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  Subjects -> BIOLOGY (Total: 2982 journals)
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BIOLOGY (1420 journals)                  1 2 3 4 5 6 7 8 | Last

Showing 1 - 200 of 1720 Journals sorted alphabetically
AAPS Journal     Hybrid Journal   (Followers: 18)
Achievements in the Life Sciences     Open Access   (Followers: 4)
ACS Synthetic Biology     Full-text available via subscription   (Followers: 20)
Acta Biologica Colombiana     Open Access   (Followers: 6)
Acta Biologica Hungarica     Full-text available via subscription   (Followers: 4)
Acta Biologica Sibirica     Open Access  
Acta Biomaterialia     Hybrid Journal   (Followers: 25)
Acta Biotheoretica     Hybrid Journal   (Followers: 5)
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 Parasitologica     Hybrid Journal   (Followers: 9)
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)
Advances in Antiviral Drug Design     Full-text available via subscription   (Followers: 3)
Advances in Bioinformatics     Open Access   (Followers: 18)
Advances in Biological Regulation     Hybrid Journal   (Followers: 4)
Advances in Biology     Open Access   (Followers: 8)
Advances in Biosensors and Bioelectronics     Open Access   (Followers: 6)
Advances in Cell Biology     Open Access   (Followers: 23)
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: 39)
Advances in Ecology     Open Access   (Followers: 13)
Advances in Environmental Sciences - International Journal of the Bioflux Society     Open Access   (Followers: 20)
Advances in Enzyme Research     Open Access   (Followers: 10)
Advances in Experimental Biology     Full-text available via subscription   (Followers: 7)
Advances in Genome Biology     Full-text available via subscription   (Followers: 12)
Advances in High Energy Physics     Open Access   (Followers: 20)
Advances in Human Biology     Open Access  
Advances in Life Science and Technology     Open Access   (Followers: 14)
Advances in Life Sciences     Open Access   (Followers: 4)
Advances in Marine Biology     Full-text available via subscription   (Followers: 16)
Advances in Molecular and Cell Biology     Full-text available via subscription   (Followers: 21)
Advances in Planar Lipid Bilayers and Liposomes     Full-text available via subscription   (Followers: 3)
Advances in Regenerative Biology     Open Access   (Followers: 1)
Advances in Structural Biology     Full-text available via subscription   (Followers: 7)
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: 7)
Aging Cell     Open Access   (Followers: 9)
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: 13)
AJP Endocrinology and Metabolism     Full-text available via subscription   (Followers: 22)
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: 12)
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 Biostatistics     Open Access   (Followers: 9)
American Journal of Human Biology     Hybrid Journal   (Followers: 12)
American Journal of Medical and Biological Research     Open Access   (Followers: 5)
American Journal of Plant Sciences     Open Access   (Followers: 20)
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: 63)
Amphibia-Reptilia     Hybrid Journal   (Followers: 6)
Anaerobe     Hybrid Journal   (Followers: 4)
Analytical Methods     Full-text available via subscription   (Followers: 7)
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: 8)
Annals of Biomedical Engineering     Hybrid Journal   (Followers: 18)
Annals of Human Biology     Hybrid Journal   (Followers: 4)
Annual Review of Biomedical Engineering     Full-text available via subscription   (Followers: 17)
Annual Review of Biophysics     Full-text available via subscription   (Followers: 25)
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: 14)
Annual Review of Genomics and Human Genetics     Full-text available via subscription   (Followers: 18)
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: 8)
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: 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: 4)
Aquatic Ecology     Hybrid Journal   (Followers: 30)
Aquatic Ecosystem Health & Management     Hybrid Journal   (Followers: 13)
Aquatic Science and Technology     Open Access   (Followers: 3)
Aquatic Toxicology     Hybrid Journal   (Followers: 19)
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: 7)
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: 2)
Artificial Photosynthesis     Open Access   (Followers: 1)
Asian Bioethics Review     Full-text available via subscription   (Followers: 1)
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: 5)
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: 3)
Asian Journal of Poultry Science     Open Access   (Followers: 4)
Australian Life Scientist     Full-text available via subscription   (Followers: 2)
Australian Mammalogy     Hybrid Journal   (Followers: 5)
Autophagy     Hybrid Journal   (Followers: 2)
Avian Biology Research     Full-text available via subscription   (Followers: 3)
Avian Conservation and Ecology     Open Access   (Followers: 7)
Bacteriology Journal     Open Access   (Followers: 2)
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     Full-text available via subscription   (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)
Biodiversidad Colombia     Open Access  
Biodiversity : Research and Conservation     Open Access   (Followers: 26)
Biodiversity and Natural History     Open Access   (Followers: 5)
Biodiversity Data Journal     Open Access   (Followers: 3)
Biodiversity Informatics     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: 9)
Biogeosciences Discussions (BGD)     Open Access   (Followers: 1)
Bioinformatics     Hybrid Journal   (Followers: 233)
Bioinformatics and Biology Insights     Open Access   (Followers: 14)
Bioinspiration & Biomimetics     Hybrid Journal   (Followers: 6)
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: 4)
Biological Control     Hybrid Journal   (Followers: 5)
Biological Invasions     Hybrid Journal   (Followers: 16)
Biological Journal of the Linnean Society     Hybrid Journal   (Followers: 14)
Biological Letters     Open Access   (Followers: 4)
Biological Procedures Online     Open Access  
Biological Psychiatry     Hybrid Journal   (Followers: 41)
Biological Psychology     Hybrid Journal   (Followers: 6)
Biological Research     Open Access  
Biological Rhythm Research     Hybrid Journal   (Followers: 2)
Biological Theory     Hybrid Journal   (Followers: 1)
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: 44)
Biologija     Open Access  
Biology     Open Access   (Followers: 5)
Biology and Philosophy     Hybrid Journal   (Followers: 16)
Biology Bulletin     Hybrid Journal   (Followers: 1)
Biology Bulletin Reviews     Hybrid Journal  
Biology Direct     Open Access   (Followers: 7)
Biology Letters     Full-text available via subscription   (Followers: 35)
Biology Methods and Protocols     Hybrid Journal  

