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  Subjects -> BIOLOGY (Total: 3041 journals)
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    - BIOLOGY (1442 journals)
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    - ZOOLOGY (136 journals)

BIOLOGY (1442 journals)                  1 2 3 4 5 6 7 8 | Last

Showing 1 - 200 of 1720 Journals sorted alphabetically
AAPS Journal     Hybrid Journal   (Followers: 22)
Achievements in the Life Sciences     Open Access   (Followers: 4)
ACS Synthetic Biology     Full-text available via subscription   (Followers: 23)
Acta Biologica Colombiana     Open Access   (Followers: 7)
Acta Biologica Hungarica     Full-text available via subscription   (Followers: 4)
Acta Biologica Sibirica     Open Access  
Acta Biomaterialia     Hybrid Journal   (Followers: 26)
Acta Biotheoretica     Hybrid Journal   (Followers: 4)
Acta Chiropterologica     Full-text available via subscription   (Followers: 6)
acta ethologica     Hybrid Journal   (Followers: 4)
Acta Limnologica Brasiliensia     Open Access   (Followers: 3)
Acta Médica Costarricense     Open Access   (Followers: 2)
Acta Musei Silesiae, Scientiae Naturales : The Journal of Silesian Museum in Opava     Open Access  
Acta Neurobiologiae Experimentalis     Open Access  
Acta Parasitologica     Hybrid Journal   (Followers: 10)
Acta Scientiarum. Biological Sciences     Open Access   (Followers: 2)
Acta Scientifica Naturalis     Open Access   (Followers: 2)
Actualidades Biológicas     Open Access   (Followers: 1)
Advanced Health Care Technologies     Open Access   (Followers: 4)
Advanced Studies in Biology     Open Access  
Advances in Antiviral Drug Design     Full-text available via subscription   (Followers: 4)
Advances in Bioinformatics     Open Access   (Followers: 20)
Advances in Biological Regulation     Hybrid Journal   (Followers: 4)
Advances in Biosensors and Bioelectronics     Open Access   (Followers: 7)
Advances in Cell Biology     Open Access   (Followers: 25)
Advances in Cellular and Molecular Biology of Membranes and Organelles     Full-text available via subscription   (Followers: 13)
Advances in Developmental Biology     Full-text available via subscription   (Followers: 12)
Advances in DNA Sequence-Specific Agents     Full-text available via subscription   (Followers: 6)
Advances in Ecological Research     Full-text available via subscription   (Followers: 47)
Advances in Environmental Sciences - International Journal of the Bioflux Society     Open Access   (Followers: 21)
Advances in Enzyme Research     Open Access   (Followers: 9)
Advances in Experimental Biology     Full-text available via subscription   (Followers: 9)
Advances in Genome Biology     Full-text available via subscription   (Followers: 11)
Advances in High Energy Physics     Open Access   (Followers: 19)
Advances in Human Biology     Open Access   (Followers: 2)
Advances in Life Science and Technology     Open Access   (Followers: 14)
Advances in Life Sciences     Open Access   (Followers: 6)
Advances in Marine Biology     Full-text available via subscription   (Followers: 16)
Advances in Molecular and Cell Biology     Full-text available via subscription   (Followers: 23)
Advances in Organ Biology     Full-text available via subscription   (Followers: 2)
Advances in Planar Lipid Bilayers and Liposomes     Full-text available via subscription   (Followers: 3)
Advances in Regenerative Biology     Open Access   (Followers: 1)
Advances in Space Biology and Medicine     Full-text available via subscription   (Followers: 5)
Advances in Structural Biology     Full-text available via subscription   (Followers: 8)
Advances in Virus Research     Full-text available via subscription   (Followers: 6)
African Journal of Range & Forage Science     Hybrid Journal   (Followers: 6)
AFRREV STECH : An International Journal of Science and Technology     Open Access   (Followers: 1)
Ageing Research Reviews     Hybrid Journal   (Followers: 9)
Aging Cell     Open Access   (Followers: 11)
Agrokémia és Talajtan     Full-text available via subscription   (Followers: 2)
Agrokreatif Jurnal Ilmiah Pengabdian kepada Masyarakat     Open Access  
AJP Cell Physiology     Full-text available via subscription   (Followers: 14)
AJP Endocrinology and Metabolism     Full-text available via subscription   (Followers: 23)
AJP Lung Cellular and Molecular Physiology     Full-text available via subscription   (Followers: 3)
Al-Kauniyah : Jurnal Biologi     Open Access  
Alasbimn Journal     Open Access   (Followers: 1)
AMB Express     Open Access   (Followers: 1)
Ambix     Hybrid Journal   (Followers: 3)
American Biology Teacher     Full-text available via subscription   (Followers: 13)
American Fern Journal     Full-text available via subscription   (Followers: 1)
American Journal of Agricultural and Biological Sciences     Open Access   (Followers: 10)
American Journal of Bioethics     Hybrid Journal   (Followers: 10)
American Journal of Human Biology     Hybrid Journal   (Followers: 13)
American Journal of Medical and Biological Research     Open Access   (Followers: 8)
American Journal of Plant Sciences     Open Access   (Followers: 18)
American Journal of Primatology     Hybrid Journal   (Followers: 15)
American Malacological Bulletin     Full-text available via subscription   (Followers: 3)
American Naturalist     Full-text available via subscription   (Followers: 74)
Amphibia-Reptilia     Hybrid Journal   (Followers: 6)
Anaerobe     Hybrid Journal   (Followers: 4)
Analytical Methods     Full-text available via subscription   (Followers: 11)
Anatomical Science International     Hybrid Journal   (Followers: 2)
Animal Cells and Systems     Hybrid Journal   (Followers: 4)
Annales de Limnologie - International Journal of Limnology     Hybrid Journal   (Followers: 1)
Annales françaises d'Oto-rhino-laryngologie et de Pathologie Cervico-faciale     Full-text available via subscription   (Followers: 3)
Annales Henri Poincaré     Hybrid Journal   (Followers: 3)
Annales UMCS, Biologia     Open Access   (Followers: 1)
Annals of Applied Biology     Hybrid Journal   (Followers: 7)
Annals of Biomedical Engineering     Hybrid Journal   (Followers: 18)
Annals of Human Biology     Hybrid Journal   (Followers: 5)
Annual Review of Biomedical Engineering     Full-text available via subscription   (Followers: 14)
Annual Review of Biophysics     Full-text available via subscription   (Followers: 23)
Annual Review of Cancer Biology     Full-text available via subscription   (Followers: 1)
Annual Review of Cell and Developmental Biology     Full-text available via subscription   (Followers: 37)
Annual Review of Food Science and Technology     Full-text available via subscription   (Followers: 16)
Annual Review of Genomics and Human Genetics     Full-text available via subscription   (Followers: 22)
Annual Review of Phytopathology     Full-text available via subscription   (Followers: 10)
Anthropological Review     Open Access   (Followers: 24)
Anti-Infective Agents     Hybrid Journal   (Followers: 3)
Antibiotics     Open Access   (Followers: 9)
Antioxidants     Open Access   (Followers: 4)
Antioxidants & Redox Signaling     Hybrid Journal   (Followers: 9)
Antonie van Leeuwenhoek     Hybrid Journal   (Followers: 5)
Anzeiger für Schädlingskunde     Hybrid Journal   (Followers: 1)
Apidologie     Hybrid Journal   (Followers: 4)
Apmis     Hybrid Journal   (Followers: 1)
APOPTOSIS     Hybrid Journal   (Followers: 8)
Applied Bionics and Biomechanics     Open Access   (Followers: 8)
Applied Vegetation Science     Full-text available via subscription   (Followers: 9)
Aquaculture Environment Interactions     Open Access   (Followers: 2)
Aquaculture International     Hybrid Journal   (Followers: 22)
Aquaculture Reports     Open Access   (Followers: 3)
Aquaculture, Aquarium, Conservation & Legislation - International Journal of the Bioflux Society     Open Access   (Followers: 6)
Aquatic Biology     Open Access   (Followers: 5)
Aquatic Ecology     Hybrid Journal   (Followers: 32)
Aquatic Ecosystem Health & Management     Hybrid Journal   (Followers: 14)
Aquatic Science and Technology     Open Access   (Followers: 3)
Aquatic Toxicology     Hybrid Journal   (Followers: 21)
Archaea     Open Access   (Followers: 3)
Archiv für Molluskenkunde: International Journal of Malacology     Full-text available via subscription   (Followers: 3)
Archives of Biomedical Sciences     Open Access   (Followers: 7)
Archives of Microbiology     Hybrid Journal   (Followers: 8)
Archives of Natural History     Hybrid Journal   (Followers: 8)
Archives of Oral Biology     Hybrid Journal   (Followers: 2)
Archives of Virology     Hybrid Journal   (Followers: 5)
Archivum Immunologiae et Therapiae Experimentalis     Hybrid Journal   (Followers: 2)
Arid Ecosystems     Hybrid Journal   (Followers: 3)
Arquivos do Instituto Biológico     Open Access   (Followers: 1)
Arquivos do Museu Dinâmico Interdisciplinar     Open Access  
Arthropod Structure & Development     Hybrid Journal   (Followers: 2)
Arthropods     Open Access   (Followers: 1)
Artificial DNA: PNA & XNA     Hybrid Journal   (Followers: 3)
Artificial Photosynthesis     Open Access   (Followers: 1)
Asian Bioethics Review     Full-text available via subscription   (Followers: 2)
Asian Journal of Biodiversity     Open Access   (Followers: 5)
Asian Journal of Biological Sciences     Open Access   (Followers: 3)
Asian Journal of Cell Biology     Open Access   (Followers: 6)
Asian Journal of Developmental Biology     Open Access   (Followers: 2)
Asian Journal of Medical and Biological Research     Open Access   (Followers: 2)
Asian Journal of Nematology     Open Access   (Followers: 4)
Asian Journal of Poultry Science     Open Access   (Followers: 4)
Australian Life Scientist     Full-text available via subscription   (Followers: 2)
Australian Mammalogy     Hybrid Journal   (Followers: 6)
Autophagy     Hybrid Journal   (Followers: 2)
Avian Biology Research     Full-text available via subscription   (Followers: 5)
Avian Conservation and Ecology     Open Access   (Followers: 13)
Bacteriology Journal     Open Access   (Followers: 2)
Bacteriophage     Full-text available via subscription   (Followers: 4)
Bangladesh Journal of Bioethics     Open Access  
Bangladesh Journal of Plant Taxonomy     Open Access  
Bangladesh Journal of Scientific Research     Open Access   (Followers: 2)
Berita Biologi     Open Access   (Followers: 1)
Between the Species     Open Access   (Followers: 1)
Bio Tribune Magazine     Hybrid Journal  
BIO Web of Conferences     Open Access  
BIO-Complexity     Open Access  
Bio-Grafía. Escritos sobre la Biología y su enseñanza     Open Access  
Bioanalytical Reviews     Hybrid Journal   (Followers: 2)
Biocatalysis and Biotransformation     Hybrid Journal   (Followers: 6)
Biochemistry and Cell Biology     Hybrid Journal   (Followers: 14)
Biochimie     Hybrid Journal   (Followers: 7)
BioControl     Hybrid Journal   (Followers: 5)
Biocontrol Science and Technology     Hybrid Journal   (Followers: 5)
Biodemography and Social Biology     Hybrid Journal   (Followers: 1)
BioDiscovery     Open Access   (Followers: 2)
Biodiversity : Research and Conservation     Open Access   (Followers: 29)
Biodiversity and Natural History     Open Access   (Followers: 6)
Biodiversity Data Journal     Open Access   (Followers: 3)
Biodiversity Informatics     Open Access   (Followers: 1)
Biodiversity Information Science and Standards     Open Access  
Bioedukasi : Jurnal Pendidikan Biologi FKIP UM Metro     Open Access  
Bioeksperimen : Jurnal Penelitian Biologi     Open Access  
Bioelectrochemistry     Hybrid Journal   (Followers: 2)
Bioelectromagnetics     Hybrid Journal   (Followers: 1)
Bioenergy Research     Hybrid Journal   (Followers: 2)
Bioengineering and Bioscience     Open Access   (Followers: 1)
BioEssays     Hybrid Journal   (Followers: 10)
Bioethics     Hybrid Journal   (Followers: 14)
BioéthiqueOnline     Open Access  
Biofabrication     Hybrid Journal   (Followers: 3)
Biogeosciences (BG)     Open Access   (Followers: 10)
Biogeosciences Discussions (BGD)     Open Access   (Followers: 1)
Bioinformatics     Hybrid Journal   (Followers: 287)
Bioinformatics and Biology Insights     Open Access   (Followers: 15)
Bioinspiration & Biomimetics     Hybrid Journal   (Followers: 7)
Biointerphases     Open Access   (Followers: 1)
Biojournal of Science and Technology     Open Access  
Biologia     Hybrid Journal  
Biologia on-line : Revista de divulgació de la Facultat de Biologia     Open Access  
Biological Bulletin     Partially Free   (Followers: 5)
Biological Control     Hybrid Journal   (Followers: 4)
Biological Invasions     Hybrid Journal   (Followers: 17)
Biological Journal of the Linnean Society     Hybrid Journal   (Followers: 18)
Biological Letters     Open Access   (Followers: 5)
Biological Procedures Online     Open Access  
Biological Psychiatry     Hybrid Journal   (Followers: 45)
Biological Psychology     Hybrid Journal   (Followers: 6)
Biological Research     Open Access  
Biological Rhythm Research     Hybrid Journal   (Followers: 2)
Biological Theory     Hybrid Journal   (Followers: 2)
Biological Trace Element Research     Hybrid Journal  
Biologicals     Full-text available via subscription   (Followers: 9)
Biologics: Targets & Therapy     Open Access   (Followers: 1)
Biologie Aujourd'hui     Full-text available via subscription  
Biologie in Unserer Zeit (Biuz)     Hybrid Journal   (Followers: 41)
Biologija     Open Access  
Biology     Open Access   (Followers: 5)
Biology and Philosophy     Hybrid Journal   (Followers: 17)
Biology Bulletin     Hybrid Journal   (Followers: 1)
Biology Bulletin Reviews     Hybrid Journal  

