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: 7.63

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 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
Year

Additional details

5-year impact 6.33
Cited half-life 4.50
Immediacy index 1.50
Eigenfactor 0.01
Article influence 1.93
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

  • 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
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    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: Drosophila is one of the most convenient model organisms in the genetics of aging and longevity. Unlike the nematodes, which allow for the detection of new pro-aging genes by knockout and RNAi-mediated knock-down, Drosophila also provides an opportunity to find new pro-longevity genes by driver-induced overexpression. Similar studies on other models are extremely rare. In this review we focused on genes whose overexpression prolongs the life of fruit flies. The majority of longevity-associated genes regulates metabolism and stress resistance, and belong to the IGF-1R, PI3K, PKB, AMPK and TOR metabolic regulation cluster and the FOXO, HDAC, p53 stress response cluster. Copyright © 2015. Published by Elsevier B.V.
    Ageing research reviews 08/2015; DOI:10.1016/j.arr.2015.08.005
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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: Apart from the classical function of regulating intestinal, bone and kidney calcium and phosphorus absorption as well as bone mineralization, there is growing evidence for the neuroprotective function of vitamin D3 through neuronal calcium regulation, the antioxidative pathway, immunomodulation and detoxification. Vitamin D3 and its derivates influence directly or indirectly almost all metabolic processes such as proliferation, differentiation, apoptosis, inflammatory processes and mutagenesis (Fig 1.). Such multifactorial effects of vitamin D3 can be a profitable source of new therapeutic solutions for two radically divergent diseases, cancer and neurodegeneration. Interestingly, an unusual association seems to exist between the occurrence of these two pathological states, called "inverse comorbidity". Patients with cognitive dysfunctions or dementia have considerably lower risk of cancer, whereas survivors of cancer have lower prevalence of central nervous system (CNS) disorders. To our knowledge, there are few publications analyzing the role of vitamin D3 in biological pathways existing in carcinogenic and neuropathological disorders. Copyright © 2015. Published by Elsevier B.V.
    Ageing research reviews 07/2015; DOI:10.1016/j.arr.2015.07.008
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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
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    ABSTRACT: Diabetes, a group of metabolic and age-related diseases, is a major global health problem, the incidence of which has increased dramatically in recent decades. Type 1 diabetes mellitus (T1DM) is a complex, T cell-mediated autoimmune disease characterized by immune cell infiltration and chronic inflammation in the islets of Langerhans. Type 2 diabetes mellitus (T2DM) is a complex metabolic disease characterized by hyperglycemia (high blood sugar) resulting from insulin resistance and β-cell dysfunction. The involvement of inflammatory processes, such as immune cell infiltration, and chronic inflammation in the pathogenesis of diabetes is less well understood in T2DM than in T1DM. However, studies conducted in the past decade have shown a strong link between inflammation and metabolic dysfunction. They have also shown that chronic inflammation plays a key role in the pathogenesis of both T1DM and T2DM. Two immunological factors commonly contribute to the pathogenesis of diabetes: the activation of inflammasomes and the release of proinflammatory cytokines in response to damage-associated molecular patterns (DAMPs). Inflammasomes are intracellular multiprotein molecular platforms. DAMPs act as endogenous danger signals. Here, we review current research on the function(s) of inflammasomes and DAMPs and discuss their pathological relevance and therapeutic implications in diabetes. Copyright © 2015 Elsevier B.V. All rights reserved.
    Ageing research reviews 07/2015; DOI:10.1016/j.arr.2015.06.004
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    ABSTRACT: Accumulating evidence points to a link between age-related hearing loss and cognitive decline, but their relationship is not clear. Does one cause the other, or does some third factor produce both? The answer has critical implications for prevention, rehabilitation, and health policy but has been difficult to establish for several reasons. First, determining a causal relationship in natural, correlational samples is problematic, and hearing and cognition are difficult to measure independently. Here, we critically review the evidence for a link between hearing loss and cognitive decline. We conclude that the evidence is convincing, but that the effects are small when hearing is measured audiometrically. We review four different directional hypotheses that have been offered as explanations for such a link, and conclude that no single hypothesis is sufficient. We introduce a framework that highlights that hearing and cognition rely on shared neurocognitive resources, and relate to each other in several different ways. We also discuss interventions for sensory and cognitive decline that may permit more causal inferences. Copyright © 2015. Published by Elsevier B.V.
    Ageing research reviews 06/2015; DOI:10.1016/j.arr.2015.06.002
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    ABSTRACT: This essay begins by proposing that muscle weakness of old age from sarcopenia is due in large part to reduced capillary density in the muscles, as documented in 9 reports of aged persons and animals. Capillary density (CD) is determined by local levels of various angiogenic factors, which also decline in muscles with aging, as reported in 7 studies of old persons and animals. There are also numerous reports of reduced CD in the aged brain and other studies showing reduced CD in the kidney and heart of aged animals. Thus a waning angiogenesis throughout the body may be a natural occurrence in later years and may account significantly for the lesser ailments (physical and cognitive) of elderly people. Old age is regarded here as a deficiency state which may be corrected by therapeutic angiogenesis, much as a hormonal deficiency can be relieved by the appropriate hormone therapy. Such therapy could employ recombinant angiogenic factors which are now commercially available. Copyright © 2015 Elsevier B.V. All rights reserved.
    Ageing research reviews 06/2015; DOI:10.1016/j.arr.2015.03.005