        1 2 3 4 5 6 7 8 | Last

Journal Cover Ageing Research Reviews
  [SJR: 3.289]   [H-I: 78]   [7 followers]  Follow
    
   Hybrid Journal Hybrid journal (It can contain Open Access articles)
   ISSN (Print) 1568-1637
   Published by Elsevier Homepage  [3031 journals]
  • Frailty and sarcopenia: The potential role of an aged immune system
    • Authors: Daisy Wilson; Thomas Jackson; Elizabeth Sapey; Janet M. Lord
      Pages: 1 - 10
      Abstract: Publication date: July 2017
      Source:Ageing Research Reviews, Volume 36
      Author(s): Daisy Wilson, Thomas Jackson, Elizabeth Sapey, Janet M. Lord
      Frailty is a common negative consequence of ageing. Sarcopenia, the syndrome of loss of muscle mass, quality and strength, is more common in older adults and has been considered a precursor syndrome or the physical manifestation of frailty. The pathophysiology of both syndromes is incompletely described with multiple causes, inter-relationships and complex pathways proposed. Age-associated changes to the immune system (both immunesenescence, the decline in immune function with ageing, and inflammageing, a state of chronic inflammation) have been suggested as contributors to sarcopenia and frailty but a direct causative role remains to be established. Frailty, sarcopenia and immunesenescence are commonly described in older adults but are not ubiquitous to ageing. There is evidence that all three conditions are reversible and all three appear to share common inflammatory drivers. It is unclear whether frailty, sarcopenia and immunesenescence are separate entities that co-occur due to coincidental or potentially confounding factors, or whether they are more intimately linked by the same underlying cellular mechanisms. This review explores these possibilities focusing on innate immunity, and in particular associations with neutrophil dysfunction, inflammation and known mechanisms described to date. Furthermore, we consider whether the age-related decline in immune cell function (such as neutrophil migration), increased inflammation and the dysregulation of the phosphoinositide 3-kinase (PI3K)-Akt pathway in neutrophils could contribute pathogenically to sarcopenia and frailty.

      PubDate: 2017-02-25T01:56:12Z
      DOI: 10.1016/j.arr.2017.01.006
      Issue No: Vol. 36 (2017)
       