        1 2 3 4 5 6 7 8 | Last

Journal Cover Ageing Research Reviews
  [SJR: 3.289]   [H-I: 78]   [9 followers]  Follow
    
   Hybrid Journal Hybrid journal (It can contain Open Access articles)
   ISSN (Print) 1568-1637
   Published by Elsevier Homepage  [3120 journals]
  • Procancerogenic activity of senescent cells: A case of the peritoneal
           mesothelium
    • Authors: Justyna Mikuła-Pietrasik; Łukasz Stryczyński; Paweł Uruski; Andrzej Tykarski; Krzysztof Książek
      Pages: 1 - 9
      Abstract: Publication date: May 2018
      Source:Ageing Research Reviews, Volume 43
      Author(s): Justyna Mikuła-Pietrasik, Łukasz Stryczyński, Paweł Uruski, Andrzej Tykarski, Krzysztof Książek
      Human peritoneal mesothelial cells belong to a narrow group of somatic cells in which both the triggers and the mechanisms of senescence have already been well defined. Importantly, senescent mesothelial cells have been found in the peritoneal cavity in vivo. From a clinical point of view, peritoneal mesothelial cells have been recognized as playing a critical role in the intraperitoneal development of tumor metastases. The pro-cancerogenic behavior of mesothelial cells is even more pronounced when the cells exhaust their proliferative capacity and become senescent. In this review, we summarize the current state of art regarding the contribution of peritoneal mesothelial cells in the progression of ovarian, colorectal, and pancreatic carcinomas, with particular attention paid to the cancer-promoting activity of their senescent counterparts. Moreover, we delineate the mechanisms, mediators, and signaling pathways that are engaged by the senescent mesothelial cells to support such vital elements of cancer progression as adhesion, proliferation, migration, invasion, epithelial-mesenchymal transition, and angiogenesis. Finally, we discuss the experimental evidence regarding both natural and synthetic compounds that may either prevent or restrict cancer development by delaying senescence of mesothelial cells.

      PubDate: 2018-02-05T17:23:51Z
      DOI: 10.1016/j.arr.2018.01.002
      Issue No: Vol. 43 (2018)
       
  • Cellular senescence: Immunosurveillance and future immunotherapy
    • Authors: Dominick G.A. Burton; Alexandra Stolzing
      Pages: 17 - 25
      Abstract: Publication date: May 2018
      Source:Ageing Research Reviews, Volume 43
      Author(s): Dominick G.A. Burton, Alexandra Stolzing
      In response to persistent DNA damage, induction into cell senescence promotes an immunogenic program which facilitates immune clearance of these damaged cells. Under physiological conditions, senescent cells can activate both innate and adaptive immune responses, functioning to maintain tissue homeostasis. In addition, emerging findings suggest that programmed induction of cell senescence may be important for regulating reproductive processes, partly facilitated by immune clearance. However, likely owing to ageing of the immune system, a failure to eliminate senescent cells can contribute to their persistence in tissues, leading to the development and progression of age-related diseases. Such immune failure may in part be due to activation of the senescence program in immune cells, leading to their dysfunction. Furthermore, senescent cells under certain biological contexts have been shown to instead promote immune suppression, a response that may reflect differences between an acute verses chronic senescent phenotype. In this review, we provide an overview of the research to date concerning senescence immunosurviellance, including a focused discussion on the mechanisms by which macrophages may recognise senescent cells. Senescence immunotherapy strategies as an alternative to senolytics for the removal of senescent cells will also be discussed.

      PubDate: 2018-02-15T17:45:05Z
      DOI: 10.1016/j.arr.2018.02.001
      Issue No: Vol. 43 (2018)
       
  • Poor cognitive ageing: Vulnerabilities, mechanisms and the impact of
           nutritional interventions
    • Authors: Sophie Miquel; Claire Champ; Jon Day; Esther Aarts; Ben A. Bahr; Martijntje Bakker; Diána Bánáti; Vittorio Calabrese; Tommy Cederholm; John Cryan; Louise Dye; Jonathan A. Farrimond; Aniko Korosi; Sophie Layé; Stuart Maudsley; Dragan Milenkovic; M.Hasan Mohajeri; John Sijben; Alina Solomon; Jeremy P.E. Spencer; Sandrine Thuret; Wim Vanden Berghe; David Vauzour; Bruno Vellas; Keith Wesnes; Peter Willatts; Raphael Wittenberg; Lucie Geurts
      Pages: 40 - 55
      Abstract: Publication date: March 2018
      Source:Ageing Research Reviews, Volume 42
      Author(s): Sophie Miquel, Claire Champ, Jon Day, Esther Aarts, Ben A. Bahr, Martijntje Bakker, Diána Bánáti, Vittorio Calabrese, Tommy Cederholm, John Cryan, Louise Dye, Jonathan A. Farrimond, Aniko Korosi, Sophie Layé, Stuart Maudsley, Dragan Milenkovic, M.Hasan Mohajeri, John Sijben, Alina Solomon, Jeremy P.E. Spencer, Sandrine Thuret, Wim Vanden Berghe, David Vauzour, Bruno Vellas, Keith Wesnes, Peter Willatts, Raphael Wittenberg, Lucie Geurts
      Background Ageing is a highly complex process marked by a temporal cascade of events, which promote alterations in the normal functioning of an individual organism. The triggers of normal brain ageing are not well understood, even less so the factors which initiate and steer the neuronal degeneration, which underpin disorders such as dementia. A wealth of data on how nutrients and diets may support cognitive function and preserve brain health are available, yet the molecular mechanisms underlying their biological action in both normal ageing, age-related cognitive decline, and in the development of neurodegenerative disorders have not been clearly elucidated. Objectives This review aims to summarise the current state of knowledge of vulnerabilities that predispose towards dysfunctional brain ageing, highlight potential protective mechanisms, and discuss dietary interventions that may be used as therapies. A special focus of this paper is on the impact of nutrition on neuroprotection and the underlying molecular mechanisms, and this focus reflects the discussions held during the 2nd workshop ‘Nutrition for the Ageing Brain: Functional Aspects and Mechanisms’ in Copenhagen in June 2016. The present review is the most recent in a series produced by the Nutrition and Mental Performance Task Force under the auspice of the International Life Sciences Institute Europe (ILSI Europe). Conclusion Coupling studies of cognitive ageing with studies investigating the effect of nutrition and dietary interventions as strategies targeting specific mechanisms, such as neurogenesis, protein clearance, inflammation, and non-coding and microRNAs is of high value. Future research on the impact of nutrition on cognitive ageing will need to adopt a longitudinal approach and multimodal nutritional interventions will likely need to be imposed in early-life to observe significant impact in older age.

      PubDate: 2018-02-15T17:45:05Z
      DOI: 10.1016/j.arr.2017.12.004
      Issue No: Vol. 42 (2018)
       
  • Altered function of neuronal L-type calcium channels in ageing and
           neuroinflammation: Implications in age-related synaptic dysfunction and
           cognitive decline
    • Authors: Sheeja Navakkode; Chao Liu; Tuck Wah Soong
      Pages: 86 - 99
      Abstract: Publication date: March 2018
      Source:Ageing Research Reviews, Volume 42
      Author(s): Sheeja Navakkode, Chao Liu, Tuck Wah Soong
      The rapid developments in science have led to an increase in human life expectancy and thus, ageing and age-related disorders/diseases have become one of the greatest concerns in the 21st century. Cognitive abilities tend to decline as we get older. This age-related cognitive decline is mainly attributed to aberrant changes in synaptic plasticity and neuronal connections. Recent studies show that alterations in Ca2+ homeostasis underlie the increased vulnerability of neurons to age-related processes like cognitive decline and synaptic dysfunctions. Dysregulation of Ca2+ can lead to dramatic changes in neuronal functions. We discuss in this review, the recent advances on the potential role of dysregulated Ca2+ homeostasis through altered function of L-type voltage gated Ca2+ channels (LTCC) in ageing, with an emphasis on cognitive decline. This review therefore focuses on age-related changes mainly in the hippocampus, and with mention of other brain areas, that are important for learning and memory. This review also highlights age-related memory deficits via synaptic alterations and neuroinflammation. An understanding of these mechanisms will help us formulate strategies to reverse or ameliorate age-related disorders like cognitive decline.

