Gerontology Journal Impact Factor & Information

Publisher: Karger

Journal description

As the ratio of people over sixty-five continues to rise, understanding the basic mechanisms of aging and age-related diseases has become a matter of urgent necessity. ëGerontologyí responds to this need by drawing experimental contributions from diverse medical, biological and behavioral disciplines to provide a primary source of high-quality papers covering all aspects of aging in man and animals. Recent research on the clinical problems of aging and the practical applications of laboratory results is also included to support the fundamental goals of extending active life and enhancing its quality. Informative reviews and an open debate section for stimulating, speculative articles carry strong reader approval.

Current impact factor: 3.06

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 3.059
2013 Impact Factor 2.681
2012 Impact Factor 2.676
2011 Impact Factor 2.777
2010 Impact Factor 2.203
2009 Impact Factor 1.661
2008 Impact Factor 1.69
2007 Impact Factor 1.358
2006 Impact Factor 1.439
2005 Impact Factor 1.636
2004 Impact Factor 1.31
2003 Impact Factor 1.6
2002 Impact Factor 1.48
2001 Impact Factor 1.418
2000 Impact Factor 1.424
1999 Impact Factor 1.711
1998 Impact Factor 1.5
1996 Impact Factor 0.969
1995 Impact Factor 0.778
1994 Impact Factor 1.101
1993 Impact Factor 1.17
1992 Impact Factor 1.074