  • Relationship between depression and frailty in older adults: A systematic
           review and meta-analysis
    • Authors: Pinar Soysal; Nicola Veronese; Trevor Thompson; Kai G. Kahl; Brisa S. Fernandes; A. Matthew Prina; Marco Solmi; Patricia Schofield; Ai Koyanagi; Ping-Tao Tseng; Pao-Yao Lin; Che-Sheng Chu; Theodore D. Cosco; Matteo Cesari; Andre F. Carvalho; Brendon Stubbs
      Pages: 78 - 87
      Abstract: Publication date: July 2017
      Source:Ageing Research Reviews, Volume 36
      Author(s): Pinar Soysal, Nicola Veronese, Trevor Thompson, Kai G. Kahl, Brisa S. Fernandes, A. Matthew Prina, Marco Solmi, Patricia Schofield, Ai Koyanagi, Ping-Tao Tseng, Pao-Yao Lin, Che-Sheng Chu, Theodore D. Cosco, Matteo Cesari, Andre F. Carvalho, Brendon Stubbs
      Aim Depression and frailty are prevalent and burdensome in older age. However, the relationships between these entities are unclear and no quantitative meta- analysis exists. We conducted a systematic review and meta-analysis to investigate the associations between depression and frailty. Methods Two authors searched major electronic databases from inception until November-2016 for cross-sectional/longitudinal studies investigating depression and frailty. The strength of the reciprocal associations between frailty and depression was assessed through odds ratios (ORs) adjusted for potential confounders. Results From 2306 non duplicated hits, 24 studies were included. The overall prevalence of depression in 8023 people with frailty was 38.60% (95% CI 30.07–47.10, I2 =94%). Those with frailty were at increased odds of having depression (OR adjusted for publication bias 4.42, 95%CI 2.66–7.35, k=11), also after adjusting for potential confounders (OR=2.64; 95%CI: 1.59–4.37, I2 =55%, k=4). The prevalence of frailty in 2167 people with depression was 40.40% (95%CI 27.00–55.30, I2 =97%). People with depression were at increased odds of having frailty (OR=4.07, 95%CI 1.93–8.55, k=8). The pooled OR for incident frailty, adjusted for a median of 7 confounders, was 3.72 (95%CI 1.95–7.08, I2 =98%, k=4), whilst in two studies frailty increased the risk of incident depression with an OR=1.90 (95%CI 1.55–2.32, I2 =0%). Conclusion This meta-analysis points to a reciprocal interaction between depression and frailty in older adults. Specifically, each condition is associated with an increased prevalence and incidence of the other, and may be a risk factor for the development of the other. However, further prospective investigations are warranted.

      PubDate: 2017-04-04T23:33:50Z
      DOI: 10.1016/j.arr.2017.03.005
      Issue No: Vol. 36 (2017)
       
  • HIV-associated cellular senescence: A contributor to accelerated aging
    • Authors: Justin Cohen; Claudio Torres
      Pages: 117 - 124
      Abstract: Publication date: July 2017
      Source:Ageing Research Reviews, Volume 36
      Author(s): Justin Cohen, Claudio Torres
      Due to the advent of antiretroviral therapy HIV is no longer a terminal disease and the HIV infected patients are becoming increasingly older. While this is a major success, with increasing age comes an increased risk for disease. The age-related comorbidities that HIV infected patients experience suggest that they suffer from accelerated aging. One possible contributor to this accelerated aging is cellular senescence, an age-associated response that can occur prematurely in response to stress, and that is emerging as a contributor to disease and aging. HIV patients experience several stressors such as the virus itself, antiretroviral drugs and to a lesser extent, substance abuse that can induce cellular senescence. This review summarizes the current knowledge of senescence induction in response to these stressors and their relation to the comorbidities in HIV patients. Cellular senescence may be a possible therapeutic target for these comorbidities.

      PubDate: 2017-04-19T01:43:40Z
      DOI: 10.1016/j.arr.2016.12.004
      Issue No: Vol. 36 (2017)
       
  • Gut microbiota: A player in aging and a target for anti-aging intervention
    • Authors: Alexander M. Vaiserman; Alexander K. Koliada; Francesco Marotta
      Pages: 36 - 45
      Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35
      Author(s): Alexander M. Vaiserman, Alexander K. Koliada, Francesco Marotta
      Aging-associated alterations in composition, diversity and functional features of intestinal microbiota are well-described in the modern literature. They are suggested to be caused by an age-related decline in immune system functioning (immunosenescence) and a low-grade chronic inflammation (inflammaging), which accompany many aging-associated pathologies. The microbiota-targeted dietary and probiotic interventions have been shown to favorably affect the host health and aging by an enhancement of antioxidant activity, improving immune homeostasis, suppression of chronic inflammation, regulation of fat deposition and metabolism and prevention of insulin resistance. Recently, a high effectiveness and safety of novel therapeutic application such as fecal microbiota transplantation in the prevention and treatment of age-related pathological conditions including atherosclerosis, type 2 diabetes and Parkinson’s disease has been demonstrated. In this review, recent research findings are summarized on the role of gut micribiota in aging processes with emphasis on therapeutic potential of microbiome-targeted interventions in anti-aging medicine,

