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BIOLOGY (1469 journals)                  1 2 3 4 5 6 7 8 | Last

Showing 1 - 200 of 1720 Journals sorted alphabetically
AAPS Journal     Hybrid Journal   (Followers: 21)
Achievements in the Life Sciences     Open Access   (Followers: 5)
ACS Synthetic Biology     Full-text available via subscription   (Followers: 24)
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: 27)
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: 3)
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: 2)
Advances in Bioinformatics     Open Access   (Followers: 17)
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: 12)
Advances in Developmental Biology     Full-text available via subscription   (Followers: 11)
Advances in DNA Sequence-Specific Agents     Full-text available via subscription   (Followers: 5)
Advances in Ecological Research     Full-text available via subscription   (Followers: 42)
Advances in Environmental Sciences - International Journal of the Bioflux Society     Open Access   (Followers: 17)
Advances in Enzyme Research     Open Access   (Followers: 9)
Advances in Experimental Biology     Full-text available via subscription   (Followers: 7)
Advances in Genome Biology     Full-text available via subscription   (Followers: 8)
Advances in High Energy Physics     Open Access   (Followers: 18)
Advances in Human Biology     Open Access   (Followers: 3)
Advances in Life Science and Technology     Open Access   (Followers: 16)
Advances in Life Sciences     Open Access   (Followers: 6)
Advances in Marine Biology     Full-text available via subscription   (Followers: 15)
Advances in Molecular and Cell Biology     Full-text available via subscription   (Followers: 21)
Advances in Organ Biology     Full-text available via subscription   (Followers: 1)
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: 5)
Advances in Virus Research     Full-text available via subscription   (Followers: 5)
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: 10)
Aging Cell     Open Access   (Followers: 12)
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)
Alces : A Journal Devoted to the Biology and Management of Moose     Open Access  
AMB Express     Open Access   (Followers: 1)
Ambix     Hybrid Journal   (Followers: 3)
American Biology Teacher     Full-text available via subscription   (Followers: 14)
American Fern Journal     Full-text available via subscription   (Followers: 1)
American Journal of Agricultural and Biological Sciences     Open Access   (Followers: 8)
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: 14)
American Malacological Bulletin     Full-text available via subscription   (Followers: 3)
American Naturalist     Full-text available via subscription   (Followers: 70)
Amphibia-Reptilia     Hybrid Journal   (Followers: 6)
Anaerobe     Hybrid Journal   (Followers: 4)
Analytical Methods     Full-text available via subscription   (Followers: 10)
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: 15)
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: 13)
Annual Review of Genomics and Human Genetics     Full-text available via subscription   (Followers: 23)
Annual Review of Phytopathology     Full-text available via subscription   (Followers: 10)
Anthropological Review     Open Access   (Followers: 23)
Anti-Infective Agents     Hybrid Journal   (Followers: 3)
Antibiotics     Open Access   (Followers: 9)
Antioxidants     Open Access   (Followers: 4)
Antioxidants & Redox Signaling     Hybrid Journal   (Followers: 8)
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: 10)
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: 33)
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 Biological Sciences     Open Access  
Archives of Microbiology     Hybrid Journal   (Followers: 8)
Archives of Natural History     Hybrid Journal   (Followers: 6)
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: 2)
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: 3)
Asian Journal of Biodiversity     Open Access   (Followers: 4)
Asian Journal of Biological Sciences     Open Access   (Followers: 3)
Asian Journal of Cell Biology     Open Access   (Followers: 5)
Asian Journal of Developmental Biology     Open Access   (Followers: 2)
Asian Journal of Medical and Biological Research     Open Access   (Followers: 3)
Asian Journal of Nematology     Open Access   (Followers: 4)
Asian Journal of Poultry Science     Open Access   (Followers: 3)
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: 4)
Avian Conservation and Ecology     Open Access   (Followers: 11)
Bacteriology Journal     Open Access   (Followers: 1)
Bacteriophage     Full-text available via subscription   (Followers: 3)
Bangladesh Journal of Bioethics     Open Access  
Bangladesh Journal of Plant Taxonomy     Open Access  
Bangladesh Journal of Scientific Research     Open Access   (Followers: 1)
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: 15)
Biochimie     Hybrid Journal   (Followers: 7)
BioControl     Hybrid Journal   (Followers: 5)
Biocontrol Science and Technology     Hybrid Journal   (Followers: 5)
Biodemography and Social Biology     Hybrid Journal  
BioDiscovery     Open Access   (Followers: 2)
Biodiversitas : Journal of Biological Diversity     Open Access  
Biodiversity : Research and Conservation     Open Access   (Followers: 26)
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: 5)
Biofilms     Full-text available via subscription   (Followers: 1)
Biogeosciences (BG)     Open Access   (Followers: 10)
Biogeosciences Discussions (BGD)     Open Access   (Followers: 2)
Bioinformatics     Hybrid Journal   (Followers: 291)
Bioinformatics and Biology Insights     Open Access   (Followers: 11)
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: 6)
Biological Control     Hybrid Journal   (Followers: 4)
Biological Invasions     Hybrid Journal   (Followers: 18)
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: 7)
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   (Followers: 1)
Biologie in Unserer Zeit (Biuz)     Hybrid Journal   (Followers: 40)
Biologija     Open Access  
Biology     Open Access   (Followers: 3)
Biology and Philosophy     Hybrid Journal   (Followers: 19)

