeroScience老年科学

GeroScience(英文缩写 GEROSCIENCE),ISSN 2509-2715,eISSN 2509-2723,中文译名:老年科学 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。

2026 年数据 · 影响因子
6.000
JCR 分区
Q1
CAS 分区
B2
近一年发文量
783
本站 PubMed 收录统计

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。

ISSN: 2509-2715 · eISSN: 2509-2723 · 缩写: GEROSCIENCE ·中文: 老年科学

期刊介绍

选择期刊介绍栏目

期刊简介

GeroScience 是一本聚焦衰老生物学与老年医学的跨学科期刊,涵盖从基础机制到临床转化的广泛议题。主要领域包括衰老的分子与细胞机制、年龄相关疾病、长寿干预及老年综合征。读者群为从事衰老研究的科研人员、临床医生及公共卫生专家,旨在促进对衰老过程的理解并推动健康老龄化策略。

研究方向

主要研究方向包括衰老的遗传与表观遗传调控、细胞衰老、代谢与衰老、神经退行性变、免疫衰老及老年干预措施。论文类型涵盖原创研究、综述、评论和短篇报告,鼓励多学科交叉研究,尤其关注将基础发现转化为临床应用的成果。

期刊特色

期刊强调机制探索与转化潜力并重,论文通常要求有扎实的实验数据和明确的理论意义。其特点在于整合分子、细胞、动物及人类研究,适合从事衰老基础研究或老年临床研究的学者,以及关注年龄相关疾病新靶点的药物研发人员。

投稿难度

投稿难度中等偏上,对研究的创新性和完整性要求较高。建议在投稿前确保实验设计严谨、数据充分,并清晰阐述与衰老领域的关联。由于期刊覆盖范围广,跨学科研究需注意逻辑连贯性,综述类文章需提供批判性视角而非简单罗列。

历年影响因子趋势

JCR 数据年份影响因子JCR 分区
20217.581Q1
20225.600Q2
20235.300Q1
20245.400Q1
20256.000Q1

GeroScience 最新收录文献

  1. JCR分区: Q1 CAS分区: B2 影响因子: 6

    1. Sensory gamma entrainment in older adults with or without cognitive impairment: a systematic review and exploratory meta-analysis.

    1. 患有或不患有认知障碍的老年人的感觉伽马节律夹带:系统综述与探索性荟萃分析
    作者:
    Myeonghae Hyun, Yeseung Park, Seo Yoon Park, Ki Woong Kim
    日期:
    2026-10-03

    Gamma entrainment using sensory stimulation (GENUS) is a noninvasive approach under investigation in older adults with and without cognitive impairment, including Alzheimer's disease; however, human evidence remains scattered across structural, functional, biomarker, electrophysiological, and cognitive domains. We searched PubMed, Embase, Scopus, and Web of Science for English-language articles published from January 2016 to December 2025, following PRISMA 2020 guidelines and a retrospectively registered PROSPERO protocol. Eligible studies evaluated non-invasive sensory gamma-frequency stimulation in adults aged 60 years, including Alzheimer's disease-spectrum and cognitively normal older adults, with quantitative outcomes reported in at least one relevant domain. Narrative synthesis was the primary approach, supplemented by an exploratory random-effects meta-analysis of hippocampal and ventricular volume change. Eight studies were included, spanning single-session to 6-month interventions. Findings were directionally favorable across domains but derived from small, heterogeneous studies with nonoverlapping outcomes. Fluid biomarker evidence was limited to exploratory immune-related findings from a single uncontrolled study. Controlled structural studies suggested possible attenuation of hippocampal atrophy, ventricular enlargement, and white matter decline. Functional connectivity findings suggested possible preservation of connectivity in Alzheimer's disease-relevant networks. Electroencephalography studies supported target engagement, with entrainment strength and propagation varying according to stimulation parameters and individual characteristics. Cognitive findings from small exploratory studies did not establish a consistent benefit. Exploratory pooled effects for ventricular and hippocampal volume change were favorable but not robust to conservative sensitivity analysis. Human evidence for GENUS is promising but preliminary and hypothesis-generating; larger, adequately powered, standardized trials are needed before firm efficacy conclusions can be drawn.

