Ageing research reviews (Ageing Res Rev)

Publisher: Elsevier Masson

Journal description

As the average human life expectancy has increased, so too has the impact of ageing and age-related disease on ou society. Ageing research is now the focus of thousands of laboratories that include leaders in the areas of genetics, molecular and cellular biology, biochemistry, and behaviour. Ageing Research Reviews (ARR) covers the trends in this field. It is designed to fill a large void, namely, a source for critical reviews and viewpoints on emerging findings on mechanisms of ageing and age-related disease. Rapid advances in understanding of mechanisms that control cellular proliferation, differentiation and survival are leading to new insight into the regulation of ageing. From telomerase to stem cells to energy and oxyradical metabolism, this is an exciting new era in the multidisciplinary field of ageing research. The cellular and molecular underpinnings of manipulations that extend lifespan, such as caloric restriction, are being identified and novel approaches for preventing age-related diseases are being developed. ARR publishes articles on focussed topics selected from the broad field of ageing research, with an emphasis on cellular and molecular mechanisms of the aging process and age-related diseases such as cancer, cardiovascular disease, diabetes and neurodegenerative disorders. Applications of basic ageing research to lifespan extension and disease prevention are also covered in this journal.

Current impact factor: 4.94

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 4.94
2013 Impact Factor 7.628
2012 Impact Factor 5.953
2011 Impact Factor 6.174
2010 Impact Factor 9
2009 Impact Factor 5.622
2008 Impact Factor 6.209
2007 Impact Factor 6.365
2006 Impact Factor 4.526
2005 Impact Factor 4.151
2004 Impact Factor 4.953
2003 Impact Factor 3.795

Impact factor over time

Impact factor

Additional details

5-year impact 6.36
Cited half-life 4.50
Immediacy index 1.54
Eigenfactor 0.01
Article influence 1.81
Website Ageing Research Reviews website
ISSN 1872-9649