Impact factor over time

Impact factor

Additional details

5-year impact 3.23
Cited half-life 7.60
Immediacy index 0.80
Eigenfactor 0.01
Article influence 1.04
Website Gerontology website
Other titles Gerontology (Online)
ISSN 0304-324X
OCLC 44723306
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • On author's server or institutional server
    • Server must be non-commercial
    • Publisher's version/PDF cannot be used
    • Publisher copyright and source must be acknowledged
    • Must link to publisher version
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Aging is one of the primary risk factors for the development of obesity, a pathology that develops due to an imbalance of increased energy consumption over reduced expenditure. Brown adipocytes are responsible for thermogenesis and could therefore counter obesity by increasing energy expenditure. It is by now well established that humans possess thermogenesis-competent brown adipocytes throughout life, and recent findings indicate that brown fat is actively involved in metabolic control and body weight regulation in adults. Aging is accompanied by a loss of classical brown adipocytes as well as the brown-like adipocytes found in white adipose tissue, suggesting that loss of their energy-expending capacity might contribute to an obesity-prone phenotype with increased age. We here discuss the hypothesis that the age-related loss of brown adipocyte regenerative capacity is a result of dysfunctional stem/progenitor cells. The possible molecular mechanisms that lead to an age-related decline in brown adipogenic stem/progenitor cell function include cell-autonomous and external effects. General loss of mitochondrial biogenesis and function has repeatedly been linked to age-related perturbation of metabolic processes. We also discuss the possibility that alterations in neuronal control by the sympathetic nervous system may contribute to impaired regeneration and thermogenesis in aged brown adipocytes. Finally, age-related changes of endocrine signals have been proposed to exacerbate the loss of brown adipose tissue. In conclusion, age-induced impairment of brown adipogenic stem/progenitor cell function could contribute to the loss of brown adipocyte regeneration, thereby promoting the development of obesity and other metabolic disorders with age. © 2014 S. Karger AG, Basel.
    Gerontology 12/2014; 61(3). DOI:10.1159/000366557
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    ABSTRACT: Background: Zebrafish have become a valuable model for the study of developmental biology and human disease, such as cardiovascular disease. It is difficult to discriminate between disease-related and age-related alterations. Objective: This study was aimed to investigate the effects and potential mechanisms of age-related cardiac modifications in an older zebrafish population. Methods: In this study, we calculated the survival rate and measured the spinal curvature through the aging process. A swimming challenge test was performed and showed that swimming capacity and endurance dramatically dropped in older fish groups. Results: To find out the effect of stress on zebrafish during the aging process, we recorded electrocardiograms on zebrafish and showed that during stress, aging not only led to a significant reduction in heart rate, but also caused other age-related impairments, such as arrhythmias and ST-T depression. Echocardiography showed a marked increase in end-diastolic ventricular dimensions and in isovolumic relaxation time and a notably slower mean and peak velocity of the bulboventricular valve in older zebrafish, but stroke volume and cardiac output were not different in young and old zebrafish. Both nppa and nppb (cardiac fetal genes for natriuretic factor) expression detected by real-time polymerase chain reaction analysis increased in older fish compared to the younger group. Histological staining revealed fibrosis within cardiomyocytes and an increase in ventricular myocardial density and a decrease in epicardial vessel dimensions in older fish hearts that may correlate with a deterioration of cardiac function and exercise capacity. Conclusion: These data suggest that cardiac functional modifications in zebrafish are comparable to those in humans and may partly be due to changes in the cardiovascular system including cardiac fetal gene reprogramming, myocardial density, and epicardial vessel dimensions. © 2014 S. Karger AG, Basel.
    Gerontology 12/2014; 61(5). DOI:10.1159/000369094
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    ABSTRACT: Background: Future time perspective has been associated with subjective well-being, though depending on the line of research considered either an open-ended future time perspective or a limited future time perspective has been associated with high well-being. Most of this research however has conceptualized future time perspective as a one-dimensional construct, whereas recent evidence has demonstrated that there are likely at least two different underlying dimensions, a focus on opportunities and a focus on limitations. This project first seeks to replicate the two-dimensional structure of the Future Time Perspective Scale, and then examines the associations these dimensions may have with different measures of subjective well-being and a biological index of chronic stress. Objective: To test if the two dimensions of the Future Time Perspective Scale, a focus on opportunities and a focus on limitations, differentially associate with two measures of subjective well-being and a biological indicator of chronic stress, namely hair cortisol. Method: Sixty-six community-dwelling participants