        1 2 3 4 5 6 7 8 | Last

Journal Cover Ageing Research Reviews
  [SJR: 3.289]   [H-I: 78]   [10 followers]  Follow
   Hybrid Journal Hybrid journal (It can contain Open Access articles)
   ISSN (Print) 1568-1637
   Published by Elsevier Homepage  [3177 journals]
  • Multi-tissue DNA methylation age: Molecular relationships and perspectives
           for advancing biomarker utility
    • Authors: Jamaji C. Nwanaji-Enwerem; Marc G. Weisskopf; Andrea A. Baccarelli
      Pages: 15 - 23
      Abstract: Publication date: August 2018
      Source:Ageing Research Reviews, Volume 45
      Author(s): Jamaji C. Nwanaji-Enwerem, Marc G. Weisskopf, Andrea A. Baccarelli
      The multi-tissue DNA methylation estimator of chronological age (DNAm-age) has been associated with a wide range of exposures and health outcomes. Still, it is unclear how DNAm-age can have such broad relationships and how it can be best utilized as a biomarker. Understanding DNAm-age’s molecular relationships is a promising approach to address this critical knowledge gap. In this review, we discuss the existing literature regarding DNAm-age’s molecular relationships in six major categories: animal model systems, cancer processes, cellular aging processes, immune system processes, metabolic processes, and nucleic acid processes. We also present perspectives regarding the future of DNAm-age research, including the need to translate a greater number of ongoing research efforts to experimental and animal model systems.
      Graphical abstract image

      PubDate: 2018-04-26T08:29:02Z
      DOI: 10.1016/j.arr.2018.04.005
      Issue No: Vol. 45 (2018)
  • Dysbiosis of gut microbiota and microbial metabolites in Parkinson’s
    • Authors: Meng-Fei Sun; Yan-Qin Shen
      Pages: 53 - 61
      Abstract: Publication date: August 2018
      Source:Ageing Research Reviews, Volume 45
      Author(s): Meng-Fei Sun, Yan-Qin Shen
      Gut microbial dysbiosis and alteration of microbial metabolites in Parkinson’s disease (PD) have been increasingly reported. Dysbiosis in the composition and abundance of gut microbiota can affect both the enteric nervous system and the central nervous system (CNS), indicating the existence of a microbiota-gut-brain axis and thereby causing CNS diseases. Disturbance of the microbiota-gut-brain axis has been linked to specific microbial products that are related to gut inflammation and neuroinflammation. Future directions should therefore focus on the exploration of specific gut microbes or microbial metabolites that contribute to the development of PD. Microbiota-targeted interventions, such as antibiotics, probiotics and fecal microbiota transplantation, have been shown to favorably affect host health. In this review, recent findings regarding alterations and the role of gut microbiota and microbial metabolites in PD are summarized, and potential molecular mechanisms and microbiota-targeted interventions in PD are discussed.

      PubDate: 2018-05-02T20:50:34Z
      DOI: 10.1016/j.arr.2018.04.004
      Issue No: Vol. 45 (2018)
  • PGC-1α sparks the fire of neuroprotection against neurodegenerative
    • Authors: Jianjun Lv; Shuai Jiang; Zhi Yang; Wei Hu; Zheng Wang; Tian Li; Yang Yang
      Pages: 8 - 21
      Abstract: Publication date: July 2018
      Source:Ageing Research Reviews, Volume 44
      Author(s): Jianjun Lv, Shuai Jiang, Zhi Yang, Wei Hu, Zheng Wang, Tian Li, Yang Yang
      Recently, growing evidence has demonstrated that peroxisome proliferator activated receptor γ (PPARγ) coactivator-1α (PGC-1α) is a superior transcriptional regulator that acts via controlling the expression of anti-oxidant enzymes and uncoupling proteins and inducing mitochondrial biogenesis, which plays a beneficial part in the central nervous system (CNS). Given the significance of PGC-1α, we summarize the current literature on the molecular mechanisms and roles of PGC-1α in the CNS. Thus, in this review, we first briefly introduce the basic characteristics regarding PGC-1α. We then depict some of its important cerebral functions and discuss upstream modulators, partners, and downstream effectors of the PGC-1α signaling pathway. Finally, we highlight recent progress in research on the involvement of PGC-1α in certain major neurodegenerative disorders (NDDs), including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis. Collectively, the data presented here may be useful for supporting the future potential of PGC-1α as a therapeutic target.