      PubDate: 2017-01-22T14:21:57Z
      DOI: 10.1016/j.arr.2017.01.001
      Issue No: Vol. 35 (2017)
       
  • The role of the anti-ageing protein Klotho in vascular physiology and
           pathophysiology
    • Authors: Rik Mencke; Jan-Luuk Hillebrands
      Pages: 124 - 146
      Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35
      Author(s): Rik Mencke, Jan-Luuk Hillebrands
      Klotho is an anti-ageing protein that functions in many pathways that govern ageing, like regulation of phosphate homeostasis, insulin signaling, and Wnt signaling. Klotho expression levels and levels in blood decline during ageing. The vascular phenotype of Klotho deficiency features medial calcification, intima hyperplasia, endothelial dysfunction, arterial stiffening, hypertension, and impaired angiogenesis and vasculogenesis, with characteristics similar to aged human arteries. Klotho-deficient phenotypes can be prevented and rescued by Klotho gene expression or protein supplementation. High phosphate levels are likely to be directly pathogenic and are a prerequisite for medial calcification, but more important determinants are pathways that regulate cellular senescence, suggesting that deficiency of Klotho renders cells susceptible to phosphate toxicity. Overexpression of Klotho is shown to ameliorate medial calcification, endothelial dysfunction, and hypertension. Endogenous vascular Klotho expression is a controversial subject and, currently, no compelling evidence exists that supports the existence of vascular membrane-bound Klotho expression, as expressed in kidney. In vitro, Klotho has been shown to decrease oxidative stress and apoptosis in both SMCs and ECs, to reduce SMC calcification, to maintain the contractile SMC phenotype, and to prevent μ-calpain overactivation in ECs. Klotho has many protective effects with regard to the vasculature and constitutes a very promising therapeutic target. The purpose of this review is to explore the etiology of the vascular phenotype of Klotho deficiency and the therapeutic potential of Klotho in vascular disease.

      PubDate: 2017-03-17T06:00:14Z
      DOI: 10.1016/j.arr.2016.09.001
      Issue No: Vol. 35 (2017)
       
  • Neuromuscular contributions to the age-related reduction in muscle power:
           Mechanisms and potential role of high velocity power training
    • Authors: Neal B. McKinnon; Denise M. Connelly; Charles L. Rice; Susan W. Hunter; Timothy J. Doherty
      Pages: 147 - 154
      Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35
      Author(s): Neal B. McKinnon, Denise M. Connelly, Charles L. Rice, Susan W. Hunter, Timothy J. Doherty
      Although much of the literature on neuromuscular changes with aging has focused on loss of muscle mass and isometric strength, deficits in muscle power are more pronounced with aging and may be a more sensitive measure of neuromuscular degeneration. This review aims to identify the adaptations to the neuromuscular system with aging, with specific emphasis on changes that result in decreased muscle power. We discuss how these changes in neuromuscular performance can affect mobility, and ultimately contribute to an increased risk for falls in older adults. Finally, we evaluate the literature regarding high-velocity muscle power training (PT), and its potential advantages over conventional strength training for improving functional performance and mitigating fall risk in older adults.

      PubDate: 2017-03-17T06:00:14Z
      DOI: 10.1016/j.arr.2016.09.003
      Issue No: Vol. 35 (2017)
       
  • Targeting chaperones, heat shock factor-1, and unfolded protein response:
           Promising therapeutic approaches for neurodegenerative disorders
    • Authors: Shambhunath Bose; Jungsook Cho
      Pages: 155 - 175
      Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35
      Author(s): Shambhunath Bose, Jungsook Cho
      Protein misfolding, which is known to cause several serious diseases, is an emerging field that addresses multiple therapeutic areas. Misfolding of a disease-specific protein in the central nervous system ultimately results in the formation of toxic aggregates that may accumulate in the brain, leading to neuronal cell death and dysfunction, and associated clinical manifestations. A large number of neurodegenerative diseases in humans, including Alzheimer’s, Parkinson’s, Huntington’s, and prion diseases, are primarily caused by protein misfolding and aggregation. Notably, the cellular system is equipped with a protein quality control system encompassing chaperones, ubiquitin proteasome system, and autophagy, as a defense mechanism that monitors protein folding and eliminates inappropriately folded proteins. As the intrinsic molecular mechanisms of protein misfolding become more clearly understood, the novel therapeutic approaches in this arena are gaining considerable interest. The present review will describe the chaperones network and different approaches as the therapeutic targets for neurodegenerative diseases. Current and emerging therapeutic approaches to combat neurodegenerative diseases, addressing the roles of molecular, chemical, and pharmacological chaperones, as well as heat shock factor-1 and the unfolded protein response, are also discussed in detail.