with a mean age of 72 years (SD = 5.83) completed the Future Time Perspective Scale, Center for Epidemiologic Studies Depression Scale, and Philadelphia Geriatric Center Morale Scale. Participants also provided a 3-cm-long hair strand to index cortisol accumulation over the past 3 months. Following the results of a factor analysis, a mediation model was created for each dimension of the Future Time Perspective Scale, and significance testing was done through a bootstrapping approach to harness maximal statistical power. Results: Factor analysis results replicated the two-dimensional structure of the Future Time Perspective Scale. Both dimensions were then found to have unique associations with well-being. Specifically, a high focus on opportunities was associated with fewer depressive symptoms and higher morale, whereas a low focus on limitations was associated with reduced hair cortisol, though this association was mediated by subjective well-being. Conclusion: Results replicate and extend previous research by pointing to the multi-dimensional nature of the Future Time Perspective Scale. While an open future time perspective was overall beneficial for well-being, the exact association each dimension had with well-being differed depending on whether subjective measures of well-being or biological indices of chronic stress were considered. © 2014 S. Karger AG, Basel.
    Gerontology 12/2014; 61(2). DOI:10.1159/000368716
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    ABSTRACT: Technologies that provide immersive experiences continue to become more ubiquitous across all age groups. This paper presents a review of the literature to provide a snapshot of the current state of research involving the use of immersive technologies and the elderly. A narrative literature review was conducted using the ScienceDirect, EBSCOhost, Springerlink and ERIC databases to summarize primary studies from which conclusions were drawn into a holistic interpretation. The majority of the studies examined the effect of immersive technologies on elder peoples' age-related declines, including sensory and motor changes (vision, hearing, motor skills), cognitive changes and social changes. Various immersive technologies have been described and tested to address these age-related changes, and have been categorized as 'games and simulations', 'robotics' and 'social technologies'. In most cases, promising results were found for immersive technologies to challenge age-related declines, especially through the increase of morale. © 2014 S. Karger AG, Basel.
    Gerontology 12/2014; 61(2). DOI:10.1159/000365754
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    ABSTRACT: Sarcopenia is age-associated deterioration of muscle mass and function caused by a wide scope of physiological and pathological changes ranging from hormonal disorders to loss of subcellular homeostasis. Recent research indicates that mitochondrial dysregulation with advanced age plays a central role in the development of sarcopenia due to the multifactorial functions of this organelle in energy supply, redox regulation, crosstalk with nuclear gene expression and apoptosis. In order to fulfill these roles, it is crucial that mitochondria maintain their own structural and functional integrity through biogenesis, antioxidant defense, fusion/fission dynamics and autophagy (mitophagy). Unfortunately, mitochondria undergo age-associated changes that compromise the above-mentioned properties that eventually contribute to the development of sarcopenia. The peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is involved in the transcriptional regulation of numerous nuclear and mitochondrial gene products participating in the cellular events that control muscle mass and function. Thus, it is not surprising that maintaining an optimal intracellular PGC-1α level and signaling activity is crucial in protecting the muscle from many degradative and destructive processes, such as proteolysis, oxidative damage, inflammation, uncontrolled autophagy and apoptosis. Physical exercise is a powerful stimulus to PGC-1α expression and signaling. Recent research indicates that PGC-1α-controlled mitochondrial biogenesis is not limited by old age per se and that elderly individuals can still benefit from increased muscular activity in terms of skeletal muscle health that ultimately contributes to quality of life in old age. © 2014 S. Karger AG, Basel.
    Gerontology 12/2014; 61(2). DOI:10.1159/000365947
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    ABSTRACT: Background: Little information is available on the potential association between polypharmacy and risk of mortality. Objective: To determine in a population-based study whether polypharmacy is associated with increased risk of mortality in elderly persons. Methods: In this population-based, prospective study of 5,052 people aged 65 years and older (Neurological Disorders in Central Spain), current medications were recorded. Cox proportional hazards models, adjusted for sociodemographics and comorbidity factors, were used to assess the risk of death up to 13.3 years later, comparing the polypharmacy group (≥6 drugs) to those who were taking 1-5 drugs and those in a nonmedicated group (0 drugs). Results: Out of 5,052 participants, 2,550 (50.5%) died over a median follow-up of 6.5 years, including 361 (28.8%) deaths among 931 nonmedicated participants, 1,946 (51.4%) deaths among 3,787 participants taking 1-5 drugs daily, and 243 (72.8%) among 334 participants on polypharmacy. In an unadjusted Cox model, risk of mortality was increased in participants on polypharmacy [hazard ratio (HR) = 2.78, 95% confidence interval [CI]: 2.36-3.27, p < 0.001) and in those taking between 1 and 5 drugs (HR = 1.47, 95% CI: 1.31-1.64, p < 0.001) versus those who were nonmedicated (reference group). In a Cox model that adjusted for a variety of demographic factors and comorbidities, HR remained increased in participants on polypharmacy (HR = 1.83, 95% CI: 1.51-2.21, p < 0.001). Conclusion: This study provides evidence that polypharmacy is associated with increased risk of mortality in elderly people. The extent to which polypharmacy is the proximate cause rather than a marker of this increase risk remains to be determined. © 2014 S. Karger AG, Basel.