      PubDate: 2018-04-19T08:19:36Z
      DOI: 10.1016/j.arr.2018.03.004
      Issue No: Vol. 44 (2018)
  • Sirtuins in mitochondrial stress: Indispensable helpers behind the scenes
    • Authors: Shuangzhe Lin; Haiping Xing; Tongtong Zang; Xin Ruan; Lulu Wo; Ming He
      Pages: 22 - 32
      Abstract: Publication date: July 2018
      Source:Ageing Research Reviews, Volume 44
      Author(s): Shuangzhe Lin, Haiping Xing, Tongtong Zang, Xin Ruan, Lulu Wo, Ming He
      Mitochondria play an essential part in guaranteeing normal cellular physiological functions through providing ATP and participating in diverse processes and signaling pathways. Recently, more and more studies have revealed the vital roles of mitochondria in coping with stressors in the aging process, metabolic disturbances and neurological disorders. Mitochondrial stress responses, including the mitochondrial unfolded protein response (UPRmt), antioxidant defense, mitochondrial fission, mitochondrial fusion and mitophagy, are induced to maintain cellular integrity in response to stress. The sirtuin family, a group of NAD+-dependent deacetylases, has been the focus of much attention in recent years for their multiple regulatory functions, especially in aging and metabolism. Recent reports validated the significant link between mitochondrial stress responses and the sirtuin family, which may help to elucidate the pathogenesis and therapies for diseases such as Alzheimer’s disease or Parkinson’s disease. This review will summarize recent related studies and illuminate the interplay between sirtuins and mitochondrial stress.

      PubDate: 2018-04-19T08:19:36Z
      DOI: 10.1016/j.arr.2018.03.006
      Issue No: Vol. 44 (2018)
  • Beyond ROS clearance: Peroxiredoxins in stress signaling and aging
    • Authors: Giel Detienne; Wouter De Haes; Lucas Mergan; Samantha L. Edwards; Liesbet Temmerman; Sven Van Bael
      Pages: 33 - 48
      Abstract: Publication date: July 2018
      Source:Ageing Research Reviews, Volume 44
      Author(s): Giel Detienne, Wouter De Haes, Lucas Mergan, Samantha L. Edwards, Liesbet Temmerman, Sven Van Bael
      Antioxidants were long predicted to have lifespan-promoting effects, but in general this prediction has not been well supported. While some antioxidants do seem to have a clear effect on longevity, this may not be primarily as a result of their role in the removal of reactive oxygen species, but rather mediated by other mechanisms such as the modulation of intracellular signaling. In this review we discuss peroxiredoxins, a class of proteinaceous antioxidants with redox signaling and chaperone functions, and their involvement in regulating longevity and stress resistance. Peroxiredoxins have a clear role in the regulation of lifespan and survival of many model organisms, including the mouse, Caenorhabditis elegans and Drosophila melanogaster. Recent research on peroxiredoxins − in these models and beyond − has revealed surprising new insights regarding the interplay between peroxiredoxins and longevity signaling, which will be discussed here in detail. As redox signaling is emerging as a potentially important player in the regulation of longevity and aging, increased knowledge of these fascinating antioxidants and their mode(s) of action is paramount.

      PubDate: 2018-04-19T08:19:36Z
      DOI: 10.1016/j.arr.2018.03.005
      Issue No: Vol. 44 (2018)
  • Auditory system dysfunction in Alzheimer disease and its prodromal states:
           A review
    • Authors: Gabriel M. Swords; Lydia T. Nguyen; Raksha A. Mudar; Daniel A. Llano
      Pages: 49 - 59
      Abstract: Publication date: July 2018
      Source:Ageing Research Reviews, Volume 44
      Author(s): Gabriel M. Swords, Lydia T. Nguyen, Raksha A. Mudar, Daniel A. Llano
      Recent findings suggest that both peripheral and central auditory system dysfunction occur in the prodromal stages of Alzheimer Disease (AD), and therefore may represent early indicators of the disease. In addition, loss of auditory function itself leads to communication difficulties, social isolation and poor quality of life for both patients with AD and their caregivers. Developing a greater understanding of auditory dysfunction in early AD may shed light on the mechanisms of disease progression and carry diagnostic and therapeutic importance. Herein, we review the literature on hearing abilities in AD and its prodromal stages investigated through methods such as pure-tone audiometry, dichotic listening tasks, and evoked response potentials. We propose that screening for peripheral and central auditory dysfunction in at-risk populations is a low-cost and effective means to identify early AD pathology and provides an entry point for therapeutic interventions that enhance the quality of life of AD patients.