      PubDate: 2018-02-05T17:23:51Z
      DOI: 10.1016/j.arr.2018.01.001
      Issue No: Vol. 42 (2018)
       
  • Use of near-infrared spectroscopy in the investigation of brain activation
           during cognitive aging: A systematic review of an emerging area of
           research
    • Authors: Nounagnon F. Agbangla; Michel Audiffren; Cédric T. Albinet
      Pages: 52 - 66
      Abstract: Publication date: September 2017
      Source:Ageing Research Reviews, Volume 38
      Author(s): Nounagnon F. Agbangla, Michel Audiffren, Cédric T. Albinet
      The cognitive neuroscience of aging is a growing and stimulating research area. The development of neuroimaging techniques in the past two decades has considerably increased our understanding of the brain mechanisms that might underlie cognitive performance and resulting changes due to normal aging. Beside traditional metabolic neuroimaging techniques, such as Positron Emission Tomography and functional Magnetic Resonance Imaging, near infrared spectroscopy (NIRS), an optical imaging technique allowing to monitor real-time cerebral blood oxygenation, has gained recent interest in this field. The aim of the present review paper, after briefly presenting the NIRS technique, is to review and to summarize the recent results of neuroimaging studies using this technique in the field of cognitive aging. The reviewed literature shows that, despite low spatial resolution and cerebral depth penetration, this technique provides consistent findings on the reduced hemodynamic activity as a function of chronological age, mainly in the prefrontal cortex. Important moderators of brain hemodynamics, such as cognitive load, subjects’ characteristics and experimental conditions, for which the NIRS technique is sensitive, are discussed. Strengths and weaknesses of functional NIRS in the field of cognitive aging are presented and finally, novel perspectives of research are proposed.

      PubDate: 2018-02-15T17:45:05Z
      DOI: 10.1016/j.arr.2017.07.003
      Issue No: Vol. 38 (2018)
       
  • Oxidative stress, genomic features and DNA repair in frail elderly: A
           systematic review
    • Authors: María Sánchez-Flores; Diego Marcos-Pérez; Solange Costa; João Paulo Teixeira; Stefano Bonassi; Eduardo Pásaro; Blanca Laffon; Vanessa Valdiglesias
      Pages: 1 - 15
      Abstract: Publication date: August 2017
      Source:Ageing Research Reviews, Volume 37
      Author(s): María Sánchez-Flores, Diego Marcos-Pérez, Solange Costa, João Paulo Teixeira, Stefano Bonassi, Eduardo Pásaro, Blanca Laffon, Vanessa Valdiglesias
      Frailty is an emerging geriatric syndrome characterized by higher vulnerability to stressors, with an increased risk of adverse health outcomes such as mortality, morbidity, disability, hospitalization, and institutionalization. Although it is generally recognized to have a biological basis, no particular biological trait has been consistently associated to frailty status so far. In this work, epidemiological studies evaluating association of frailty status with alterations at cellular level − namely oxidative stress, genomic instability and DNA damage and repair biomarkers −were revised and compared. A total of 25 studies fulfilled inclusion/exclusion criteria and, consequently, were included in the review. Variations of oxidative stress biomarkers were often associated to frailty status in older people. On the contrary, genomic instability seems not to be linked to frailty. The only study which addressed the possible relationship between DNA repair modulations and frailty status also failed in finding association. Despite the large number of cellular alterations known to be associated with frailty, studies on this issue are still very scarce and limited to some of the possible cellular targets. The established link between DNA repair, genomic instability, and age and age-related disorders, encourage deeper investigations on this line.

      PubDate: 2018-02-15T17:45:05Z
      DOI: 10.1016/j.arr.2017.05.001
      Issue No: Vol. 37 (2018)
       
  • Circuit resistance training is an effective means to enhance muscle
           strength in older and middle aged adults
    • Authors: Assaf Buch; Ofer Kis; Eli Carmeli; Lital Keinan-Boker; Yitshal Berner; Yael Barer; Gabi Shefer; Yonit Marcus; Naftali Stern
      Pages: 16 - 27
      Abstract: Publication date: August 2017
      Source:Ageing Research Reviews, Volume 37
      Author(s): Assaf Buch, Ofer Kis, Eli Carmeli, Lital Keinan-Boker, Yitshal Berner, Yael Barer, Gabi Shefer, Yonit Marcus, Naftali Stern
      Background Physical exercise, particularly resistance training (RT), is proven treatment to reduce the accelerated decline in muscle strength exhibited by older adults, but its effect is hindered by low adherence rate, even under well-structured programs. Objective and data sources We investigated the efficacy of circuit resistance training (CRT) on muscle strength, lean mass and aerobic capacity in older adults based on report in MEDLINE, EMBASE, ClinicalTrials.gov and Cochrane electronic (through 8/2016). Study eligibility criteria: middle and older aged men and/or women who followed a structured program, assigned to CRT. Study appraisal and synthesis methods: Out of 237 originally identified articles, 10 articles were included with a total of 362 patients with mean: age −64.5±7.4 years; 3±1.15 sessions/week; session duration 41.8±15.9min. Results Upper body strength modestly increased, by 1.14kg (95% CI; 0.28–2.00), whereas larger increment was seen in lower body strength (11.99; 2.92–21.06). Higher program volume (>24 sessions) positively influenced upper body strength and aerobic capacity. Limitations (1) variability in the studies’ validity; (2) relatively low number of studies. Conclusion CRT is a valid alternative to conventional RT. Its shorter duration and lower intensity relative to traditional RT, may increase adherence to training in older adults.

      PubDate: 2018-02-15T17:45:05Z
      DOI: 10.1016/j.arr.2017.04.003
      Issue No: Vol. 37 (2018)
       
  • GIT2—a keystone in ageing and age-related disease
    • Authors: Jaana van Gastel; Jan Boddaert; Areta Jushaj; Richard T. Premont; Louis M. Luttrell; Jonathan Janssens; Bronwen Martin; Stuart Maudsley
      Abstract: Publication date: Available online 13 February 2018
      Source:Ageing Research Reviews
      Author(s): Jaana van Gastel, Jan Boddaert, Areta Jushaj, Richard T. Premont, Louis M. Luttrell, Jonathan Janssens, Bronwen Martin, Stuart Maudsley
      Since its discovery, G protein-coupled receptor kinase-interacting protein 2, GIT2, and its family member, GIT1, have received considerable interest concerning their potential key roles in regulating multiple inter-connected physiological and pathophysiological processes. GIT2 was first identified as a multifunctional protein that is recruited to G protein-coupled receptors (GPCRs) during the process of receptor internalization. Recent findings have demonstrated that perhaps one of the most important effects of GIT2 in physiology concerns its role in controlling multiple aspects of the complex ageing process. Ageing can be considered the most prevalent pathophysiological condition in humans, affecting all tissue systems and acting as a driving force for many common and intractable disorders. The ageing process involves a complex interplay among various deleterious activities that profoundly disrupt the body’s ability to cope with damage, thus increasing susceptibility to pathophysiologies such as neurodegeneration, central obesity, osteoporosis, type 2 diabetes mellitus and atherosclerosis. The biological systems that control ageing appear to function as a series of interconnected complex networks. The inter-communication among multiple lower-complexity signaling systems within the global ageing networks is likely coordinated internally by keystones or hubs, which regulate responses to dynamic molecular events through protein-protein interactions with multiple distinct partners. Multiple lines of research have suggested that GIT2 may act as one of these network coordinators in the ageing process. Identifying and targeting keystones, such as GIT2, is thus an important approach in our understanding of, and eventual ability to, medically ameliorate or interdict age-related progressive cellular and tissue damage.

      PubDate: 2018-02-15T17:45:05Z
      DOI: 10.1016/j.arr.2018.02.002
       
  • Healthy brain aging: interplay between reactive species, inflammation and
           energy supply
    • Authors: O. Garaschuk; H.M. Semchyshyn; V.I. Lushchak
      Abstract: Publication date: Available online 13 February 2018
      Source:Ageing Research Reviews
      Author(s): O. Garaschuk, H.M. Semchyshyn, V.I. Lushchak
      Brains’ high energy expenditure with preferable utilization of glucose and ketone bodies, defines the specific features of its energy homeostasis. The extensive oxidative metabolism is accompanied by a concomitant generation of high amounts of reactive oxygen, nitrogen, and carbonyl species, which will be here collectively referred to as RONCS. Such metabolism in combination with high content of polyunsaturated fatty acids creates specific problems in maintaining brains’ redox homeostasis. While the levels of products of interaction between RONCS and cellular components increase slowly during the first two trimesters of individuals’ life, their increase is substantially accelerated towards the end of life. Here we review the main mechanisms controlling the redox homeostasis of the mammalian brain, their age-dependencies as well as their adaptive potential, which might turn out to be much higher than initially assumed. According to recent data, the organism seems to respond to the enhancement of aging-related toxicity by forming a new homeostatic set point. Therefore, further research will focus on understanding the properties of the new set point(s), the general nature of this phenomenon and will explore the limits of brains’ adaptivity.
      Graphical abstract image

      PubDate: 2018-02-15T17:45:05Z
      DOI: 10.1016/j.arr.2018.02.003
       
  • IFC: Aims and Scope
    • Abstract: Publication date: August 2017
      Source:Ageing Research Reviews, Volume 37


      PubDate: 2018-02-15T17:45:05Z
       
  • Mandibuloacral dysplasia: A premature ageing disease with aspects of
           physiological ageing
    • Authors: Vittoria Cenni; Maria Rosaria D’Apice; Paolo Garagnani; Marta Columbaro; Giuseppe Novelli; Claudio Franceschi; Giovanna Lattanzi
      Pages: 1 - 13
      Abstract: Publication date: March 2018
      Source:Ageing Research Reviews, Volume 42
      Author(s): Vittoria Cenni, Maria Rosaria D’Apice, Paolo Garagnani, Marta Columbaro, Giuseppe Novelli, Claudio Franceschi, Giovanna Lattanzi
      Mandibuloacral dysplasia (MAD) is a rare genetic condition characterized by bone abnormalities including localized osteolysis and generalized osteoporosis, skin pigmentation, lipodystrophic signs and mildly accelerated ageing. The molecular defects associated with MAD are mutations in LMNA or ZMPSTE24 (FACE1) gene, causing type A or type B MAD, respectively. Downstream of LMNA or ZMPSTE24 mutations, the lamin A precursor, prelamin A, is accumulated in cells and affects chromatin dynamics and stress response. A new form of mandibuloacral dysplasia has been recently associated with mutations in POLD1 gene, encoding DNA polymerase delta, a major player in DNA replication. Of note, involvement of prelamin A in chromatin dynamics and recruitment of DNA repair factors has been also determined under physiological conditions, at the border between stress response and cellular senescence. Here, we review current knowledge on MAD clinical and pathogenetic aspects and highlight aspects typical of physiological ageing.