  2. JCR分区: Q1 CAS分区: B2 影响因子: 6

    2. The role of social white matter tracts in susceptibility to phishing in aging.

    2. 社会白质束在老年人网络钓鱼易感性中的作用
    作者:
    Chun-Che Hung, Tian Lin, Tzu-Chen Lung, Ryan Faulkner, Kristen M Kennedy, Natalie C Ebner
    日期:
    2026-10-03

    Vulnerability to fraud and financial exploitation among older adults is an increasing public health concern. Growing evidence supports that cognitive and socioemotional changes with age contribute to greater exploitation risk among older adults, while the neural mechanisms of heightened susceptibility to deception in aging are not well understood. Of note, white matter tracts are particularly impacted in aging and are likely implicated in deception detection. This study, for the first time, examined the extent to which age-related differences in white matter pathways subserving social cognition mediated susceptibility to email phishing, a potent, fast-evolving Internet deception threat. Fifty-one younger (21.82 ± 3.47 years) and 46 cognitively healthy older (68.87 ± 6.56 years) adults underwent diffusion-weighted imaging and completed the ecologically-valid PHishing Internet Task (PHIT), which provides a behavioral measure of real-life susceptibility to email phishing. Deterministic tractography-generated a priori tracts of interest included the cingulum, uncinate fasciculus (UF), anterior thalamic radiation (ATR), and superior longitudinal fasciculus-collectively referred to as "social white matter." White matter integrity metrics (i.e., mean diffusivity [MD] and fractional anisotropy [FA]) were extracted from these tracts. Regression-based mediation analyses controlling for sex, education, general cognition, and global MD and FA (separately) showed that both increased right ATR MD and decreased left UF FA partially mediated the effects of age group on phishing susceptibility (higher PHIT scores with greater age). These findings advance a social white matter-based account of age-related exploitation risk, shedding light on the neurobiology underlying social decision-making deficits in aging.

  3. JCR分区: Q1 CAS分区: B2 影响因子: 6

    3. Mapping the evolution of dual-task paradigms in cognitive aging: A bibliometric analysis of research landscapes and translational applications.

    3. 映射认知老化中双任务范式的演变:研究图景与转化应用的文献计量分析
    作者:
    Shi Zhang, Ruoning Wu, Yuqi Xu, Hanbing Li, Cong Chen, Zhiqing Lin, Xiaofeng Wang, Shanyi Yang, Caiwei Yang, Jiajing Zhu, Jingfang Zhu
    日期:
    2026-10-02

    The increasing burden of dementia highlights the need for sensitive and ecologically relevant tools for early detection and intervention. Dual-task (DT) paradigms have emerged as promising approaches for assessing cognitive-motor alterations. This study aimed to map the 22-year evolution of DT research in cognitive aging using bibliometric analysis. We retrieved 1347 articles from the Web of Science Core Collection (January 2003-February 15, 2025) and analyzed them using CiteSpace. Co-citation, keyword burst, and collaboration network analysis were performed to identify research evolution, hotspots, knowledge structures, and international collaborations. Research showed a progressive shift from gait-focused behavioral assessment (2003-2012) to neuroimaging-based investigations (2013-2018), and subsequently toward artificial intelligence-driven, ecologically valid approaches integrating virtual reality and multimodal sensing (2019-2025). The dual-task cost emerged as a potential candidate digital biomarker associated with neural alterations and cognitive decline, while its complementary value to traditional cognitive assessment was highlighted. Dual-task training demonstrated potential benefits for improving functional outcomes and reducing fall risk; however, heterogeneity in treatment effects indicates the need for personalized intervention strategies. DT paradigms are evolving toward potential applications in precision gerontology. The proposed assessment-intervention continuum provides a conceptual framework for future research. Standardized protocols and prospective validation of DT-derived digital phenotypes are required before clinical implementation.

  4. JCR分区: Q1 CAS分区: B2 影响因子: 6

    4. Optimizing frailty care: an analysis of dual exercise targets and cognitive function among frail older adults.

    4. 优化衰弱护理:对衰弱老年人双重运动目标与认知功能的分析
    作者:
    Xiangyu Zhai, Jing Xi, Miao Miao, Doris S F Yu
    日期:
    2026-10-01