      PubDate: 2018-04-19T08:19:36Z
      DOI: 10.1016/j.arr.2018.04.001
      Issue No: Vol. 44 (2018)
  • Procancerogenic activity of senescent cells: A case of the peritoneal
    • 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)
  • The neurochemistry of agitation in Alzheimer’s disease: a systematic
    • Authors: Kathy Y. Liu; Aisling E. Stringer; Suzanne J. Reeves; Robert J. Howard
      Pages: 99 - 107
      Abstract: Publication date: May 2018
      Source:Ageing Research Reviews, Volume 43
      Author(s): Kathy Y. Liu, Aisling E. Stringer, Suzanne J. Reeves, Robert J. Howard
      Objective To provide an up-to-date systematic review of the characteristics, methodology and findings of studies that have investigated the neurochemistry of agitation in Alzheimer’s disease (AD). Methods Electronic databases were searched for published peer-reviewed articles which provided data on any neurotransmitter system in relation to agitation in AD. Screening of titles and abstracts and data extraction from full texts were conducted in duplicate. Results Forty-five studies were included. Monoamines (serotonin, dopamine and noradrenaline) were most commonly investigated. A variety of methods were used to investigate the neurochemistry underlying agitation in AD and, although there were several conflicting findings, there was evidence of serotonergic deficit, relatively preserved dopaminergic function and compensatory overactivity of postsynaptic noradrenergic neurons in agitation in AD. Conclusions Disruption of the dynamic balance between multiple neurotransmitter systems could impair functional neural networks involved in affective regulation and executive function. Differences in study design and methodology may have contributed to conflicting findings. Future studies that overcome these limitations (e.g. using standardized criteria to define agitation) and employ neuroimaging methods such as MRI/PET to investigate specific neural networks are needed to clarify the role of neurotransmitter alterations in these patients.

      PubDate: 2018-03-18T19:12:11Z
      DOI: 10.1016/j.arr.2018.03.003
      Issue No: Vol. 43 (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)
  • Inflammageing and metaflammation: The yin and yang of type 2 diabetes
    • Authors: Francesco Prattichizzo; Valeria De Nigris; Rosangela Spiga; Elettra Mancuso; Lucia La Sala; Roberto Antonicelli; Roberto Testa; Antonio Domenico Procopio; Fabiola Olivieri; Antonio Ceriello
      Pages: 1 - 17
      Abstract: Publication date: January 2018
      Source:Ageing Research Reviews, Volume 41
      Author(s): Francesco Prattichizzo, Valeria De Nigris, Rosangela Spiga, Elettra Mancuso, Lucia La Sala, Roberto Antonicelli, Roberto Testa, Antonio Domenico Procopio, Fabiola Olivieri, Antonio Ceriello
      Type 2 diabetes mellitus (T2DM) is characterised by chronic low-grade inflammation, recently referred to as ‘metaflammation’, a relevant factor contributing to the development of both diabetes and its complications. Nonetheless, ‘canonical’ anti-inflammatory drugs do not yield satisfactory results in terms of prevention of diabetes progression and of cardiovascular events, suggesting that the causal mechanisms fostering metaflammation deserve further research to identify new druggable targets. Metaflammation resembles ageing-induced low-grade inflammation, previously referred to as inflammageing, in terms of clinical presentation and the molecular profile, pointing to a common aetiology for both conditions. Along with the mechanisms proposed to fuel inflammageing, here we dissect a plethora of pathological cascades triggered by gluco- and lipotoxicity, converging on candidate phenomena possibly explaining the enduring pro-inflammatory program observed in diabetic tissues, i.e. persistent immune-system stimulation, accumulation of senescent cells, epigenetic rearrangements, and alterations in microbiota composition. We discuss the possibility of harnessing these recent discoveries in future therapies for T2DM. Moreover, we review recent evidence regarding the ability of diets and physical exercise to modulate selected inflammatory pathways relevant for the diabetic pathology. Finally, we examine the latest findings showing putative anti-inflammatory mechanisms of anti-hyperglycaemic agents with proven efficacy against T2DM-induced cardiovascular complications, in order to gain insights into quickly translatable therapeutic approaches.
      Graphical abstract image

      PubDate: 2018-03-18T19:12:11Z
      DOI: 10.1016/j.arr.2017.10.003
      Issue No: Vol. 41 (2018)
  • The role of cellular senescence in aging through the prism of Koch-like
    • Authors: Hagai Yanai; Vadim E. Fraifeld
      Pages: 18 - 33
      Abstract: Publication date: January 2018
      Source:Ageing Research Reviews, Volume 41
      Author(s): Hagai Yanai, Vadim E. Fraifeld
      Since Hayflick’s discovery of cellular senescence (CS), a great volume of knowledge in the field has been accumulated and intensively discussed. Here, we attempted to organize the evidence “for” and “against” the hypothesized causal role of CS in aging. For that purpose, we utilized robust Koch-like logical criteria, based on the assumption that some quantitative relationships between the accumulation of senescent cells and aging rate should exist. If so, it could be expected that (i) the “CS load” would be greater in the premature aging phenotype and lesser in longevity phenotype; (ii) CS would promote age-related diseases, and (iii) the interventions that modulate the levels of senescent cells should also modulate health/lifespan. The analysis shows that CS can be considered a causal factor of aging and an important player in various age-related diseases, though its contribution may greatly vary across species. While the relative impact of senescent cells to aging could overall be rather limited and their elimination is hardly expected to be the “fountain of youth”, the potential benefits of the senolytic strategy seems a promising option in combating age-related diseases and extending healthspan.
      Graphical abstract image