      PubDate: 2017-12-11T21:29:24Z
      DOI: 10.1016/j.arr.2017.12.001
      Issue No: Vol. 42 (2017)
       
  • Insulin-like Growth Factor 1 (IGF-1) as a marker of cognitive decline in
           normal ageing: A review
    • Authors: Julanne Frater; David Lie; Perry Bartlett; John J. McGrath
      Pages: 14 - 27
      Abstract: Publication date: March 2018
      Source:Ageing Research Reviews, Volume 42
      Author(s): Julanne Frater, David Lie, Perry Bartlett, John J. McGrath
      Insulin-like Growth Factor 1 (IGF-1) and its signaling pathway play a primary role in normal growth and ageing, however serum IGF-1 is known to reduce with advancing age. Recent findings suggest IGF-1 is essential for neurogenesis in the adult brain, and this reduction of IGF-1 with ageing may contribute to age-related cognitive decline. Experimental studies have shown manipulation of the GH/GF-1 axis can slow rates of cognitive decline in animals, making IGF-1 a potential biomarker of cognition, and/or its signaling pathway a possible therapeutic target to prevent or slow age-related cognitive decline. A systematic literature review and qualitative narrative summary of current evidence for IGF-1 as a biomarker of cognitive decline in the ageing brain was undertaken. Results indicate IGF-1 concentrations do not confer additional diagnostic information for those with cognitive decline, and routine clinical measurement of IGF-1 is not currently justified. In cases of established cognitive impairment, it remains unclear whether increasing circulating or brain IGF-1 may reverse or slow down the rate of further decline. Advances in neuroimaging, genetics, neuroscience and the availability of large well characterized biobanks will facilitate research exploring the role of IGF-1 in both normal ageing and age-related cognitive decline.

      PubDate: 2017-12-11T21:29:24Z
      DOI: 10.1016/j.arr.2017.12.002
      Issue No: Vol. 42 (2017)
       
  • Role of microglia-neuron interactions in diabetic encephalopathy
    • Authors: Yuan Liu; Mingchao Li; Zuo Zhang; Yun Ye; Jiyin Zhou
      Pages: 28 - 39
      Abstract: Publication date: March 2018
      Source:Ageing Research Reviews, Volume 42
      Author(s): Yuan Liu, Mingchao Li, Zuo Zhang, Yun Ye, Jiyin Zhou
      In the central nervous system, the primary immune cells, the microglia, prevent pathogenic invasion as the first line of defense. Microglial energy consumption is dependent on their degree of activity. Microglia express transporters for the three primary energy substrates (glucose, fatty acids, glutamine) and regulate diabetic encephalopathy via microglia-neuron interactions. Microglia may play a sentry role for rapid protection or even ablation of impaired neurons. Neurons exhibit hyperactivity in response to hyperglycemia, hyperlipidemia, and neurotoxic factors and release potential microglial activators. Microglial activation is also regulated by proinflammatory factors, caspase-3 activity, P2X7 receptor, interferon regulatory factor-8, and glucocorticoids. Modulation of microglia in diabetic encephalopathy may involve CX3CL1, p38 MAPK, purinergic, and CD200/CD200R signaling pathways, and pattern recognition receptors. The microglia-neuron interactions play an important role in diabetic encephalopathy, and modulation of microglial activation may be a therapeutic target for diabetic encephalopathy.

      PubDate: 2017-12-24T07:51:03Z
      DOI: 10.1016/j.arr.2017.12.005
      Issue No: Vol. 42 (2017)
       
  • Sirtuins, epigenetics and longevity
    • Authors: Mateusz Wątroba; Ilona Dudek; Marta Skoda; Aleksandra Stangret; Przemysław Rzodkiewicz; Dariusz Szukiewicz
      Pages: 11 - 19
      Abstract: Publication date: November 2017
      Source:Ageing Research Reviews, Volume 40
      Author(s): Mateusz Wątroba, Ilona Dudek, Marta Skoda, Aleksandra Stangret, Przemysław Rzodkiewicz, Dariusz Szukiewicz
      Aging of organisms begins from a single cell at the molecular level. It includes changes related to telomere shortening, cell senescence and epigenetic modifications. These processes accumulate over the lifespan. Research studies show that epigenetic signaling contributes to human disease, tumorigenesis and aging. Epigenetic DNA modifications involve changes in the gene activity but not in the DNA sequence. An epigenome consists of chemical modifications to the DNA and histone proteins without the changes in the DNA sequence. These modifications strongly depend on the environment, could be reversible and are potentially transmittable to daughter cells. Epigenetics includes DNA methylation, noncoding RNA interference, and modifications of histone proteins. Sirtuins, a family of nicotine adenine dinucleotide (NAD+)-dependent enzymes, are involved in the cell metabolism and can regulate many cellular functions including DNA repair, inflammatory response, cell cycle or apoptosis. Literature shows the strong interconnection between sirtuin expression and aging processes. However, the direct relationship is still unknown. Here, we would like to summarize the existing knowledge about epigenetic processes in aging, especially those related to sirtuin expression. Another objective is to explain why some negative correlations between sirtuin activity and the rate of aging can be assumed.

      PubDate: 2017-08-15T14:35:35Z
      DOI: 10.1016/j.arr.2017.08.001
      Issue No: Vol. 40 (2017)
       
  • The role of the immune system in Alzheimer disease: Etiology and treatment
    • Authors: Stefan Jevtic; Ameet S. Sengar; Michael W. Salter; JoAnne McLaurin
      Pages: 84 - 94
      Abstract: Publication date: November 2017
      Source:Ageing Research Reviews, Volume 40
      Author(s): Stefan Jevtic, Ameet S. Sengar, Michael W. Salter, JoAnne McLaurin
      The immune system is now considered a major factor in Alzheimer Disease (AD). This review seeks to demonstrate how various aspects of the immune system, both in the brain and peripherally, interact to contribute to AD. We highlight classical nervous system immune components, such as complement and microglia, as well as novel aspects of the peripheral immune system that can influence disease, such as monocytes and lymphocytes. By detailing the roles of various immune cells in AD, we summarize an emerging perspective for disease etiology and future therapeutic targets.

      PubDate: 2017-09-23T13:11:22Z
      DOI: 10.1016/j.arr.2017.08.005
      Issue No: Vol. 40 (2017)
       
  • The science of nutritional modulation of aging
    • Authors: Luigi Fontana
      Pages: 1 - 2
      Abstract: Publication date: October 2017
      Source:Ageing Research Reviews, Volume 39
      Author(s): Luigi Fontana


      PubDate: 2017-08-26T18:09:15Z
      DOI: 10.1016/j.arr.2017.08.002
      Issue No: Vol. 39 (2017)
       
  • Dietary restriction and lifespan: Lessons from invertebrate models
    • Authors: Pankaj Kapahi; Matt Kaeberlein; Malene Hansen
      Pages: 3 - 14
      Abstract: Publication date: October 2017
      Source:Ageing Research Reviews, Volume 39
      Author(s): Pankaj Kapahi, Matt Kaeberlein, Malene Hansen
      Dietary restriction (DR) is the most robust environmental manipulation known to increase active and healthy lifespan in many species. Despite differences in the protocols and the way DR is carried out in different organisms, conserved relationships are emerging among multiple species. Elegant studies from numerous model organisms are further defining the importance of various nutrient-signaling pathways including mTOR (mechanistic target of rapamycin), insulin/IGF-1-like signaling and sirtuins in mediating the effects of DR. We here review current advances in our understanding of the molecular mechanisms altered by DR to promote lifespan in three major invertebrate models, the budding yeast Saccharomyces cerevisiae, the nematode Caenorhabditis elegans, and the fruit fly Drosophila melanogaster.

      PubDate: 2017-08-26T18:09:15Z
      DOI: 10.1016/j.arr.2016.12.005
      Issue No: Vol. 39 (2017)
       
  • Nutrition, metabolism, and targeting aging in nonhuman primates
    • Authors: Priya Balasubramanian; Julie A. Mattison; Rozalyn M. Anderson
      Pages: 29 - 35
      Abstract: Publication date: October 2017
      Source:Ageing Research Reviews, Volume 39
      Author(s): Priya Balasubramanian, Julie A. Mattison, Rozalyn M. Anderson
      This short review focuses on the importance of nonhuman primate nutrition and aging studies and makes the case that a targeted expansion of the use of this highly translatable model would be advantageous to the biology of aging field. First, we describe the high degree of similarity of the model in terms of aging phenotypes including incidence and prevalence of common human age-related diseases. Second, we discuss the importance of the nonhuman primate nutrition and aging studies and the extent to which the outcomes of two ongoing long-term studies of caloric restriction are congruent with short-term equivalent studies in humans. Third, we showcase a number of pharmacological agents previously employed in nonhuman primate studies that display some potential as caloric restriction mimetics. Finally, we present nonhuman primates as an important model for translation of mechanisms of delayed aging identified in studies of shorter-lived animals. Proof of efficacy and safety of candidate longevity agents in nonhuman primates would be a cost-effective means to bring these exciting new avenues a step closer to clinical application.

      PubDate: 2017-08-26T18:09:15Z
      DOI: 10.1016/j.arr.2017.02.002
      Issue No: Vol. 39 (2017)
       
  • Calorie restriction in humans: An update
    • Authors: Jasper Most; Valeria Tosti; Leanne M. Redman; Luigi Fontana
      Pages: 36 - 45
      Abstract: Publication date: October 2017
      Source:Ageing Research Reviews, Volume 39
      Author(s): Jasper Most, Valeria Tosti, Leanne M. Redman, Luigi Fontana
      Calorie restriction (CR), a nutritional intervention of reduced energy intake but with adequate nutrition, has been shown to extend healthspan and lifespan in rodent and primate models. Accumulating data from observational and randomized clinical trials indicate that CR in humans results in some of the same metabolic and molecular adaptations that have been shown to improve health and retard the accumulation of molecular damage in animal models of longevity. In particular, moderate CR in humans ameliorates multiple metabolic and hormonal factors that are implicated in the pathogenesis of type 2 diabetes, cardiovascular diseases, and cancer, the leading causes of morbidity, disability and mortality. In this paper, we will discuss the effects of CR in non-obese humans on these physiological parameters. Special emphasis is committed to recent clinical intervention trials that have investigated the feasibility and effects of CR in young and middle-aged men and women on parameters of energy metabolism and metabolic risk factors of age-associated disease in great detail. Additionally, data from individuals who are either naturally exposed to CR or those who are self-practicing this dietary intervention allows us to speculate on longer-term effects of more severe CR in humans.

