Mechanisms of ageing and development

Publisher: Elsevier

Journal description

Current impact factor: 3.51

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 3.51
2012 Impact Factor 3.264
2011 Impact Factor 3.439
2010 Impact Factor 4.857
2009 Impact Factor 4.179
2008 Impact Factor 3.915
2007 Impact Factor 4.308
2006 Impact Factor 3.846
2005 Impact Factor 2.812
2004 Impact Factor 2.866
2003 Impact Factor 3.214
2002 Impact Factor 2.867
2001 Impact Factor 1.841
2000 Impact Factor 1.897
1999 Impact Factor 1.788
1998 Impact Factor 1.583
1997 Impact Factor 1.143
1996 Impact Factor 0.89
1995 Impact Factor 1.182
1994 Impact Factor 1.124
1993 Impact Factor 1.349
1992 Impact Factor 1.571

Impact factor over time

Impact factor

Additional details

5-year impact 3.91
Cited half-life 6.70
Immediacy index 0.63
Eigenfactor 0.02
Article influence 1.36
ISSN 1872-6216

Publisher details


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    • Voluntary deposit by author of authors post-print allowed on authors' personal website, 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 .
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    • 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

  • Sara Martire, Luciana Mosca, Maria D
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    ABSTRACT: DNA damage is the prime activator of the enzyme poly(ADP-ribose) polymerase1 (PARP-1) whose overactivation has been proven to be associated with the pathogenesis of numerous central nervous system disorders such as ischemia, neuroinflammation and neurodegenerative diseases. Under oxidative stress conditions PARP-1 activity increases, leading to an accumulation of ADP-ribose polymers and NAD(+) depletion, that induces energy crisis and finally cell death. This review aims to explain the contribution of PARP-1 in neurodegenerative diseases, focusing on Alzheimer's and Parkinson's disease, to stimulate further studies on this issue and thereby engage a new perspective regarding the design of possible therapeutic agents or the identification of biomarkers. Copyright © 2015. Published by Elsevier Ireland Ltd.
    Mechanisms of ageing and development 04/2015; DOI:10.1016/j.mad.2015.04.001
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    ABSTRACT: Changes in the abundance and post-translational modification of proteins and accumulation of some covalently modified proteins have been proposed to represent hallmarks of biological ageing. Within the frame of the Mark-Age project, the workpackage dedicated to "markers based on proteins and their modifications" has been firstly focused on enzymatic and non-enzymatic post-translational modifications of serum proteins by carbohydrates. The second focus of the workpackage has been directed towards protein maintenance systems that are involved either in protein quality control (ApoJ/Clusterin) or in the removal of oxidatively damaged proteins through degradation and repair (proteasome and methionine sulfoxide reductase systems). This review describes the most relevant features of these protein modifications and maintenance systems, their fate during ageing and/or their implication in ageing and longevity. Copyright © 2015 Z. Published by Elsevier Ireland Ltd.. All rights reserved.
    Mechanisms of ageing and development 04/2015; 83. DOI:10.1016/j.mad.2015.03.009
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    ABSTRACT: In multicellular organisms the proper system functionality is ensured by the balance between cell division, differentiation, senescence and death. This balance is changed during aging. Immunosenescence plays a crucial role in aging and leads to the shrinkage of T cell repertoire and the propensity to apoptosis. The elimination of expanded T cells at the end of immune response is crucial to maintain homeostasis and avoid any uncontrolled inflammation. Resting mature T lymphocytes, when activated via their antigen-specific receptor (TCR) and CD28 co-receptor, start to proliferate and then undergo the so called Activation Induced Cell Death (AICD), which mechanistically is triggered by the death receptor and leads to activation of the extrinsic signaling apoptotic pathway overlapping with mitochondrial (intrinsic) signaling to apoptosis. T lymphocytes, like other cells, are also exposed to damage, which can trigger the so called damage-induced cell death (DICD). It was hypothesized that oxidative stress and chronic antigenic load increasing with age reduced lymphocyte susceptibility to DICD and enhanced a proinflamatory status leading to increased AICD. However, data collected so far are inconsistent and does not support this assumption. Systematic and comprehensive studies are still needed for conclusive elucidation of the role of AICD and DICD in human immunosenescence, including the role of autophagy and necroptosis in the processes. Copyright © 2015. Published by Elsevier Ireland Ltd.
    Mechanisms of ageing and development 04/2015; DOI:10.1016/j.mad.2015.03.011
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    ABSTRACT: Though defective genome maintenance and DNA repair have long been know to promote phenotypes of premature aging, the role protein methylation plays in these processes is only now emerging. We have recently identified the first N-terminal methyltransferase, NRMT1, which regulates protein-DNA interactions and is necessary for both accurate mitotic division and nucleotide excision repair. To demonstrate if complete loss of NRMT1 subsequently resulted in developmental or aging phenotypes, we constructed the first NRMT1 knockout (Nrmt1(-/-)) mouse. The majority of these mice die shortly after birth. However, the ones that survive exhibit decreased body size, female-specific infertility, kyphosis, decreased mitochondrial function, and early-onset liver degeneration; phenotypes characteristic of other mouse models deficient in DNA repair. The livers from Nrmt1(-/-) mice produce less reactive oxygen species (ROS) than wild type controls, and Nrmt1(-/-) mouse embryonic fibroblasts show a decreased capacity for handling oxidative damage. This indicates that decreased mitochondrial function may benefit Nrmt1(-/-) mice and protect them from excess internal ROS and subsequent DNA damage. These studies position the NRMT1 knockout mouse as a useful new system for studying the effects of genomic instability and defective DNA damage repair on organismal and tissue-specific aging. Copyright © 2015. Published by Elsevier Ireland Ltd.