      PubDate: 2018-03-18T19:12:11Z
      DOI: 10.1016/j.arr.2017.10.004
      Issue No: Vol. 41 (2018)
  • Connecting chaperone-mediated autophagy dysfunction to cellular senescence
    • Authors: Daniel Moreno-Blas; Elisa Gorostieta-Salas; Susana Castro-Obregón
      Pages: 34 - 41
      Abstract: Publication date: January 2018
      Source:Ageing Research Reviews, Volume 41
      Author(s): Daniel Moreno-Blas, Elisa Gorostieta-Salas, Susana Castro-Obregón
      Chaperone-mediated autophagy (CMA) is one of the main pathways of the lysosome-autophagy proteolytic system. It regulates different cellular process through the selective degradation of cytosolic proteins. In ageing, the function of CMA is impaired causing an inefficient stress response and the accumulation of damaged, oxidized or misfolded proteins, which is associated with numerous age-related diseases. Deficient protein degradation alters cellular proteostasis and activates signaling pathways that culminate in the induction of cellular senescence, whose accumulation is a typical feature of ageing. However, the relationship between CMA activity and cellular senescence has been poorly studied. Here, we review and integrate evidence showing that CMA dysfunction correlates with the acquisition of many hallmarks of cellular senescence and propose that loss of CMA function during aging promotes cellular senescence.

      PubDate: 2018-03-18T19:12:11Z
      DOI: 10.1016/j.arr.2017.11.001
      Issue No: Vol. 41 (2018)
  • FOXO1/3: Potential suppressors of fibrosis
    • Authors: Zhenlong Xin; Zhiqiang Ma; Wei Hu; Shuai Jiang; Zhi Yang; Tian Li; Fulin Chen; Guozhan Jia; Yang Yang
      Pages: 42 - 52
      Abstract: Publication date: January 2018
      Source:Ageing Research Reviews, Volume 41
      Author(s): Zhenlong Xin, Zhiqiang Ma, Wei Hu, Shuai Jiang, Zhi Yang, Tian Li, Fulin Chen, Guozhan Jia, Yang Yang
      Fibrosis is a universally age-related disease that involves nearly all organs. It is typically initiated by organic injury and eventually results in organ failure. There are still few effective therapeutic strategy targets for fibrogenesis. Forkhead box proteins O1 and O3 (FOXO1/3) have been shown to have favorable inhibitory effects on fibroblast activation and subsequent extracellular matrix production and can ameliorate fibrosis levels in numerous organs, including the heart, liver, lung, and kidney; they are therefore promising targets for anti-fibrosis therapy. Moreover, we can develop appropriate strategies to make the best use of FOXO1/3’s anti-fibrosis properties. The information reviewed here should be significant for understanding the roles of FOXO1/3 in fibrosis and should contribute to the design of further studies related to FOXO1/3 and the fibrotic response and shed light on a potential treatment for fibrosis.

      PubDate: 2018-03-18T19:12:11Z
      DOI: 10.1016/j.arr.2017.11.002
      Issue No: Vol. 41 (2018)
  • Differential gene expression analysis in ageing muscle and drug discovery
    • Authors: Aicha Melouane; Abdelaziz Ghanemi; Simon Aubé; Mayumi Yoshioka; Jonny St-Amand
      Pages: 53 - 63
      Abstract: Publication date: January 2018
      Source:Ageing Research Reviews, Volume 41
      Author(s): Aicha Melouane, Abdelaziz Ghanemi, Simon Aubé, Mayumi Yoshioka, Jonny St-Amand
      Identifying therapeutic target genes represents the key step in functional genomics-based therapies. Within this context, the disease heterogeneity, the exogenous factors and the complexity of genomic structure and function represent important challenges. The functional genomics aims to overcome such obstacles via identifying the gene functions and therefore highlight disease-causing genes as therapeutic targets. Genomic technologies promise to reshape the research on ageing muscle, exercise response and drug discovery. Herein, we describe the functional genomics strategies, mainly differential gene expression methods microarray, serial analysis of gene expression (SAGE), massively parallel signature sequence (MPSS), RNA sequencing (RNA seq), representational difference analysis (RDA), and suppression subtractive hybridization (SSH). Furthermore, we review these illustrative approaches that have been used to discover new therapeutic targets for some complex diseases along with the application of these tools to study the modulation of the skeletal muscle transcriptome.

