Ageing research reviews (Ageing Res Rev )

Publisher: Elsevier

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.

  • Impact factor
    5.62
  • 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

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Pre-print allowed on any website or open access repository
    • Voluntary deposit by author of authors post-print allowed on authors' personal website, arXiv.org or institutions open scholarly website including Institutional Repository, without embargo, where there is not a policy or mandate
    • Deposit due to Funding Body, Institutional and Governmental policy or mandate only allowed where separate agreement between repository and the publisher exists.
    • 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 .
    • Set statement to accompany deposit
    • Published source must be acknowledged
    • Must link to journal home page or articles' DOI
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • NIH Authors articles will be submitted to PubMed Central after 12 months
    • Publisher last contacted on 18/10/2013
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Lipid dysfunction, inflammation, immune response and advanced aging are major factors involved in the initiation and progression of atherosclerosis. MicroRNAs (miRNAs) have emerged as important regulators of gene expression that post transcriptionally modify cellular responses and function. MiRNA's are crucially involved in several vascular pathologies which show a clear association with increasing age(Dimmeler and Nicotera, 2013). Several studies have demonstrated that miRNA dysregulation has a in atherosclerotic disease, encompassing every step from plaque formation to destabilization and rupture. This review will present the recent advances in the elucidation of the complex pathophysiological mechanisms in vascular aging by which miRNAs regulate the different phases of atherosclerotic process with a focus on endothelial cells and both, innate and adaptive immune systems. Furthermore, the future areas of research and potential clinical strategies will be discussed.
    Ageing research reviews 09/2014;
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    ABSTRACT: Non-coding RNAs, such as microRNAs and long non-coding RNAs, represent the next major step in understanding the complexity of gene regulation and expression. In the past decade, tremendous efforts have been put mainly into identifying microRNAs that are changed in Alzheimer's disease, with the goal to provide biomarkers of the disease and to better characterize molecular pathways that are deregulated concomitantly to the formation of Tau and amyloid aggregates. This review underlines the importance of correctly defining, in a deluge of high-throughput data, which microRNAs are abnormally expressed in Alzheimer's disease patients. Despite a clear lack of consensus on the topic, miR-132 is emerging as a neuronal microRNA being gradually down-regulated during disease and showing important roles in the maintenance of brain integrity. Insight into the biological importance of other classes of non-coding RNAs also rapidly increased over the last years and therefore we discuss the possible implication of long non-coding RNAs in Alzheimer's disease.
    Ageing research reviews 09/2014;
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    ABSTRACT: As the link between metabolism and major disease processes becomes more well-defined, the identification of key molecular targets is leading to new therapeutic strategies. As a result, small non-coding RNA molecules that regulate gene expression via epigenetic alterations, microRNAs have been identified as regulators of these metabolic processes. In the last decade, dietary interventions have been used to change metabolism and to potentially alter disease progression and clinical outcomes. These interventions have been linked, at a molecular level, to microRNAs. This review will summarize the role of various dietary strategies on the expression of several microRNA families.
    Ageing research reviews 05/2014;
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    ABSTRACT: The skin protects humans from the surrounding environment. Tissues undergo continuous renewal throughout an individual's lifetime; however, there is a decline in the regenerative potential of tissue with age. The accumulation of senescent cells over time probably reduces tissue regenerative capacity and contributes to the physiological ageing of the tissue itself. The mechanisms that govern ageing remain unclear and are under intense investigation, and insight could be gained by studying the mechanisms involved in cellular senescence. In vitro, keratinocytes and dermal fibroblasts undergo senescence in response to multiple cellular stresses, including the overproduction of reactive oxygen species and the shortening of telomeres, or simply by reaching the end of their replicative potential (i.e., reaching replicative senescence). Recent findings demonstrate that microRNAs play key roles in regulating the balance between a cell's proliferative capacity and replicative senescence. Here, we will focus on the molecular mechanisms regulated by senescence-associated microRNAs and their validated targets in both keratinocytes and dermal fibroblasts.