    Cognitive decline is a significant concern among frail older adults. Although aerobic and resistance exercise are recommended, their implementation remains challenging due to reduced physical capacity and vitality in this population. Understanding how cardiorespiratory fitness (CRF) and muscle strength (MS) relate to cognitive function may inform targeted exercise prescription. This cross-sectional study examined their independent and combined associations with cognitive impairment in prefrail and frail older adults. We enrolled 4477 prefrail and frail older adults (mean age 72.2 years, 72.5% female). CRF was assessed by 2-min walk test, MS by handgrip strength, and cognitive impairment by Montreal Cognitive Assessment 5-min protocol. Logistic regression analysis examined relationship of CRF and MS with cognitive impairment. Three hundred fifteen (7.0%) participants had cognitive impairment. Higher CRF was independently associated with lower odds of cognitive impairment across quartiles (Q4 vs. Q1: OR = 0.15, 95% CI 0.08-0.29; p for linear trend < 0.001). The association with MS was attenuated after adjusting for CRF, with Q3 (OR = 0.65, 95% CI 0.45-0.94) and Q4 (OR = 0.66, 95% CI 0.45-0.97) statistically significant. Findings were consistent across prefrail and frail subgroups. Joint analysis revealed that high CRF with high MS had lowest odds of cognitive impairment (OR = 0.38, 95% CI 0.26-0.56) compared to low CRF with low MS, and high CRF alone conferred 56% lower odds than high MS alone. CRF and MS were significantly associated with cognitive impairment, with CRF showing stronger independent associations, suggesting CRF as a promising target for future exercise interventions to prevent cognitive decline in prefrail and frail older adults.

  5. JCR分区: Q1 CAS分区: B2 影响因子: 6

    5. Associations between socioeconomic position index and epigenetic aging in NHANES.

    5. NHANES中社会经济地位指数与表观遗传衰老之间的关联
    作者:
    Michelle R Caunca, Katrina Kezios, Andrea L C Schneider, Hanyang Shen, David H Rehkopf, Jacqueline M Torres, Brian H Chen
    日期:
    2026-09-30

    Lower socioeconomic position (SEP) is related to poor health, and epigenetic aging represents a potential mechanism of action. We aimed to estimate associations between a novel measure of SEP and epigenetic age in a nationally representative cohort. We used data from NHANES survey waves 1999-2000 and 2001-2002. Our exposure was a novel three-category indicator of SEP, incorporating income, wealth, occupational status, and educational attainment. Our outcomes included 13 different epigenetic clocks and leukocyte telomere length. Higher SEP was associated with lower epigenetic age acceleration for a subset of epigenetic clocks tested. In adjusted models, higher (vs. lower) SEP was associated with lower epigenetic age for the GrimAgeMort (β [95% CI] = -0.94 [-1.84, -0.05]), GrimAge2Mort (β [95% CI] = -1.22 [-2.26, -0.18]), and HorvathTelo (β [95% CI] = 0.07 [0.01, 0.13]) epigenetic clocks. Higher SEP was associated with greater telomere length, though CI contained the null (β [95% CI] = 0.04 [-0.01, 0.09]). The magnitude of association was larger for men vs. women (p-value for interactions for GrimAgeMort and GrimAge2Mort < 0.05), though 95% CIs overlapped (GrimAgeMort β [95% CI] men: -2.01 [-3.18, -0.84], women: -0.31 [-1.39, 0.77], GrimAge2Mort -2.42 [-3.91, -0.94], women: -0.52 [-1.70, 0.66]). Most associations remained stable, though CI for most estimates contained the null, after adjustment for cell proportions. In this cross-sectional analysis, higher SEP was associated with lower epigenetic age acceleration for a limited number of epigenetic clocks, and associations were null controlling for cell proportions. Future work should examine whether cell composition mediates these associations.

  6. JCR分区: Q1 CAS分区: B2 影响因子: 6

    6. Sex- and age-specific patterns in bone, muscle, and fat across adulthood and their relation to osteosarcopenic adiposity phenotype: a cross-sectional study.

    作者:
    Jasminka Z Ilich, Jon Mills, Selma Cvijetic, Emily M Barlow, Semira Galijasevic, Dario Boschiero, Jeffrey Harman
    日期:
    2026-09-30

    Evidence suggests that age-associated differences in body composition-bone/muscle/adipose tissue-are nonlinear, but their timing, sex-specific features, and relation to osteosarcopenic adiposity (OSA) phenotype remain poorly defined. OSA is characterized by the coexistence of osteopenia/osteoporosis, sarcopenia, and excess or redistributed adiposity. We examined sex- and age-specific patterns and inflection points for bone, muscle, fat, and intramuscular adipose tissue (IMAT) in cross-sectional data from 9717 Caucasian adults aged 20-90 years. Body composition was assessed using BIA-ACC, a nonionizing bioelectrical impedance analysis that estimates total body bone, skeletal muscle, fat mass, and IMAT. Prespecified operational thresholds for the BIA-ACC-derived bone and muscle mass scores and sex-specific fat mass percentages were used to define reduced bone and muscle mass, adiposity, and the BIA-ACC-based OSA phenotype. LOESS nonparametric regression was used to model age-related body composition patterns without assuming a predefined functional relationship between age and each outcome and to identify inflection points. For sensitivity analyses, all LOESS curves were fitted with stiffness/span parameter (f) and confidence intervals were calculated. Men showed earlier peaks and relative midlife stability in bone and muscle, followed by lower later life values than women. Women showed lower baseline values, multiple early-life inflection points, and sharper midlife downturns, particularly around menopause. Fat mass increased steadily in men but followed multiphasic patterns in women, whereas IMAT increased progressively with age in both sexes. Adults meeting the operational BIA-ACC criteria for OSA (identified even in the youngest participants) demonstrated less stable trajectories, earlier downturns in bone and muscle components, and more complex fat and IMAT patterns. Distinct sex-specific patterns and adverse association between BIA-ACC-defined OSA and body composition patterns were identified. Early identification of this phenotype may support preventive assessment of accelerated musculoskeletal decline and increasing adiposity.