      PubDate: 2018-03-18T19:12:11Z
      DOI: 10.1016/j.arr.2017.10.006
      Issue No: Vol. 41 (2018)
  • The influence and impact of ageing and immunosenescence (ISC) on adaptive
           immunity during multiple sclerosis (MS) and the animal counterpart
           experimental autoimmune encephalomyelitis (EAE)
    • Authors: Christopher Bolton; Paul A. Smith
      Pages: 64 - 81
      Abstract: Publication date: January 2018
      Source:Ageing Research Reviews, Volume 41
      Author(s): Christopher Bolton, Paul A. Smith
      The human ageing process encompasses mechanisms that effect a decline in homeostasis with increased susceptibility to disease and the development of chronic life-threatening illness. Increasing age affects the immune system which undergoes a progressive loss of efficiency, termed immunosenescence (ISC), to impact on quantitative and functional aspects of innate and adaptive immunity. The human demyelinating disease multiple sclerosis (MS) and the corresponding animal model experimental autoimmune encephalomyelitis (EAE) are strongly governed by immunological events that primarily involve the adaptive arm of the immune response. MS and EAE are frequently characterised by a chronic pathology and a protracted disease course which thereby creates the potential for exposure to the inherent, on-going effects and consequences of ISC. Collective evidence is presented to confirm the occurrence of established and unendorsed biological markers of ISC during the development of both diseases. Moreover, results are discussed from studies during the course of MS and EAE that reveal a premature upregulation of ISC-related biomarkers which indicates untimely alterations to the adaptive immune system. The effects of ISC and a prematurely aged immune system on autoimmune-associated neurodegenerative conditions such as MS and EAE are largely unknown but current evaluation of data justifies and encourages further investigation.

      PubDate: 2018-03-18T19:12:11Z
      DOI: 10.1016/j.arr.2017.10.005
      Issue No: Vol. 41 (2018)
  • Werner syndrome (WRN) gene variants and their association with altered
           function and age-associated diseases
    • Authors: Michel Lebel; Raymond J. Monnat
      Pages: 82 - 97
      Abstract: Publication date: January 2018
      Source:Ageing Research Reviews, Volume 41
      Author(s): Michel Lebel, Raymond J. Monnat
      Werner syndrome (WS) is a heritable autosomal recessive human disorder characterized by the premature onset of several age-associated pathologies including cancer. The protein defective in WS patients, WRN, is encoded by a member of the human RECQ gene family that contains both a DNA exonuclease and a helicase domain. WRN has been shown to participate in several DNA metabolic pathways including DNA replication, recombination and repair, as well as telomere maintenance and transcription modulation. Here we review base pair-level genetic variation that has been documented in WRN, with an emphasis on non-synonymous coding single nucleotide polymorphisms (SNPs) and their associations with anthropomorphic features, longevity and disease risk. These associations have been challenging to identify, as many reported WRN SNP associations appear to be further conditioned upon ethnic, age, gender or other environmental co-variables. The WRN variant phenotypic associations identified to date are intriguing, and several are of clear clinical import. Consequently, it will be important to extend these initial associations and to identify the mechanisms and conditions under which specific WRN variants may compromise WRN function to drive cellular and organismal phenotypes as well as disease risk.

      PubDate: 2018-03-18T19:12:11Z
      DOI: 10.1016/j.arr.2017.11.003
      Issue No: Vol. 41 (2018)
  • Muscle Morphology and Performance in Master Athletes: A Systematic Review
           and Meta-analyses
    • Authors: James Mckendry; Leigh Breen; Brandon J. Shad; Carolyn Greig
      Abstract: Publication date: Available online 30 April 2018
      Source:Ageing Research Reviews
      Author(s): James Mckendry, Leigh Breen, Brandon J. Shad, Carolyn Greig
      Introduction The extent to which chronic exercise training preserves age-related decrements in physical function, muscle strength, mass and morphology is unclear. Our aim was to conduct a systematic review of the literature to determine to what extent chronically trained master athletes (strength/power and endurance) preserve levels of physical function, muscle strength, muscle mass and morphology in older age, compared with older and younger controls and young trained individuals. Methods The systematic data search included Medline, EMBASE, SPORTDiscus, CINAHL and Web of Science databases. Inclusion criteria : i) master athletes mean exercise training duration ≥20 years ii) master athletes mean age of cohort >59 years) iii) at least one measurement of muscle mass/volume/fibre-type morphology and/or strength/physical function. Results Fifty-five eligible studies were identified. Meta-analyses were carried out on maximal aerobic capacity, maximal voluntary contraction and body composition. Master endurance athletes (42.0 ± 6.6 ml kg−1 min−1) exhibited VO2max values comparable with young healthy controls (43.1 ± 6.8 ml kg−1 min−1, P = 0.84), greater than older controls (27.1 ± 4.3−1 min−1, P < 0.01) and master strength/power athletes (26.5 ± 2.3−1.min−1, P < 0.01), and lower than young endurance trained individuals (60.0 ± 5.4 ml kg−1 min−1, P < 0.01). Master strength/power athletes (0.60 (0.28 to 0.93) P < 0.01) and young controls (0.71 (0.06 to 1.36) P < 0.05) were significantly stronger compared with the other groups. Body fat % was greater in master endurance athletes than young endurance trained (−4.44% (−8.44 to −0.43) P < 0.05) but lower compared with older controls (7.11% (5.70 to 8.52) P < 0.01). Conclusion Despite advancing age, this review suggests that chronic exercise training preserves physical function, muscular strength and body fat levels similar to that of young, healthy individuals in an exercise mode-specific manner.