    Ageing research reviews 04/2014;
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    ABSTRACT: A growing body of evidence shows that microRNA expression changes with age in animals ranging from nematode to human. Genetic studies of microRNA function in vivo provide the means to move beyond correlation and to explore cause-effect relationships. Genetic studies in C. elegans and Drosophila have identified cellular pathways involved in organismal aging. Here, we review the evidence that microRNAs act in vivo as regulators of aging pathways, with emphasis on Drosophila.
    Ageing research reviews 04/2014;
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    ABSTRACT: The generation of ROS underlies all solar infrared-affected therapeutic and pathological cutaneous effects. The signaling pathway NF-kB is responsible for the induced therapeutic effects, while the AP-1 for the pathological effects. The different signaling pathways of infrared-induced ROS and infrared-induced heat shock ROS were shown to act independently multiplying the influence on each other by increasing the doses of irradiation and/or increasing the temperature. The molecular action mechanisms of solar infrared radiation and heat on human skin are summarized and discussed in detail in the present paper. The critical doses are determined. Protection strategies against infrared-induced skin damage are proposed.
    Ageing research reviews 04/2014;
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    ABSTRACT: Angiogenesis is generally a quiescent process which, however, may be modified by different physiological and pathological conditions. The "angiogenic paradox" has been described in diabetes because this disease impairs the angiogenic response in a manner that differs depending on the organs involved and disease evolution. Aging is also associated with pro- and antiangiogenic processes. Glycation, the post-translational modification of proteins, increases with aging and the progression of diabetes. The effect of glycation on angiogenesis depends on the type of glycated proteins and cells involved. This complex link could be responsible for the "angiogenic paradox" in aging and age-related disorders and diseases. Using diabetes as a model, the present work has attempted to review the age-related angiogenic paradox, in particular the effects of glycation on angiogenesis during aging.
    Ageing research reviews 04/2014;
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    ABSTRACT: As the second most common age related neurodegenerative disease after Alzheimer's disease, the health, social and economic impact resulting from Parkinson's disease will continue to increase alongside the longevity of the population. Ageing remains the biggest risk factor for developing idiopathic Parkinson's disease. Although research into the mechanisms leading to cell death in Parkinson's disease has shed light on many aspects of the pathogenesis of this disorder, we still cannot answer the fundamental question, what specific age related factors predispose some individuals to develop this common neurodegenerative disease. In this review we focus specifically on the neuronal population associated with the motor symptoms of Parkinson's disease, the dopaminergic neurons of the substantia nigra, and try to understand how ageing puts these neurons at risk to the extent that a slight change in protein metabolism or mitochondrial function can push the cells over the edge leading to catastrophic cell death and many of the symptoms seen in Parkinson's disease. We review the evidence that ageing is important for the development of Parkinson's disease and how age related decline leads to the loss of neurons within this disease, before describing exactly how advancing age may lead to substantia nigra neuronal loss and Parkinson's disease in some individuals.
    Ageing research reviews 02/2014;
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    ABSTRACT: Parkinson's disease (PD) is the most common motor system disorder affecting 1-2% of people over the age of sixty-five. Although PD is generally a sporadic neurological disorder, the discovery of monogenic, hereditable forms of the disease, representing 5-10% of all cases, has been very important in helping to partially delineate the molecular pathways that lead to this pathology. These mechanisms include impairment of the intracellular protein-degradation pathways, protein aggregation, mitochondria dysfunction, oxidative stress and neuroinflammation. Some of these features are also supported by post-mortem analyses. One of the main pathological hallmarks of PD is the preferential degeneration of dopaminergic neurons, which supports a direct role of dopamine itself in promoting the disorder. This review presents a comprehensive overview of the existing literature that links the aforementioned pathways to the oxidative chemistry of dopamine, ultimately leading to the formation of free radicals and reactive quinone species. We emphasize, in particular, how the reaction of dopamine-derived quinones with several cellular targets could foster the processes involved in the pathogenesis of PD and contribute to the progression of the disorder.
    Ageing research reviews 01/2014;