  7. JCR分区: Q1 CAS分区: B2 影响因子: 6

    7. Autologous cytokine-induced NK cells as candidate cellular senolytics: evidence, obstacles, and the experiments still needed.

    7. 自体细胞因子诱导的NK细胞作为候选细胞衰老清除剂:证据、障碍及仍需进行的实验
    作者:
    Ramon E Coronado
    日期:
    2026-09-29

    Cellular senescence and chronic low-grade inflammation occupy a central, mechanistically coupled position among the hallmarks of aging. Natural killer (NK) cells decline in per-cell cytotoxicity with age, and lower NK cell cytotoxicity has been associated with higher cancer incidence and infection-related mortality in older adults. NK cells are also endogenous effectors of senescent-cell clearance, engaging stress-induced NKG2D and DNAM-1 ligands and depending on perforin-mediated cytolysis. These literatures meet at a hypothesis: that autologous cytokine-induced NK cells, manufactured from a patient's own peripheral blood mononuclear cells (PBMCs), might be developed as candidate cellular senolytics. Cytokine-induced killer (CIK) and cytokine-induced memory-like (CIML) manufacturing platforms are mature, with registry safety data across more than 2700 predominantly oncology patients and a first autologous NK cell trial in a non-cancer, aging-related indication (Alzheimer's disease). Yet no trial has tested such a product against a senescent-cell-burden or biological-age endpoint. This review maps the evidence across NK cell aging, NK cell-mediated senolysis, and autologous NK cell clinical experience; separates what is established in humans from what remains preclinical or hypothetical; and confronts three obstacles: the HLA-E/NKG2A evasion axis, the heterogeneity of senescent-cell surface phenotypes across tissue and inducing stimulus, and the physiological roles of senescent cells in wound healing, tissue remodeling, development, and tumor suppression that make indiscriminate clearance non-trivial. We conclude that the rationale is defensible but not yet trial-ready, and specify the precursor experiments (autologous NK cell cytotoxicity against autologous senescent cells from older donors, and a preclinical infusion model) that should gate any first-in-human program.

  8. JCR分区: Q1 CAS分区: B2 影响因子: 6

    8. Box C/D snoRNPs and MDT-15/MED15 regulate mitochondrial surveillance and mitophagy via fatty acid metabolism.

    8. Box C/D snoRNPs 和 MDT-15/MED15 通过脂肪酸代谢调控线粒体监视与线粒体自噬
    作者:
    Lois Armendariz, Alicia Chan, Elissa Tjahjono, Meggie Wang, Yvette Acevedo, Natalia V Kirienko
    日期:
    2026-09-26

    In response to constant homeostatic threats, organisms have developed complex regulatory networks to monitor cellular functions and restore normal function. Here, we identify MDT-15 and its effectors, the fatty acid desaturases FAT-5, FAT-6, and FAT-7, as activators of the Ethanol and Stress Response (ESRE) mitochondrial surveillance pathway. Our data show that box C/D snoRNPs, which were previously linked to ESRE activation, also regulate FAT-6 and FAT-7 protein levels. Notably, knockdown of mdt-15 or fib-1, a component of the box C/D snoRNP complex, increased accumulation of the mitophagic activator PINK-1, the first step in licensing mitophagy, suggesting a relationship between ESRE surveillance and mitophagic activation. Our results show that both MDT-15 and FAT-6 are required for host defense against liquid-based Pseudomonas aeruginosa pathogenesis, linking this mitochondrial surveillance network to resistance against acute infection. Supplementation with downstream unsaturated fatty acid products of FAT-6 and FAT-7 enhanced ESRE and mitophagic activation, but did not affect the mitochondrial unfolded protein response (UPR) pathway. Since fatty acids activated ESRE and PINK-1 in wild-type and mutant genetic backgrounds, they are likely to act via a mechanism independent of FAT-6 and FAT-7 function. Our results provide insight into a novel interplay between box C/D snoRNPs, MDT-15, and fatty acids in the regulation of mitochondrial surveillance, mitophagy, and host defense.