      PubDate: 2018-05-02T20:50:34Z
      DOI: 10.1016/j.arr.2018.04.007
    • Authors: Eldris Iglesias; Alba Pesini; Nuria Garrido-Pérez; Patricia Meade; M. Pilar Bayona-Bafaluy; Julio Montoya; Eduardo Ruiz-Pesini
      Abstract: Publication date: Available online 22 April 2018
      Source:Ageing Research Reviews
      Author(s): Eldris Iglesias, Alba Pesini, Nuria Garrido-Pérez, Patricia Meade, M. Pilar Bayona-Bafaluy, Julio Montoya, Eduardo Ruiz-Pesini
      Late-onset Parkinson disease is a multifactorial and multietiological disorder, age being one of the factors implicated. Genetic and/or environmental factors, such as pesticides, can also be involved. Up to 80% of dopaminergic neurons of the substantia nigra are lost before motor features of the disorder begin to appear. In humans, these neurons are only formed a few weeks after fertilization. Therefore, prenatal exposure to pesticides or industrial chemicals during crucial steps of brain development might also alter their proliferation and differentiation. Oxidative phosphorylation is one of the metabolic pathways sensitive to environmental toxicants and it is crucial for neuronal differentiation. Many inhibitors of this biochemical pathway, frequently found as persistent organic pollutants, affect dopaminergic neurogenesis, promote the degeneration of these neurons and increase the risk of suffering late-onset Parkinson disease. Here, we discuss how an early, prenatal, exposure to these oxidative phosphorylation xenobiotics might trigger a late-onset, old age, Parkinson disease.

      PubDate: 2018-04-26T08:29:02Z
      DOI: 10.1016/j.arr.2018.04.006
  • Effective multicomponent interventions in comparison to active control and
           no interventions on physical capacity, cognitive function and instrumental
           activities of daily living in elderly people with and without mild
           impaired cognition – A systematic review and network meta-analysis
    • Authors: Marina Bruderer-Hofstetter; Anne-Kathrin Rausch-Osthoff; André Meichtry; Thomas Münzer; Karin Niedermann
      Abstract: Publication date: Available online 18 April 2018
      Source:Ageing Research Reviews
      Author(s): Marina Bruderer-Hofstetter, Anne-Kathrin Rausch-Osthoff, André Meichtry, Thomas Münzer, Karin Niedermann
      Multicomponent interventions (MCT) combine physical exercises and cognitive training and seem to be most effective in improving cognition in elderly people. However, literature is inconclusive if MCTs are superior to active comparison interventions, if delivery modes matter, and if people can transfer achieved effects to instrumental activities of daily living (IADL). This network meta-analysis aimed to a) identify MCTs that were effective on physical capacity and/or cognitive function and able to transfer these effects into IADL in elderly people with normal cognition (NC) and mild cognitive impairment (MCI); b) provide a rating on the best interventions per outcome; c) evaluate MCTs’ mode of delivery. Eligible studies were randomized controlled trials comparing MCTs to active comparison or no treatments. Six studies in participants with MCI (n = 1088) and eleven studies in participants with NC (n = 670) were included. Five effective MCTs that were superior to physical exercises or cognitive training alone in improving physical capacity and/or cognitive function were detected, however none of these MCTs improved IADL. In people with NC MCTs performed separately or simultaneously were effective. However, in people with MCI MCTs performed separately were more effective. A framework needs to be developed to better understand the mediating effects of physical capacity and cognitive function on IADL and to design MCTs that effectively improve IADL.