Publisher details

Elsevier Masson

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 01/05/2015
    • 'Elsevier Masson' is an imprint of 'Elsevier'
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: This systematic review and meta-analysis of randomized controlled trials assessed the effects of exercise on behavioral and psychological symptoms of dementia (BPSD, including depression) in people with dementia (PWD). Secondary outcomes for the effects of exercise were mortality and antipsychotic use. Twenty studies were included in this review (n=18 in the meta-analysis). Most studies used a multicomponent exercise training (n=13) as intervention; the control group was often a usual care (n=10) or a socially-active (n=8) group. Exercise did not reduce global levels of BPSD (n=4. Weighted mean difference -3.884; 95% CI -8.969 to 1.201; I(2)=69.4%). Exercise significantly reduced depression levels in PWD (n=7. Standardized mean difference -0.306; 95% CI -0.571 to -0.041; I(2)=46.8%); similar patterns were obtained in sensitivity analysis performed among studies with: institutionalized people (p=0.038), multicomponent training (p=0.056), social control group (p=0.08), and low risk of attrition bias (p=0.11). Exploratory analysis showed that the principal BPSD (other than depression) positively affected by exercise was aberrant motor behaviour. Exercise had no effect on mortality. Data on antipsychotics were scarce. In conclusion, exercise reduces depression levels in PWD. Future studies should examine whether exercise reduces the use (and doses) of antipsychotics and other drugs often used to manage BPSD.
    Ageing research reviews 09/2015; DOI:10.1016/j.arr.2015.09.001
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    ABSTRACT: Skeletal muscle homeostasis depends on an intricate balance between muscle hypertrophy, atrophy and regeneration. As we age, maintenance of muscle homeostasis is perturbed, resulting in a loss of muscle mass and function, termed sarcopenia. Individuals with sarcopenia exhibit impaired balance, increased falls (leading to subsequent injury) and an overall decline in quality of life. The mechanisms mediating sarcopenia are still not fully understood but clarity in our understanding of the precise pathophysiological changes occurring during skeletal muscle ageing has improved dramatically. Advances in transcriptomics has highlighted significant deregulation in skeletal muscle gene expression with ageing, suggesting epigenetic alterations may play a crucial and potentially causative role in the skeletal muscle ageing process. microRNAs (miRNAs, miRs), novel regulators of gene expression, can modulate many processes in skeletal muscle, including myogenesis, tissue regeneration and cellular programming. Expression of numerous evolutionary conserved miRNAs is disrupted in skeletal muscle with age. Given that a single miRNA can simultaneously affect the functionality of multiple signaling pathways, miRNAs are potent modulators of pathophysiological changes. miRNA-based interventions provide a promising new therapeutic strategy against alterations in muscle homeostasis. The aim of this review is two-fold; firstly to outline the latest understanding of the pathophysiological alterations impacting the deregulation of skeletal muscle mass and function with ageing, and secondly, to highlight the mounting evidence for a role of miRNAs in modulating muscle mass, and the need to explore their specific role in sarcopenia. Copyright © 2015. Published by Elsevier B.V.
    Ageing research reviews 09/2015; DOI:10.1016/j.arr.2015.08.007
  • Ageing research reviews 09/2015; 23(Pt A):1-2. DOI:10.1016/j.arr.2015.06.001
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    ABSTRACT: Autophagy, a major catabolic pathway responsible of the elimination of damaged proteins and organelles, is now recognized as an anti-aging process. In addition to its basal role in cell homeostasis, autophagy is also a stress-responsive mechanism for survival purposes. Here, we review recent literature to highlight the autophagy role in the different bone cell types, i.e. osteoblasts, osteoclasts and osteocytes. We also discuss the effects of autophagy modulators in bone physiology and of bone anabolic compounds in autophagy. Finally, we analyzed studies regarding bone cell autophagy-deficient mouse models to obtain a more general view on how autophagy modulates bone physiology and pathophysiology, particularly during aging. Copyright © 2015. Published by Elsevier B.V.
    Ageing research reviews 08/2015; DOI:10.1016/j.arr.2015.08.004
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    ABSTRACT: Alzheimer's disease (AD) disproportionally affects women and men. The female susceptibility for AD has been largely associated with the loss of ovarian sex hormones during menopause. This review examines current understanding of the role of estrogen receptor β (ERβ) in the regulation of neurological health and its implication in the development and intervention of AD. Since its discovery in 1996, research conducted over the last 15-20 years has documented a great deal of evidence indicating that ERβ plays a pivotal role in a broad spectrum of brain activities from development to aging. ERβ genetic polymorphisms have been associated with cognitive impairment and increased risk for AD predominantly in women. The role of ERβ in the intervention of AD has been demonstrated by the alteration of AD pathology in response to treatment with ERβ-selective modulators in transgenic models that display pronounced plaque and tangle histopathological presentations as well as learning and memory deficits. Future studies that explore the potential interactions between ERβ signaling and the genetic isoforms of human apolipoprotein E (APOE) in brain aging and development of AD-risk phenotype are critically needed. The current trend of lost-in-translation in AD drug development that has primarily been based on early-onset familial AD (FAD) models underscores the urgent need for novel models that recapitulate the etiology of late-onset sporadic AD (SAD), the most common form of AD representing more than 95% of the current human AD population. Combining the use of FAD-related models that generally have excellent face validity with SAD-related models that hold more reliable construct validity would together increase the predictive validity of preclinical findings for successful translation into humans. Copyright © 2015. Published by Elsevier B.V.
    Ageing research reviews 08/2015; DOI:10.1016/j.arr.2015.08.001
  • [Show abstract] [Hide abstract]
    ABSTRACT: Medical advancements have increased life expectancy but have consequently increased the incidence of age-related disease. Fasting or dietary restriction (DR) can help prevent these via anti-ageing effects; however, these effects in neurons are less well characterized. Here, a series of animal and human studies of the effects of DR on the structural and functional integrity of neurons and the underlying mechanisms are analyzed. DR improves the integrity of animal neurons via a wide range of possible mechanisms including changes in metabolism, oxidative damage, stress responses, growth factors and gene expression. These mechanisms are extensively interlinked and point to an optimum range of calorie intake, above calorie deprivation and below burdensome calorie excess. Human studies also suggest that DR improves neuron integrity; however due to ethical and methodological limitations, the most conclusive data on DR hinge upon on-going life-long monkey experiments. Rather than developing pharmacological mimetics of DR, our focus should be on educating the public about DR in order to minimize age-related disease. Copyright © 2015. Published by Elsevier B.V.
    Ageing research reviews 08/2015; DOI:10.1016/j.arr.2015.07.010
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    ABSTRACT: Age-related cognitive changes often include difficulties in retrieving memories, particularly those that rely on personal experiences within their temporal and spatial contexts (i.e., episodic memories). This decline may vary depending on the studied phase (i.e., encoding, storage or retrieval), according to inter-individual differences, and whether we are talking about normal or pathological (e.g., Alzheimer disease; AD) aging. Such cognitive changes are associated with different structural and functional alterations in the human neural network that underpins episodic memory. The prefrontal cortex is the first structure to be affected by age, followed by the medial temporal lobe (MTL), the parietal cortex and the cerebellum. In AD, however, the modifications occur mainly in the MTL (hippocampus and adjacent structures) before spreading to the neocortex. In this review, we will present results that attempt to characterize normal and pathological cognitive aging at multiple levels by integrating structural, behavioral, inter-individual and neuroimaging measures of episodic memory. Copyright © 2015. Published by Elsevier B.V.
    Ageing research reviews 08/2015; DOI:10.1016/j.arr.2015.08.006
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    ABSTRACT: Influenza A virus (IAV) is a serious global health problem worldwide due to frequent and severe outbreaks. IAV causes significant morbidity and mortality in the elderly population, due to the ineffectiveness of the vaccine and the alteration of T cell immunity with ageing. The cellular and molecular link between ageing and virus infection is unclear and it is possible that damage associated molecular patterns (DAMPs) may play a role in the raised severity and susceptibility of virus infections in the elderly. DAMPs which are released from damaged cells following activation, injury or cell death can activate the immune response through the stimulation of the inflammasome through several types of receptors found on the plasma membrane, inside endosomes after endocytosis as well as in the cytosol. In this review, the detriment in the immune system during aging and the links between influenza virus infection and ageing will be discussed. In addition, the role of DAMPs such as HMGB1 and S100/Annexin in ageing, and will in the enhanced morbidity and mortality to severe influenza infection in ageing will be highlighted. Copyright © 2015. Published by Elsevier B.V.
    Ageing research reviews 07/2015; DOI:10.1016/j.arr.2015.07.005