  9. JCR分区: Q1 CAS分区: B2 影响因子: 6

    9. Plasma and cerebrospinal fluid proteomics reveal distinct patterns of senescence and neuropathology in aging rhesus macaques.

    作者:
    Giovanne B Diniz, Kayla Schwartz, Carissa T Erices, Sean P Ott, Devon J Griggs, Justin H Mendiola, Courtney L Sutphen, Danielle Beckman, Thomas C Register, Patrick R Hof, Edward N Wilson, John H Morrison
    日期:
    2026-09-26

    Aging is the primary risk factor for neurodegenerative disease, yet the protein signatures that distinguish physiological brain aging from pathological decline remain incompletely defined in translational models. Using the targeted NULISAseq proteomic platform, we profiled cerebrospinal fluid (CSF) and plasma from 66 rhesus macaques (Macaca mulatta) spanning adult, pre-geriatric, and geriatric ages, and benchmarked the results against human reference samples. Age-related differences were broader and predominantly positive in plasma, whereas comparatively fewer CSF proteins differed with age. Canonical neurosenescence markers of axonal, astrocytic, and microglial biology, including neurofilaments, GFAP, and TREM2, showed age-related patterns similar to those reported in human aging. Synaptic and barrier proteins behaved differently by compartment: neuronal pentraxins and pleiotrophin were lower in the CSF of older animals, while choroid plexus proteins FOLR1 and IGFBP7 were lower in pre-geriatric animals. While immunohistochemistry confirmed extensive parenchymal amyloid deposition in geriatric brains alongside sparse tau pathology, plasma amyloid-beta and phosphorylated tau species tracked age and cortical amyloid burden more closely than their CSF counterparts. Systemic inflammatory and metabolic stress proteins, including IL6 and GDF15, were higher in older animals, resembling human inflammaging. Finally, we describe a subclustering of geriatric animals based on CSF proteomic signatures that is not explained by chronological age. Together, these results map compartment-specific signatures of senescence and early neuropathology across the non-human primate (NHP) lifespan and support the use of NHP models in translational biomarker studies.

  10. JCR分区: Q1 CAS分区: B2 影响因子: 6

    10. Motor speech markers of Alzheimer's risk.

    作者:
    Julia Giffard, Aidan D Bindoff, Eddy Roccati, Renjie Li, Adam P Vogel, Lynette R Goldberg, Quan Bai, Anna E King, James C Vickers, Jane Alty
    日期:
    2026-09-26

    Motor changes are increasingly recognized as part of the Alzheimer's disease (AD) phenotype, yet motor speech function and its clinical utility for early AD risk stratification remain underexplored. This cross-sectional study investigated whether measures of motor speech performance in home-based rapid syllable repetition (diadochokinesis [DDK]) tasks are associated with the established AD risk indicators of subjective cognitive decline (SCD), apolipoprotein E ε4 (APOE ε4) carriage, and plasma phosphorylated tau 181 (p-tau181). A community sample of 339 cognitively unimpaired adults (238 asymptomatic control (AC), 66.3 ± 6.5 years, 71.4% female; 101 SCD, 66.0 ± 6.6 years, 72.3% female) from the Island Study Linking Aging and Neurodegenerative Disease remotely self-administered four DDK tasks ("pa", "ta", "ka", "pataka") from the self-administered online Tasmanian Test protocol. Self-reported cognitive changes were used to classify AC or SCD groups. We conducted nonparametric analyses and percentile-LASSO multiple regression to predict risk indicators from motor speech performance measures, allowing for age, sex, education, anxiety, and depression. No nonparametric associations with SCD or APOE ε4 remained significant after adjustment for multiple comparisons. One measure of relative repetition variability remained significantly associated with plasma p-tau181. In covariate-adjusted regression analyses, motor speech measures were associated with SCD (AUC 0.700), APOE ε4 (AUC 0.715), and natural log-transformed p-tau181 (MAE 0.323). Sensitivity analyses for hearing loss, incomplete data, and depression-screened subsets revealed potentially mitigating effects of depression and blood biomarker data availability bias. This indicates that additional work, especially longitudinal follow-up, is needed to verify these preliminary findings in the search for scalable screening tools for preclinical dementia risk.

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