      PubDate: 2017-08-26T18:09:15Z
      DOI: 10.1016/j.arr.2016.08.005
      Issue No: Vol. 39 (2017)
       
  • Impact of intermittent fasting on health and disease processes
    • Authors: Mark P. Mattson; Valter D. Longo; Michelle Harvie
      Pages: 46 - 58
      Abstract: Publication date: October 2017
      Source:Ageing Research Reviews, Volume 39
      Author(s): Mark P. Mattson, Valter D. Longo, Michelle Harvie
      Humans in modern societies typically consume food at least three times daily, while laboratory animals are fed ad libitum. Overconsumption of food with such eating patterns often leads to metabolic morbidities (insulin resistance, excessive accumulation of visceral fat, etc.), particularly when associated with a sedentary lifestyle. Because animals, including humans, evolved in environments where food was relatively scarce, they developed numerous adaptations that enabled them to function at a high level, both physically and cognitively, when in a food-deprived/fasted state. Intermittent fasting (IF) encompasses eating patterns in which individuals go extended time periods (e.g., 16–48h) with little or no energy intake, with intervening periods of normal food intake, on a recurring basis. We use the term periodic fasting (PF) to refer to IF with periods of fasting or fasting mimicking diets lasting from 2 to as many as 21 or more days. In laboratory rats and mice IF and PF have profound beneficial effects on many different indices of health and, importantly, can counteract disease processes and improve functional outcome in experimental models of a wide range of age-related disorders including diabetes, cardiovascular disease, cancers and neurological disorders such as Alzheimer’s disease Parkinson’s disease and stroke. Studies of IF (e.g., 60% energy restriction on 2days per week or every other day), PF (e.g., a 5day diet providing 750–1100kcal) and time-restricted feeding (TRF; limiting the daily period of food intake to 8h or less) in normal and overweight human subjects have demonstrated efficacy for weight loss and improvements in multiple health indicators including insulin resistance and reductions in risk factors for cardiovascular disease. The cellular and molecular mechanisms by which IF improves health and counteracts disease processes involve activation of adaptive cellular stress response signaling pathways that enhance mitochondrial health, DNA repair and autophagy. PF also promotes stem cell-based regeneration as well as long-lasting metabolic effects. Randomized controlled clinical trials of IF versus PF and isoenergetic continuous energy restriction in human subjects will be required to establish the efficacy of IF in improving general health, and preventing and managing major diseases of aging.

      PubDate: 2017-08-26T18:09:15Z
      DOI: 10.1016/j.arr.2016.10.005
      Issue No: Vol. 39 (2017)
       
  • Circadian rhythms, time-restricted feeding, and healthy aging
    • Authors: Emily N.C. Manoogian; Satchidananda Panda
      Pages: 59 - 67
      Abstract: Publication date: October 2017
      Source:Ageing Research Reviews, Volume 39
      Author(s): Emily N.C. Manoogian, Satchidananda Panda
      Circadian rhythms optimize physiology and health by temporally coordinating cellular function, tissue function, and behavior. These endogenous rhythms dampen with age and thus compromise temporal coordination. Feeding-fasting patterns are an external cue that profoundly influence the robustness of daily biological rhythms. Erratic eating patterns can disrupt the temporal coordination of metabolism and physiology leading to chronic diseases that are also characteristic of aging. However, sustaining a robust feeding-fasting cycle, even without altering nutrition quality or quantity, can prevent or reverse these chronic diseases in experimental models. In humans, epidemiological studies have shown erratic eating patterns increase the risk of disease, whereas sustained feeding-fasting cycles, or prolonged overnight fasting, is correlated with protection from breast cancer. Therefore, optimizing the timing of external cues with defined eating patterns can sustain a robust circadian clock, which may prevent disease and improve prognosis.
      Graphical abstract image

      PubDate: 2017-08-26T18:09:15Z
      DOI: 10.1016/j.arr.2016.12.006
      Issue No: Vol. 39 (2017)
       
  • Protective effects of short-term dietary restriction in surgical stress
           and chemotherapy
    • Authors: Sebastian Brandhorst; Eylul Harputlugil; James R. Mitchell; Valter D. Longo
      Pages: 68 - 77
      Abstract: Publication date: October 2017
      Source:Ageing Research Reviews, Volume 39
      Author(s): Sebastian Brandhorst, Eylul Harputlugil, James R. Mitchell, Valter D. Longo
      Reduced caloric intake including fasting, as well as the dietary composition or the timing of food intake, impact longevity, likely through a modification in the onset or the severity of chronic aging-related diseases such as cancer. As with pre- and post-operative dietary recommendations, evidence-based nutritional advice from healthcare professionals during and after cancer treatment is often vague or conflicting. We hypothesize that preventive dietary recommendations can help in the context of both chronic cancer treatment efficacy and the avoidance of development of secondary malignancies, as well as in the context of protection from the acute stress of surgery. In this perspective review, we will discuss the latest findings on the potential role of short-term dietary restriction in cancer treatment and improvement of surgical outcome.
      Graphical abstract image

      PubDate: 2017-08-26T18:09:15Z
      DOI: 10.1016/j.arr.2017.02.001
      Issue No: Vol. 39 (2017)
       
  • Dietary protein, aging and nutritional geometry
    • Authors: Stephen J. Simpson; David G. Le Couteur; David Raubenheimer; Samantha M. Solon-Biet; Gregory J. Cooney; Victoria C. Cogger; Luigi Fontana
      Pages: 78 - 86
      Abstract: Publication date: October 2017
      Source:Ageing Research Reviews, Volume 39
      Author(s): Stephen J. Simpson, David G. Le Couteur, David Raubenheimer, Samantha M. Solon-Biet, Gregory J. Cooney, Victoria C. Cogger, Luigi Fontana
      Nearly a century of research has shown that nutritional interventions can delay aging and age- related diseases in many animal models and possibly humans. The most robust and widely studied intervention is caloric restriction, while protein restriction and restriction of various amino acids (methionine, tryptophan) have also been shown to delay aging. However, there is still debate over whether the major impact on aging is secondary to caloric intake, protein intake or specific amino acids. Nutritional geometry provides new perspectives on the relationship between nutrition and aging by focusing on calories, macronutrients and their interactions across a landscape of diets, and taking into account compensatory feeding in ad libitum-fed experiments. Nutritional geometry is a state-space modelling approach that explores how animals respond to and balance changes in nutrient availability. Such studies in insects and mice have shown that low protein, high carbohydrate diets are associated with longest lifespan in ad libitum fed animals suggesting that the interaction between macronutrients may be as important as their total intake.

      PubDate: 2017-08-26T18:09:15Z
      DOI: 10.1016/j.arr.2017.03.001
      Issue No: Vol. 39 (2017)
       
  • Cutting back on the essentials: Can manipulating intake of specific amino
           acids modulate health and lifespan'
    • Authors: Holly M. Brown-Borg; Rochelle Buffenstein
      Pages: 87 - 95
      Abstract: Publication date: October 2017
      Source:Ageing Research Reviews, Volume 39
      Author(s): Holly M. Brown-Borg, Rochelle Buffenstein
      With few exceptions, nutritional and dietary interventions generally impact upon both old-age quality of life and longevity. The life prolonging effects, commonly observed with dietary restriction reportedly are linked to alterations in protein intake and specifically limiting the dietary intake of certain essential amino acids. There is however a paucity of data methodically evaluating the various essential amino acids on health- and lifespan and the mechanisms involved. Rodent diets containing either lower methionine content, or tryptophan, than that found in commercially available chow, appear to elicit beneficial effects. It is unclear whether all of these favorable effects associated with restricted intake of methionine and tryptophan are due to their specific unique properties or if restriction of other essential amino acids, or proteins in general, may produce similar results. Considerably more work remains to be done to elucidate the mechanisms by which limiting these vital molecules may delay the onset of age-associated diseases and improve quality of life at older ages.

      PubDate: 2017-08-26T18:09:15Z
      DOI: 10.1016/j.arr.2016.08.007
      Issue No: Vol. 39 (2017)
       
  • Nutrition in early life and age-associated diseases
    • Authors: Jane L. Tarry-Adkins; Susan E. Ozanne
      Pages: 96 - 105
      Abstract: Publication date: October 2017
      Source:Ageing Research Reviews, Volume 39
      Author(s): Jane L. Tarry-Adkins, Susan E. Ozanne
      The prevalence of age-associated disease is increasing at a striking rate globally. It is known that a strong association exists between a suboptimal maternal and/or early-life environment and increased propensity of developing age-associated disease, including cardiovascular disease (CVD), type-2 diabetes (T2D) and obesity. The dissection of underlying molecular mechanisms to explain this phenomenon, which is known as ‘developmental programming’ is still emerging; however three common mechanisms have emerged in many models of developmental programming. These mechanisms are (a) changes in tissue structure, (b) epigenetic regulation and (c) accelerated cellular ageing. This review will examine the epidemiological evidence and the animal models of suboptimal maternal environments, focusing upon these molecular mechanisms and will discuss the progress being made in the development of safe and effective intervention strategies which ultimately could target those ‘programmed’ individuals who are known to be at-risk of age-associated disease.
      Graphical abstract image

      PubDate: 2017-08-26T18:09:15Z
      DOI: 10.1016/j.arr.2016.08.003
      Issue No: Vol. 39 (2017)
       
  • Nutrition and other lifestyle influences on arterial aging
    • Authors: Thomas J. LaRocca; Christopher R. Martens; Douglas R. Seals
      Pages: 106 - 119
      Abstract: Publication date: October 2017
      Source:Ageing Research Reviews, Volume 39
      Author(s): Thomas J. LaRocca, Christopher R. Martens, Douglas R. Seals
      As our world’s population ages, cardiovascular diseases (CVD) will become an increasingly urgent public health problem. A key antecedent to clinical CVD and many other chronic disorders of aging is age-related arterial dysfunction, characterized by increased arterial stiffness and impaired arterial endothelial function. Accumulating evidence demonstrates that diet and nutrition may favorably modulate these arterial functions with aging, but many important questions remain. In this review, we will summarize the available information on dietary patterns and nutritional factors that have been studied for their potential to reduce arterial stiffness and improve endothelial function with age, with an emphasis on: 1) underlying physiological mechanisms, and 2) emerging areas of research on nutrition and arterial aging that may hold promise for preventing age-related CVD.

      PubDate: 2017-08-26T18:09:15Z
      DOI: 10.1016/j.arr.2016.09.002
      Issue No: Vol. 39 (2017)
       
  • AMPK orchestrates an elaborate cascade protecting tissue from fibrosis and
           aging
    • Authors: Shuai Jiang; Tian Li; Zhi Yang; Wei Yi; Shouyin Di; Yang Sun; Dongjin Wang; Yang Yang
      Pages: 18 - 27
      Abstract: Publication date: September 2017
      Source:Ageing Research Reviews, Volume 38
      Author(s): Shuai Jiang, Tian Li, Zhi Yang, Wei Yi, Shouyin Di, Yang Sun, Dongjin Wang, Yang Yang
      Fibrosis is a common process characterized by excessive extracellular matrix (ECM) accumulation after inflammatory injury, which is also a crucial cause of aging. The process of fibrosis is involved in the pathogenesis of most diseases of the heart, liver, kidney, lung, and other organs/tissues. However, there are no effective therapies for this pathological alteration. Annually, fibrosis represents a huge financial burden for the USA and the world. 5′-AMP-activated protein kinase (AMPK) is a pivotal energy sensor that alleviates or delays the process of fibrogenesis. In this review, we first present basic background information on AMPK and fibrogenesis and describe the protective roles of AMPK in three fibrogenic phases. Second, we analyze the protective action of AMPK during fibrosis in myocardial, hepatic, renal, pulmonary, and other organs/tissues. Third, we present a comprehensive discussion of AMPK during fibrosis and draw a conclusion. This review highlights recent advances, vital for basic research and clinical drug design, in the regulation of AMPK during fibrosis.