    Mechanisms of ageing and development 04/2015; 146. DOI:10.1016/j.mad.2015.03.012
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    ABSTRACT: In the context of the MARK-AGE study, anthropometric, clinical and social data as well as samples of venous blood, buccal mucosal cells and urine were systematically collected from 3337 volunteers. Information from about 500 standardised questions and about 500 analysed biomarkers needed to be documented per individual. On the one hand handling with such a vast amount of data necessitates the use of appropriate informatics tools and the establishment of a database. On the other hand personal information on subjects obtained as a result of such studies has, of course, to be kept confidential, and therefore the investigators must ensure that the subjects' anonymity will be maintained. Such secrecy obligation implies a well-designed and secure system for data storage. In order to fulfil the demands of the MARK-AGE study we established a phenotypic database for storing information on the study subjects by using a doubly coded system. Copyright © 2015. Published by Elsevier Ireland Ltd.
    Mechanisms of ageing and development 03/2015; DOI:10.1016/j.mad.2015.03.005
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    ABSTRACT: Oxidized LDL (oxLDL) and nitric oxide (NO) exert contradictory actions within the vascular endothelium microenvironment influencing key events in atherogenesis. OxLDL and NO are so far regarded as representative parameters of oxidative stress and endothelial dysfunction, new targets in prevention, diagnosis and therapy of cardiovascular diseases, and also as candidate biomarkers in evaluating the human biological age. The aim of this review is to explore recent literature on molecular mechanisms and pathophysiological relationships between LDL oxidation, NO synthesis and vascular endothelium function/dysfunction in ageing, focusing on the following aspects: (1) the impact of metabolic status on both LDL oxidation and NO synthesis in relation with oxidative stress, (2) the use of oxidized LDL and NO activity as biomarkers in human studies reporting on cardiovascular outcomes, and (3) evidences supporting the importance of oxidized LDL and NO activity as relevant biomarkers in vascular ageing and age-related diseases. Copyright © 2015. Published by Elsevier Ireland Ltd.
    Mechanisms of ageing and development 03/2015; DOI:10.1016/j.mad.2015.03.003
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    ABSTRACT: Genes which confer a relative longevity advantage may be regulated at the level of transcription or translation. Alternatively, pro-longevity genes may mediate their effects at the level of protein structure-functional relationships that are beneficially optimized in long-lived species. Longevity associated genes (LAGs) may be operationally defined as genes that confer beneficial effects and are relatively more conserved among long-lived species. Global and local protein sequence alignments of over 10,000 genes across at least 30 mammalian species were examined to identify LAGs. Known LAGs, including growth hormone receptor (GHR), and breast cancer 1, early onset (BRCA1), have strong associations with maximum lifespan by our analysis. Several common categories of protein function were observed among genes ranked with the strongest associations with MLS identified by all regression models. These genes included those that function in the immune system, cell cycle regulation, and DNA damage response. We provide a ranking of genes with the strongest associations with species maximum lifespan (MLS) by several phylogenetic generalized least squares regression models, including adjustment for confounding variables such as body weight and gestation length. Copyright © 2015. Published by Elsevier Ireland Ltd.
    Mechanisms of ageing and development 03/2015; DOI:10.1016/j.mad.2015.03.004
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    ABSTRACT: p53 and NF-κB are key transcription factors in regulating the gene expression program of cellular and organismal senescence. PPM1B is a member of the protein phosphatase 2 C family and plays a role in negatively regulating p53 and NF-κB thereby possibly attenuating the gene expression program of cellular senescence. Here, possible involvement of PPM1B in replicative senescence has been investigated using the in vitro aging model of IMR-90 cells. PPM1B protein levels are progressively decreased in a replicative age-dependent manner. Importantly, PPM1B depletion induces a robust senescence phenotype as evidenced by significant growth arrest and senescence marker expression. Given that PPM1B depletion-induced senescence is partially rescued by inactivating p38 MAPK, our results identify PPM1B as a critical regulator of both p38 MAPK-dependent and -independent senescence pathways during normal cellular aging process.
    Mechanisms of ageing and development 06/2014; DOI:10.1016/j.mad.2014.03.003
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    ABSTRACT: Does aging in itself lead to alteration in adrenocortical mitochondrial oxidative phosphorylation? Mitochondria from Fischer 344 (F344) rats (6 and 24 months old), Brown Norway rats (6 and 32 months old) and F344-Brown Norway hybrid rats (6 and 30 months old) were compared. Mitochondria were isolated from extirpated adrenal cortex. The yields of mitochondria were quantitatively similar in all rat strains irrespective of age. In order to assess the activity of each mitochondrial complex, several different substrates were tested and the rate of oxidative phosphorylation measured. Aging does not affect mitochondrial activity except in the F344 rat adrenal cortex where the maximal ADP-stimulated oxidative phosphorylation decreased with age. We hypothesize that impaired synthesis of steroid hormones by the adrenal cortex with age in F344 rats might be due to decreased adrenocortical mitochondrial oxidative phosphorylation. We conclude that aging results in adrenocortical mitochondria effects that are non-uniform across different rat strains.
    Mechanisms of ageing and development 01/2014; DOI:10.1016/j.mad.2014.01.009