      PubDate: 2018-04-19T08:19:36Z
      DOI: 10.1016/j.arr.2018.04.002
  • The multiple functions of melatonin in regenerative medicine
    • Authors: Maryam Majidinia; Russel J. Reiter; Seyed-Kazem Shakouri; Iraj Mohebbi; Mojgan Rasteghar; Mojtaba Kaviani; Saber Ghazizadeh Darband; Rana Jahanban-Esfahlan; Seyed Mohammad Nabavi; Bahman Yousefik
      Abstract: Publication date: Available online 6 April 2018
      Source:Ageing Research Reviews
      Author(s): Maryam Majidinia, Russel J. Reiter, Seyed-Kazem Shakouri, Iraj Mohebbi, Mojgan Rasteghar, Mojtaba Kaviani, Saber Ghazizadeh Darband, Rana Jahanban-Esfahlan, Seyed Mohammad Nabavi, Bahman Yousefik
      Melatonin research has been experiencing hyper growth in the last two decades; this relates to its numerous physiological functions including anti-inflammation, oncostasis, circadian and endocrine rhythm regulation, and its potent antioxidant activity. Recently, a large number of studies have focused on the role of melatonin in the regeneration of cells or tissues after their partial loss. In this review, we discuss the recent findings on the molecular involvement of melatonin in the regeneration of various tissues including the nervous system, liver, bone, kidney, bladder, skin, and muscle, among others.

      PubDate: 2018-04-19T08:19:36Z
      DOI: 10.1016/j.arr.2018.04.003
  • Interventional programmes to improve cognition during healthy and
           pathological ageing: Cortical modulations and evidence for brain
    • Authors: Jesús Cespón; Carlo Miniussi; Maria Concetta Pellicciari
      Abstract: Publication date: Available online 6 March 2018
      Source:Ageing Research Reviews
      Author(s): Jesús Cespón, Carlo Miniussi, Maria Concetta Pellicciari
      A growing body of evidence suggests that healthy elderly individuals and patients with Alzheimer’s disease retain an important potential for neuroplasticity. This review summarizes studies investigating the modulation of neural activity and structural brain integrity in response to interventions involving cognitive training, physical exercise and non-invasive brain stimulation in healthy elderly and cognitively impaired subjects (including patients with mild cognitive impairment (MCI) and Alzheimer’s disease). Moreover, given the clinical relevance of neuroplasticity, we discuss how evidence for neuroplasticity can be inferred from the functional and structural brain changes observed after implementing these interventions. We emphasize that multimodal programmes, which combine several types of interventions, improve cognitive function to a greater extent than programmes that use a single interventional approach. We suggest specific methods for weighting the relative importance of cognitive training, physical exercise and non-invasive brain stimulation according to the functional and structural state of the brain of the targeted subject to maximize the cognitive improvements induced by multimodal programmes.

      PubDate: 2018-03-07T18:43:49Z
      DOI: 10.1016/j.arr.2018.03.001
  • Role of Sirtuin1-p53 regulatory axis in Aging, Cancer and Cellular
    • Authors: Agnes L.C. Ong; Thamil Selvee Ramasamy
      Abstract: Publication date: Available online 21 February 2018
      Source:Ageing Research Reviews
      Author(s): Agnes L.C. Ong, Thamil Selvee Ramasamy
      Regulatory role of Sirtuin 1 (SIRT1), one of the most extensively studied members of its kind in histone deacetylase family in governing multiple cellular fates, is predominantly linked to p53 activity. SIRT1 deacetylates p53 in a NAD+-dependent manner to inhibit transcription activity of p53, in turn modulate pathways that are implicated in regulation of tissue homoeostasis and many disease states. In this review, we discuss the role of SIRT1-p53 pathway and its regulatory axis in the cellular events which are implicated in cellular aging, cancer and reprogramming. It is noteworthy that these cellular events share few common regulatory pathways, including Sirt1-p53-LDHA-Myc,miR-34a,-Let7 regulatory network, which forms a positive feedback loop that controls cell cycle, metabolism, proliferation, differentiation, epigenetics and many others. In the context of aging, SIRT1 expression is reduced as a protective mechanism against oncogenesis and for maintenance of tissue homeostasis. Interestingly, its activation in aged cells is evidenced in response to DNA damage to protect the cells from p53-dependent apoptosis or senescence, predispose these cells to neoplastic transformation. Importantly, the dual roles of Sirt1-p53 axis in aging and tumourigenesis, either as tumour suppressor or tumour promoter are determined by SIRT1 localisation and type of cells. Conceptualising the distinct similarity between tumorigenesis and cellular reprogramming, this review provides a perspective discussion on involvement of SIRT1 in improving efficiency in the induction and maintenance of pluripotent state. Further research in understanding the role of SIRT1-p53 pathway and their associated regulators and strategies to manipulate this regulatory axis very likely foster the development of therapeutics and strategies for treating cancer and aging associated degenerative diseases.

      PubDate: 2018-02-25T18:11:21Z
      DOI: 10.1016/j.arr.2018.02.004
  • 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
  • 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 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
    • 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
    • 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
  • 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
  • Role of the AMPK Pathway in Promoting Autophagic Flux via Modulating
           Mitochondrial Dynamics in Neurodegenerative Diseases: Insight into Prion
    • 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
  • Initiation of the age-related decline of odor identification in humans: A
    • 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
  • 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
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