      PubDate: 2017-07-21T13:32:32Z
      DOI: 10.1016/j.arr.2017.07.001
      Issue No: Vol. 38 (2017)
       
  • The genetics of Parkinson disease
    • Authors: Hao Deng; Peng Wang; Joseph Jankovic
      Abstract: Publication date: Available online 26 December 2017
      Source:Ageing Research Reviews
      Author(s): Hao Deng, Peng Wang, Joseph Jankovic
      About 15% of patients with Parkinson disease (PD) have family history and 5-10% have a monogenic form of the disease with Mendelian inheritance. To date, at least 23 loci and 19 disease-causing genes for parkinsonism have been found, but many more genetic risk loci and variants for sporadic PD phenotype have been identified in various association studies. Investigating the mutated protein products has uncovered potential pathogenic pathways that provide insights into mechanisms of neurodegeneration in familial and sporadic PD. To commemorate the 200th anniversary of Parkinson’s publication of An Essay on the Shaking Palsy, we provide a comprehensive and critical overview of the current clinical, neuropathological, and genetic understanding of genetic forms of PD. We also discuss advances in screening for genetic PD-related risk factors and how they impact genetic counseling and contribute to the development of potential disease-modifying therapies.

      PubDate: 2017-12-26T22:55:17Z
      DOI: 10.1016/j.arr.2017.12.007
       
  • Cartilage regeneration and ageing: Targeting cellular plasticity in
           osteoarthritis
    • Authors: Marta Varela-Eirin; Jesus Loureiro; Eduardo Fonseca; Silvia Corrochano; Jose R. Caeiro; Manuel Collado; Maria D. Mayan
      Abstract: Publication date: Available online 16 December 2017
      Source:Ageing Research Reviews
      Author(s): Marta Varela-Eirin, Jesus Loureiro, Eduardo Fonseca, Silvia Corrochano, Jose R. Caeiro, Manuel Collado, Maria D. Mayan
      Ageing processes play a major contributing role for the development of Osteoarthritis (OA). This prototypic degenerative condition of ageing is the most common form of arthritis and is accompanied by a general decline, chronic pain and mobility deficits. The disease is primarily characterized by articular cartilage degradation, followed by subchondral bone thickening, osteophyte formation, synovial inflammation and joint degeneration. In the early stages, osteoarthritic chondrocytes undergo phenotypic changes that increase cell proliferation and cluster formation and enhance the production of matrix-remodelling enzymes. In fact, chondrocytes exhibit differentiation plasticity and undergo phenotypic changes during the healing process. Current studies are focusing on unravelling whether OA is a consequence of an abnormal wound healing response. Recent investigations suggest that alterations in different proteins, such as TGF-ß/BMPs, NF-Kß, Wnt, and Cx43, or SASP factors involved in signalling pathways in wound healing response, could be directly implicated in the initiation of OA. Several findings suggest that osteoarthritic chondrocytes remain in an immature state expressing stemness-associated cell surface markers. In fact, the efficacy of new disease-modifying OA drugs that promote chondrogenic differentiation in animal models indicates that this may be a drug-sensible state. In this review, we highlight the current knowledge regarding cellular plasticity in chondrocytes and OA. A better comprehension of the mechanisms involved in these processes may enable us to understand the molecular pathways that promote abnormal repair and cartilage degradation in OA. This understanding would be advantageous in identifying novel targets and designing therapies to promote effective cartilage repair and successful joint ageing by preventing functional limitations and disability.

      PubDate: 2017-12-24T07:51:03Z
      DOI: 10.1016/j.arr.2017.12.006
       
  • Autobiographical memory, the ageing brain and mechanisms of psychological
           interventions
    • Authors: Andrew P. Allen; Caoilainn Doyle; Seán Commins; Richard A.P. Roche
      Abstract: Publication date: Available online 12 December 2017
      Source:Ageing Research Reviews
      Author(s): Andrew P. Allen, Caoilainn Doyle, Seán Commins, Richard A.P. Roche
      Elucidating the impact of healthy cognitive ageing and dementia on autobiographical memory (AM) may help deepen our theoretical understanding of memory and underlying neural changes. The distinction between episodic and semantic autobiographical memory is particularly informative in this regard. Psychological interventions, particularly those involving reminiscence or music, have led to differential effects on episodic and semantic autobiographical memory. We propose that executive function is a key mediator of psychological therapies on autobiographical memory. We also highlight that interventions that alleviate stress and improve mood, including in major depression, can enhance autobiographical memory. Future research employing more longitudinal approaches and examining moderating factors such as gender and education level will deepen our understanding of changes in AM in later life, enhance our theoretical understanding of the neuroscience of AM and ageing, and help to develop better targeted interventions for preserving AM in older adults.
      Graphical abstract image

      PubDate: 2017-12-24T07:51:03Z
      DOI: 10.1016/j.arr.2017.12.003
       
  • IFC: Aims and Scope
    • Abstract: Publication date: November 2017
      Source:Ageing Research Reviews, Volume 40


      PubDate: 2017-11-05T16:06:50Z
       
  • Chronic Inflammation – Inflammaging – in the Ageing Cochlea: A Novel
           Target for Future Presbycusis Therapy
    • Authors: Nathan Watson; Ding Xiaoxia Zhu Robert Frisina
      Abstract: Publication date: Available online 7 October 2017
      Source:Ageing Research Reviews
      Author(s): Nathan Watson, Bo Ding, Xiaoxia Zhu, Robert D. Frisina
      Chronic, low-grade inflammation, or inflammaging, is a crucial contributor to various age-related pathologies and natural processes in aging tissue, including the nervous system. Over the past two decades, much effort has been done to understand the mechanisms of inflammaging in disease models such as type II diabetes, cardiovascular disease, Alzheimer’s disease, Parkinson’s disease, and others. However, despite being the most prevalent neurodegenerative disorder, the number one communication disorder, and one of the top three chronic medical conditions of our aged population; little research has been conducted on the potential role of inflammation in age-related hearing loss (ARHL). Recently, it has been suggested that there is an inflammatory presence in the cochlea, perhaps involving diffusion processes of the blood-brain barrier as it relates to the inner ear. Recent research has found correlations between hearing loss and markers such as C-reactive protein, IL-6, and TNF-α indicating inflammatory status in human case-cohort studies. However, there have been very few reports of in vivo research investigating the role of chronic inflammation’s in hearing loss in the aging cochlea. Future research directed at better understanding the mechanisms of inflammation in the cochlea as well as the natural changes acquired with aging may provide a better understanding of how this process can accelerate presbycusis. Animal model experimentation and pre-clinical studies designed to recognize and characterize cochlear inflammatory mechanisms may suggest novel treatment strategies for preventing or treating ARHL. In this review, we seek to summarize key research in chronic inflammation, discuss its implications for possible roles in ARHL, and finally suggest directions for future investigations.

      PubDate: 2017-10-08T14:03:31Z
       
  • Sirt1 and Parp1 as epigenome safeguards and microRNAs as SASP-associated
           signals, in cellular senescence and aging
    • Authors: Seyedhossein Hekmatimoghaddam; Ali Dehghani-Firoozabadi Mohamad Reza Zare-Khormizi Fatemeh Pourrajab
      Abstract: Publication date: Available online 6 October 2017
      Source:Ageing Research Reviews
      Author(s): Seyedhossein Hekmatimoghaddam, Ali Dehghani-Firoozabadi, Mohamad Reza Zare-Khormizi, Fatemeh Pourrajab
      Cellular senescence (CS) is underlying mechanism of organism aging and is closely interconnected with age-related diseases (ARDs). Thus, any attempt that influences CS, may be undertaken to reverse or inhibit senescence, whereby could prolong healthy life span. Until now, two main proposes are epigenetic and genetic modifications of cell fate. The first one concerns rejuvenation through effective reprogramming in cells undergoing senescence, or derived from very old or progeroid patients, by which is effective in vitro in induced pluripotent stem cells (iPSCs). The second approach concerns modification of senescence signaling pathways like as IGF-induced agents. However, senescence research has experienced an unprecedented advance over recent years, particularly with the discovery that the rate of senescence is controlled, at least to some extent, by epigenetic pathways and biochemical processes conserved in evolution. In this review we try to concentrate in very specific pathway (DNA damage response (DDR) and epigenetic modifiers) and very specific determinants (senescence-associated secretory phenotype (SASP)-miRNAs) of human premature aging. A major challenge is to dissect the interconnectedness between the candidate elements and their relative contributions to aging, with the final goal of identifying new opportunities for design of novel anti-aging treatments or avoidance of age-associated manifestations while knowing that aging is unavoidable and we cannot expect its elimination, but prolonging healthy life span is a goal worth serious consideration.

      PubDate: 2017-10-08T14:03:31Z
       
  • Alpha-synuclein, epigenetics, mitochondria, metabolism, calcium traffic,
           & circadian dysfunction in Parkinson's disease. An integrated strategy
           for management.
    • Authors: Oliver T. Phillipson
      Abstract: Publication date: Available online 3 October 2017
      Source:Ageing Research Reviews
      Author(s): Oliver T. Phillipson
      The motor deficits which characterise the sporadic form of Parkinson's disease arise from age-related loss of a subset of dopamine neurons in the substantia nigra. Although motor symptoms respond to dopamine replacement therapies, the underlying disease process remains. This review details some features of the progressive molecular pathology and proposes deployment of a combination of nutrients: R-lipoic acid, acetyl-L-carnitine, ubiquinol, melatonin (or receptor agonists) and vitamin D3, with the collective potential to slow progression of these features. The main nutrient targets include impaired mitochondria and the associated oxidative/nitrosative stress, calcium stress and impaired gene transcription induced by pathogenic forms of alpha- synuclein. Benefits may be achieved via nutrient influence on epigenetic signaling pathways governing transcription factors for mitochondrial biogenesis, antioxidant defences and the autophagy-lysosomal pathway, via regulation of the metabolic energy sensor AMP activated protein kinase (AMPK) and the mammalian target of rapamycin mTOR. Nutrients also benefit expression of the transcription factor for neuronal survival (NR4A2), trophic factors GDNF and BDNF, and age-related calcium signals. In addition a number of non-motor related dysfunctions in circadian control, clock genes and associated metabolic, endocrine and sleep-wake activity are briefly addressed, as are late-stage complications in respect of cognitive decline and osteoporosis. Analysis of the network of nutrient effects reveals how beneficial synergies may counter the accumulation and promote clearance of pathogenic alpha-synuclein.