    Gerontology 12/2014; 61(4). DOI:10.1159/000365328
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    ABSTRACT: Ageing is a prominent risk factor for atherosclerosis and cardiovascular disease. Vascular smooth muscle cells (VSMCs) are an integral part of atherosclerotic plaque formation, progression and subsequent rupture. Emerging evidence suggests that VSMC behaviour is modified by age, which in turn may affect disease outcome in the elderly. In this review, we discuss the effect of age on VSMC behaviour, proliferation, migration, apoptosis, inflammation, extracellular matrix synthesis and calcification. In addition, we discuss the multiple signalling factors underlying these behavioural changes including angiotensin-II, matrix metalloproteinases, monocyte chemotactic protein-1, and transforming growth factor-β1. Understanding the molecular processes underpinning altered VSMC behaviour with age, may lead to the identification of novel therapeutic targets for suppressing atherosclerosis in the elderly population. © 2014 S. Karger AG, Basel.
    Gerontology 12/2014; 61(5). DOI:10.1159/000368576
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    ABSTRACT: Background: Elder abuse and metabolic syndromes are both important public health issues and are associated with increased morbidity and mortality. This study aimed to examine the associations between elder abuse and risk for metabolic syndromes. Methods: The Chicago Health and Aging Project (CHAP) cohort is a population-based study (n = 4,586). We identified 676 participants with some form of elder abuse reported to a social services agency. The primary independent variable was elder abuse reported to a social services agency. Outcomes were metabolic syndrome as categorized by World Health Organization (WHO), American Heart Association (AHA) and International Diabetes Federation (IDF) criteria. Bivariate and logistic regression analyses were used to assess the association between elder abuse and different definitions of metabolic syndromes. Results: In the bivariate analyses, elder abuse victims were more likely than those without elder abuse to have metabolic syndromes [22.4 vs. 10.7% (WHO), 50.7 vs. 40.0% (AHA) and 47.7 vs. 33.5% (IDF)]. After adjusting for potential confounding factors, elder abuse was associated with an increased risk for metabolic syndromes according to WHO [OR, 3.95 (2.86-5.47)], AHA [OR, 2.03 (1.56-2.64)] and IDF [OR, 2.55 (1.97-3.29)] criteria. Interaction term analyses indicate that the association between elder abuse and metabolic syndromes may be moderated by sociodemographic characteristics but not by health-related or psychosocial factors. Conclusion: Elder abuse is associated with an increased risk for metabolic syndromes. Research is needed to examine the association between elder abuse and cardiovascular disease. © 2014 S. Karger AG, Basel.
    Gerontology 11/2014; 61(5). DOI:10.1159/000368577
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    ABSTRACT: New neurons are continuously generated and added to neural circuits in the adult brain. However, increasing age imposes changes in neural progenitor cells and their microenvironment that lead to a reduction of neurogenesis. Age-related decreased production of new neurons in the neurogenic dentate gyrus has been associated with memory impairments. Several mechanisms are known that might counteract this decline in cognitive functions. Here, we give an overview of ageing-related changes in neurogenesis in the brain of humans and rodents. We discuss possible causes for reduced neurogenesis with age, its consequences on cognition, and how neurogenesis might be restored in old age. © 2014 S. Karger AG, Basel.
    Gerontology 11/2014; 61(4). DOI:10.1159/000368575
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    ABSTRACT: The most common form of sensory disability is age-related hearing loss (ARHL), also referred to as presbycusis. ARHL is a complex disorder with a mixture of genetic and environmental components, a combination that leads to a progressive decline in hearing function with increased age. In the last 15 years, there has been a vast increase in our knowledge of the genes that underlie congenital deafness and the critical components of hearing. In contrast, knowledge of the pathological processes involved in ARHL remains very limited. The mouse has proved an essential tool in the identification of early-onset deafness genes and in revealing the basic mechanisms of hearing. As focus is now turning toward elucidating the most common form of hearing loss, ARHL, the mouse will again play a fundamental role in this research. Here, we review the need for an animal model and discuss the suitability of the mouse as an ARHL model. Finally, we outline the ways in which hearing researchers are utilising the mouse in the investigation of ARHL and provide perspectives on the need for these data to be integrated with the results of human genetic studies. © 2014 S. Karger AG, Basel.
    Gerontology 11/2014; 61(2). DOI:10.1159/000368399