      PubDate: 2017-10-08T14:03:31Z
      DOI: 10.1016/j.arr.2017.09.006
       
  • Autophagy, its mechanisms and regulation: Implications in
           neurodegenerative diseases
    • Authors: Milad Moloudizargari; Mohammad Hossein Asghari; Emad Ghobadi; Marjan Fallah; Shima Rasouli; Mohammad Abdollahi
      Abstract: Publication date: Available online 18 September 2017
      Source:Ageing Research Reviews
      Author(s): Milad Moloudizargari, Mohammad Hossein Asghari, Emad Ghobadi, Marjan Fallah, Shima Rasouli, Mohammad Abdollahi
      Autophagy is a major regulatory cellular mechanism which gives the cell an ability to cope with some of the destructive events that normally occur within a metabolically living cell. This is done by maintaining the cellular homeostasis, clearance of damaged organelles and proteins and recycling necessary molecules like amino acids and fatty acids. There is a wide array of factors that influence autophagy in the state of health and disease. Disruption of these mechanisms may not only give rise to several autophagy-related disease, but also it can occur as the result of intracellular changes induced during disease pathogenesis causing exacerbation of the disease. Our knowledge is increasing regarding the role of autophagy and its mechanisms in the pathogenesis of various neurodegenerative diseases such as multiple sclerosis, Parkinson’s disease, Alzheimer’s disease, Huntington’s disease and Amyotrophic lateral sclerosis. Indeed, getting to know about the pathways of autophagy and its regulation can provide the basis for designing therapeutic interventions. In the present paper, we review the pathways of autophagy, its regulation and the possible autophagy-targeting interventions for the treatment of neurodegenerative disorders.

      PubDate: 2017-09-23T13:11:22Z
      DOI: 10.1016/j.arr.2017.09.005
       
  • Positive effects of combined cognitive and physical exercise training on
           cognitive function in older adults with mild cognitive impairment or
           dementia: A meta-analysis
    • Authors: E.G.A. Esther Karssemeijer; J.A. Justine Aaronson; W.J. Willem Bossers; T. Tara Smits; M.G.M. Marcel Olde Rikkert; R.P.C. Roy Kessels
      Abstract: Publication date: Available online 12 September 2017
      Source:Ageing Research Reviews
      Author(s): E.G.A. Esther Karssemeijer, J.A. Justine Aaronson, W.J. Willem Bossers, T. Tara Smits, M.G.M. Marcel Olde Rikkert, R.P.C. Roy Kessels
      Combined cognitive and physical exercise interventions have potential to elicit cognitive benefits in older adults with mild cognitive impairment (MCI) or dementia. This meta-analysis aims to quantify the overall effect of these interventions on global cognitive functioning in older adults with MCI or dementia. Ten randomized controlled trials that applied a combined cognitive-physical intervention with cognitive function as an outcome measure were included. For each study effect sizes were computed (i.e., post-intervention standardized mean difference (SMD) scores) and pooled, using a random-effects meta-analysis. The primary analysis showed a small-to-medium positive effect of combined cognitive-physical interventions on global cognitive function in older adults with MCI or dementia (SMD[95% confidence interval]=0.32[0.17;0.47], p<0.00). A combined intervention was equally beneficial in patients with dementia (SMD=0.36[0.12;0.60], p<0.00) and MCI (SMD=0.39[0.15;0.63], p<0.05). In addition, the analysis showed a moderate-to-large positive effect after combined cognitive-physical interventions for activities of daily living (ADL) (SMD=0.75[0.42;1.08], p<0.01) and a small-to-medium positive effect for mood (SMD=0.27[0.48;0.96], p<0.01). These functional benefits emphasize the clinical relevance of combined cognitive and physical training strategies.

      PubDate: 2017-09-18T05:20:13Z
      DOI: 10.1016/j.arr.2017.09.003
       
  • CELL REPROGRAMMING: THERAPEUTIC POTENTIAL AND THE PROMISE OF REJUVENATION
           FOR THE AGING BRAIN
    • Authors: Micaela López-León; Tiago F. Outeiro; Rodolfo G. Goya
      Abstract: Publication date: Available online 10 September 2017
      Source:Ageing Research Reviews
      Author(s): Micaela López-León, Tiago F. Outeiro, Rodolfo G. Goya
      Aging is associated with a progressive increase in the incidence of neurodegenerative diseases, with Alzheimer’s (AD) and Parkinson's (PD) disease being the most conspicuous examples. Within this context, the absence of efficacious therapies for most age-related brain pathologies has increased the interest in regenerative medicine. In particular, cell reprogramming technologies have ushered in the era of personalized therapies that not only show a significant potential for the treatment of neurodegenerative diseases but also promise to make biological rejuvenation feasible. We will first review recent evidence supporting the emerging view that aging is a reversible epigenetic phenomenon. Next, we will describe novel reprogramming approaches that overcome some of the intrinsic limitations of conventional induced–pluripotent-stem-cell technology. One of the alternative approaches, lineage reprogramming, consists of the direct conversion of one adult cell type into another by transgenic expression of multiple lineage-specific transcription factors (TF). Another strategy, termed pluripotency factor-mediated direct reprogramming, uses universal TF to generate epigenetically unstable intermediates able to differentiate into somatic cell types in response to specific differentiation factors. In the third part we will review studies showing the potential relevance of the above approaches for the treatment of AD and PD.
      Graphical abstract image

      PubDate: 2017-09-11T00:59:20Z
      DOI: 10.1016/j.arr.2017.09.002
       
  • Role of the AMPK Pathway in Promoting Autophagic Flux via Modulating
           Mitochondrial Dynamics in Neurodegenerative Diseases: Insight into Prion
           Diseases
    • Authors: Syed Zahid Ali Shah; Deming Zhao; Tariq Hussain; Lifeng Yang
      Abstract: Publication date: Available online 10 September 2017
      Source:Ageing Research Reviews
      Author(s): Syed Zahid Ali Shah, Deming Zhao, Tariq Hussain, Lifeng Yang
      Neurons are highly energy demanding cells dependent on the mitochondrial oxidative phosphorylation system. Mitochondria generate energy via respiratory complexes that constitute the electron transport chain. Adenosine triphosphate depletion or glucose starvation act as a trigger for the activation of adenosine monophosphate-activated protein kinase (AMPK). AMPK is an evolutionarily conserved protein that plays an important role in cell survival and organismal longevity through modulation of energy homeostasis and autophagy. Several studies suggest that AMPK activation may improve energy metabolism and protein clearance in the brains of patients with vascular injury or neurodegenerative disease. Mild mitochondrial dysfunction leads to activated AMPK signaling, but severe endoplasmic reticulum stress and mitochondrial dysfunction may lead to a shift from autophagy towards apoptosis and perturbed AMPK signaling. Hence, controlling mitochondrial dynamics and autophagic flux via AMPK activation might be a useful therapeutic strategy in neurodegenerative diseases to reinstate energy homeostasis and degrade misfolded proteins. In this review article, we discuss briefly the role of AMPK signaling in energy homeostasis, the structure of AMPK, activation mechanisms of AMPK, regulation of AMPK, the role of AMPK in autophagy, the role of AMPK in neurodegenerative diseases, and finally the role of autophagic flux in prion diseases.

      PubDate: 2017-09-11T00:59:20Z
      DOI: 10.1016/j.arr.2017.09.004
       
  • Health relevance of the modification of low grade inflammation in ageing
           (inflammageing) and the role of nutrition
    • Authors: Philip C. Calder; Nabil Bosco; Raphaëlle Bourdet-Sicard; Lucile Capuron; Nathalie Delzenne; Joel Doré; Claudio Franceschi; Markus J. Lehtinen; Tobias Recker; Stefano Salvioli; Francesco Visioli
      Abstract: Publication date: Available online 9 September 2017
      Source:Ageing Research Reviews
      Author(s): Philip C. Calder, Nabil Bosco, Raphaëlle Bourdet-Sicard, Lucile Capuron, Nathalie Delzenne, Joel Doré, Claudio Franceschi, Markus J. Lehtinen, Tobias Recker, Stefano Salvioli, Francesco Visioli
      Ageing of the global population has become a public health concern with an important socio-economic dimension. Ageing is characterised by an increase in the concentration of inflammatory markers in the bloodstream, a phenomenon that has been termed “inflammageing”. The inflammatory response is beneficial as an acute, transient reaction to harmful conditions, facilitating the defence, repair, turnover and adaptation of many tissues. However, chronic and low grade inflammation is likely to be detrimental for many tissues and for normal functions. We provide an overview of low grade inflammation (LGI) and determine the potential drivers and the effects of the “inflamed” phenotype observed in the elderly. We discuss the role of gut microbiota and immune system crosstalk and the gut-brain axis. Then, we focus on major health complications associated with LGI in the elderly, including mental health and wellbeing, metabolic abnormalities and infections. Finally, we discuss the possibility of manipulating LGI in the elderly by nutritional interventions. We provide an overview of the evidence that exists in the elderly for omega-3 fatty acid, probiotic, prebiotic, antioxidant and polyphenol interventions as a means to influence LGI. We conclude that slowing, controlling or reversing LGI is likely to be an important way to prevent, or reduce the severity of, age-related functional decline and the onset of conditions affecting health and well-being; that there is evidence to support specific dietary interventions as a strategy to control LGI; and that a continued research focus on this field is warranted.

      PubDate: 2017-09-11T00:59:20Z
      DOI: 10.1016/j.arr.2017.09.001
       
  • IFC: Aims and Scope
    • Abstract: Publication date: October 2017
      Source:Ageing Research Reviews, Volume 39


      PubDate: 2017-08-26T18:09:15Z
       
  • Initiation of the age-related decline of odor identification in humans: A
           meta-analysis
    • Authors: Chenping Zhang; Xiaochun Wang
      Abstract: Publication date: Available online 19 August 2017
      Source:Ageing Research Reviews
      Author(s): Chenping Zhang, Xiaochun Wang
      Background Aging is an important contributor to olfactory system deterioration in humans, leading to increased health and safety risks as well as affecting the quality of life. However, it is currently unknown when age-related olfactory deterioration begins in humans and thus when to initiate interventions to prevent or slow it. Objective To determine the decade in which olfactory function begins to deteriorate in healthy humans by determining when odor identification is first impaired. Data Source and Study Selection Studies cited in the PubMed database were searched from its inception to March 2017 using the terms “olfac*” or “smell” and “ag*”. The effect size of each comparison was calculated. Results In this meta-analysis, the effect sizes as determined using Cohen’s d for the comparisons between 30–39.9- and 40–49.9-year-olds was 0.06 (95% CI: −0.17 to 0.29), between 40–49.9- and 50–59.9-year-olds was 0.62 (95% CI: 0.20–1.04), considered a medium effect size, and between 3555-year-olds and those >55years old was 1.12 (95% CI: 1.06–1.45), considered a very large effect. Conclusion Olfactory function deterioration, as determined by an impaired ability to identify odors, starts in the fifth decade of life in healthy humans.

      PubDate: 2017-08-26T18:09:15Z
      DOI: 10.1016/j.arr.2017.08.004
       
  • IFC: Aims and Scope
    • Abstract: Publication date: September 2017
      Source:Ageing Research Reviews, Volume 38


      PubDate: 2017-08-15T14:35:35Z
       
  • Metformin reduces all-cause mortality and diseases of ageing independent
           of its effect on diabetes control: a systematic review and meta-analysis
    • Authors: Jared M. Campbell; Susan M. Bellman; Matthew D. Stephenson; Karolina Lisy.
      Abstract: Publication date: Available online 10 August 2017
      Source:Ageing Research Reviews
      Author(s): Jared M. Campbell, Susan M. Bellman, Matthew D. Stephenson, Karolina Lisy.
      This systematic review investigated whether the insulin sensitiser metformin has a geroprotective effect in humans. Pubmed and Embase were searched along with databases of unpublished studies. Eligible research investigated the effect of metformin on all-cause mortality or diseases of ageing relative to non-diabetic populations or diabetics receiving other therapies with adjustment for disease control achieved. Overall, 260 full-texts were reviewed and 53 met the inclusion criteria. Diabetics taking metformin had significantly lower all-cause mortality than non-diabetics (hazard ratio (HR)=0.93, 95%CI 0.88-0.99), as did diabetics taking metformin compared to diabetics receiving non-metformin therapies (HR=0.72, 95%CI 0.65-0.80), insulin (HR=0.68, 95%CI 0.63-0.75) or sulphonylurea (HR=0.80, 95%CI 0.66-0.97). Metformin users also had reduced cancer compared to non-diabetics (rate ratio=0.94, 95%CI 0.92-0.97) and cardiovascular disease (CVD) compared to diabetics receiving non-metformin therapies (HR=0.76, 95%CI 0.66-0.87) or insulin (HR=0.78, 95%CI 0.73-0.83). Differences in baseline characteristics were observed which had the potential to bias findings, although statistical adjustments were made. The apparent reductions in all-cause mortality and diseases of ageing associated with metformin use suggest that metformin could be extending life and healthspans by acting as a geroprotective agent.

      PubDate: 2017-08-15T14:35:35Z
      DOI: 10.1016/j.arr.2017.08.003
       
  • Aging and Osteoarthritis: Central Role of the Extracellular Matrix
    • Authors: Maryam Rahmati; Giovanna Nalesso; Ali Mobasheri; Masoud Mozafari
      Abstract: Publication date: Available online 31 July 2017
      Source:Ageing Research Reviews
      Author(s): Maryam Rahmati, Giovanna Nalesso, Ali Mobasheri, Masoud Mozafari
      Osteoarthritis (OA), is a major cause of severe joint pain, physical disability and quality of life impairment in the aging population across the developed and developing world. Increased catabolism in the extracellular matrix (ECM) of the articular cartilage is a key factor in the development and progression of OA. The molecular mechanisms leading to an impaired matrix turnover have not been fully clarified, however cellular senescence, increased expression of inflammatory mediators as well as oxidative stress in association with an inherently limited regenerative potential of the tissue, are all important contributors to OA development. All these factors are linked to and tend to be maximized by aging. Nonetheless the role of aging in compromising joint stability and function in OA has not been completely clarified yet. This review will systematically analyze cellular and structural changes taking place in the articular cartilage and bone in the pathogenesis of OA which are linked to aging. A particular emphasis will be placed on age-related changes in the phenotype of the articular chondrocytes.

      PubDate: 2017-08-05T14:01:55Z
      DOI: 10.1016/j.arr.2017.07.004
       
  • Protein aggregation, cardiovascular diseases, and exercise training: where
           do we stand'
    • Authors: Marisol Gouveia; Ke Xia; Wilfredo Colón; Sandra I. Vieira; Fernando Ribeiro
      Abstract: Publication date: Available online 28 July 2017
      Source:Ageing Research Reviews
      Author(s): Marisol Gouveia, Ke Xia, Wilfredo Colón, Sandra I. Vieira, Fernando Ribeiro
      Cells ensure their protein quality control through the proteostasis network. Aging and age-related diseases, such as neurodegenerative and cardiovascular diseases, have been associated to the reduction of proteostasis network efficiency and, consequently, to the accumulation of protein misfolded aggregates. The decline in protein homeostasis has been associated with the development and progression of atherosclerotic cardiovascular disease, cardiac hypertrophy, cardiomyopathies, and heart failure. Exercise training is a key component of the management of patients with cardiovascular disease, consistently improving quality of life and prognosis. In this review, we give an overview on age-related protein aggregation, the role of the increase of misfolded protein aggregates on cardiovascular pathophysiology, and describe the beneficial or deleterious effects of the proteostasis network on the development of cardiovascular disease. We subsequently discuss how exercise training, a key lifestyle intervention in those with cardiovascular disease, could restore proteostasis and improve disease status.

      PubDate: 2017-08-05T14:01:55Z
      DOI: 10.1016/j.arr.2017.07.005
       
  • Modulation of dendritic cell and T cell cross-talk during aging: The
           potential role of checkpoint inhibitory molecules
    • Authors: Joanne K. Gardner; Cyril D.S. Mamotte; Connie Jackaman; Delia J. Nelson
      Abstract: Publication date: Available online 20 July 2017
      Source:Ageing Research Reviews
      Author(s): Joanne K. Gardner, Cyril D.S. Mamotte, Connie Jackaman, Delia J. Nelson
      Dendritic cells (DCs) undergo continuous changes throughout life, and there is evidence that elderly DCs have a reduced capacity to stimulate T cells, which may contribute to impaired anti-tumour immune responses in elderly people with cancer. Changes in checkpoint inhibitory molecules/pathways during aging may be one mechanism that impairs the ability of elderly DCs to activate T cells. However, little is currently known regarding the combined effects of aging and cancer on DC and T cell inhibitory molecules/pathways. In this review, we discuss our current understanding of the influence of aging and cancer on key DC and T cell inhibitory molecules/pathways, the potential underlying cellular and molecular mechanisms contributing to their modulation, and the possibility of therapeutically targeting inhibitory molecules in elderly cancer patients.

      PubDate: 2017-07-21T13:32:32Z
      DOI: 10.1016/j.arr.2017.07.002
       
  • Historical demography and longevity genetics: back to the future
    • Authors: Niels van den Berg; Marian Beekman; Ken Robert Smith; Angelique Janssens; Pieternella Eline Slagboom
      Abstract: Publication date: Available online 5 July 2017
      Source:Ageing Research Reviews
      Author(s): Niels van den Berg, Marian Beekman, Ken Robert Smith, Angelique Janssens, Pieternella Eline Slagboom
      Research into the genetic component of human longevity can provide important insights in mechanisms that may protect against age-related diseases and multi-morbidity. Thus far only a limited number of robust longevity loci have been detected in either candidate or genome wide association studies. One of the issues in these genetic studies is the definition of the trait being either lifespan, including any age at death or longevity, i.e. survival above a diverse series of thresholds. Likewise heritability and segregation research have conflated lifespan with longevity. The heritability of lifespan estimated across most studies has been rather low. Environmental factors have not been sufficiently investigated and the total amount of genetic variance contributing to longevity has not been estimated in sufficiently well-defined and powered studies. Up to now, genetic longevity studies lack the required insights into the nature and size of the genetic component and the optimal strategies for meta-analysis and subject selection for Next Generation Sequencing efforts. Historical demographic data containing deep genealogical information may help in estimating the best definition and heritability for longevity, its transmission patterns in multi-generational datasets and may allow relevant additive and modifying environmental factors such as socio-economic status, geographical background, exposure to environmental effects, birth order, and number of children to be included. In this light historical demographic data may be very useful for identifying lineages in human populations that are worth investigating further by geneticists.

      PubDate: 2017-07-10T18:38:14Z
      DOI: 10.1016/j.arr.2017.06.005
       
  • A viewpoint on considering physiological principles to study stress
           resistance and resilience with aging
    • Authors: Benjamin F. Miller; Douglas R. Seals; Karyn L. Hamilton
      Abstract: Publication date: Available online 1 July 2017
      Source:Ageing Research Reviews
      Author(s): Benjamin F. Miller, Douglas R. Seals, Karyn L. Hamilton
      Adaptation to stress is identified as one of the seven pillars of aging research. Our viewpoint discusses the importance of the distinction between stress resistance and resilience, highlights how integration of physiological principles is critical for further understanding in vivo stress resistance and resilience, and advocates for the use of early warning signs to prevent a tipping point in stress resistance and resilience.

      PubDate: 2017-07-01T18:20:01Z
      DOI: 10.1016/j.arr.2017.06.004
       
  • Physical Activity and Healthy Ageing: A Systematic Review and
           Meta-analysis of longitudinal cohort studies
    • Authors: C. Daskalopoulou; B. Stubbs; C. Kralj; A. Koukounari; M. Prince; A.M. Prina
      Abstract: Publication date: Available online 23 June 2017
      Source:Ageing Research Reviews
      Author(s): C. Daskalopoulou, B. Stubbs, C. Kralj, A. Koukounari, M. Prince, A.M. Prina
      Background Older people constitute a significant proportion of the total population and their number is projected to increase by more than half by 2050. This increasing probability of late survival comes with considerable individual, economic and social impact. Physical activity (PA) can influence the ageing process but the specific relationship with healthy ageing (HA) is unclear. Methods We conducted a systematic review and meta-analysis of longitudinal studies examining the associations of PA with HA. Studies were identified from a systematic search across major electronic databases from inception as January 2017. Random-effect meta-analysis was performed to calculate a pooled effect size (ES) and 95% CIs. Studies were assessed for methodological quality. Results Overall, 23 studies were identified including 174,114 participants (30% men) with age ranges from 20 to 87 years old. There was considerable heterogeneity in the definition and measurement of HA and PA. Most of the identified studies reported a significant positive association of PA with HA, six reported a non-significant. Meta-analysis revealed that PA is positively associated with HA (ES: 1.39, 95% CI=1.23–1.57, n=17) even if adjusted for publication bias (ES: 1.27, 95% CI=1.11–1.45, n=20). Conclusions There is consistent evidence from longitudinal observational studies that PA is positively associated with HA, regardless of definition and measurement. Future research should focus on the implementation of a single metric of HA, on the use of objective measures for PA assessment and on a full-range of confounding adjustment. In addition, our research indicated the limited research on ageing in low-and-middle income countries.

      PubDate: 2017-07-01T18:20:01Z
      DOI: 10.1016/j.arr.2017.06.003
       
  • Calorie Restriction in Rodents: Caveats to Consider
    • Authors: Donald K. Ingram; Rafael de Cabo
      Abstract: Publication date: Available online 10 June 2017
      Source:Ageing Research Reviews
      Author(s): Donald K. Ingram, Rafael de Cabo
      The calorie restriction paradigm has provided one of the most widely used and most useful tools for investigating mechanisms of aging and longevity. By far, rodent models have been employed most often in these endeavors. Over decades of investigation, claims have been made that the paradigm produces the most robust demonstration that aging is malleable. In the current review of the rodent literature, we present arguments that question the robustness of the paradigm to increase lifespan and healthspan. Specifically, there are several questions to consider as follows: (1) At what age does CR no longer produce benefits? (2) Does CR attenuate cognitive decline? (3) Are there negative effects of CR, including effects on bone health, wound healing, and response to infection? (4) How important is schedule of feeding? (5) How long does CR need to be imposed to be effective? (6) How do genotype and gender influence CR? (7) What role does dietary composition play? Consideration of these questions produce many caveats that should guide future investigations to move the field forward.

      PubDate: 2017-06-12T11:21:08Z
      DOI: 10.1016/j.arr.2017.05.008
       
 
 
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