      PubDate: 2017-03-17T06:00:14Z
      DOI: 10.1016/j.arr.2016.09.004
      Issue No: Vol. 35 (2017)
       
  • Sex differences in the prevalence and incidence of mild cognitive
           impairment: A meta-analysis
    • Authors: Bonnie Au; Sydney Dale-McGrath; Mary C. Tierney
      Pages: 176 - 199
      Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35
      Author(s): Bonnie Au, Sydney Dale-McGrath, Mary C. Tierney
      Objective More women have Alzheimer’s disease (AD) than men. Understanding sex differences in mild cognitive impairment (MCI) may further knowledge of AD etiology and prevention. We conducted a meta-analysis to examine sex differences in the prevalence and incidence of MCI, which included amnestic and non-amnestic subtypes. Method Systematic searches were performed in July 2015 using MEDLINE/PubMed, Scopus, and PsycINFO for population-or community-based studies with MCI data for men and women. Random-effects model were used. Results Fifty-six studies were included. There were no statistically significant sex differences in prevalence or incidence of amnestic MCI. There was a significantly higher prevalence (p =0.038), but not incidence, of non-amnestic MCI among women. There were no sex differences in studies that combined both subtypes of MCI. Conclusion The only statistically significant finding emerging from this study was that women have a higher prevalence of non-amnestic MCI. To better understand sex differences in the preclinical stages of dementia, studies must better characterize the etiology of the cognitive impairment.

      PubDate: 2017-03-17T06:00:14Z
      DOI: 10.1016/j.arr.2016.09.005
      Issue No: Vol. 35 (2017)
       
  • Sarcopenic obesity or obese sarcopenia: A cross talk between
           age-associated adipose tissue and skeletal muscle inflammation as a main
           mechanism of the pathogenesis
    • Authors: Alexander Kalinkovich; Gregory Livshits
      Pages: 200 - 221
      Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35
      Author(s): Alexander Kalinkovich, Gregory Livshits
      Sarcopenia, an age-associated decline in skeletal muscle mass coupled with functional deterioration, may be exacerbated by obesity leading to higher disability, frailty, morbidity and mortality rates. In the combination of sarcopenia and obesity, the state called sarcopenic obesity (SOB), some key age- and obesity-mediated factors and pathways may aggravate sarcopenia. This review will analyze the mechanisms underlying the pathogenesis of SOB. In obese adipose tissue (AT), adipocytes undergo hypertrophy, hyperplasia and activation resulted in accumulation of pro-inflammatory macrophages and other immune cells as well as dysregulated production of various adipokines that together with senescent cells and the immune cell-released cytokines and chemokines create a local pro-inflammatory status. In addition, obese AT is characterized by excessive production and disturbed capacity to store lipids, which accumulate ectopically in skeletal muscle. These intramuscular lipids and their derivatives induce mitochondrial dysfunction characterized by impaired β-oxidation capacity and increased reactive oxygen species formation providing lipotoxic environment and insulin resistance as well as enhanced secretion of some pro-inflammatory myokines capable of inducing muscle dysfunction by auto/paracrine manner. In turn, by endocrine manner, these myokines may exacerbate AT inflammation and also support chronic low grade systemic inflammation (inflammaging), overall establishing a detrimental vicious circle maintaining AT and skeletal muscle inflammation, thus triggering and supporting SOB development. Under these circumstances, we believe that AT inflammation dominates over skeletal muscle inflammation. Thus, in essence, it redirects the vector of processes from “sarcopenia→obesity” to “obesity→sarcopenia”. We therefore propose that this condition be defined as “obese sarcopenia”, to reflect the direction of the pathological pathway.
      Graphical abstract image

      PubDate: 2017-03-17T06:00:14Z
      DOI: 10.1016/j.arr.2016.09.008
      Issue No: Vol. 35 (2017)
       
  • Nutrition for the ageing brain: Towards evidence for an optimal diet
    • Authors: David Vauzour; Maria Camprubi-Robles; Sophie Miquel-Kergoat; Cristina Andres-Lacueva; Diána Bánáti; Pascale Barberger-Gateau; Gene L. Bowman; Laura Caberlotto; Robert Clarke; Eef Hogervorst; Amanda J. Kiliaan; Ugo Lucca; Claudine Manach; Anne-Marie Minihane; Ellen Siobhan Mitchell; Robert Perneczky; Hugh Perry; Anne-Marie Roussel; Jeroen Schuermans; John Sijben; Jeremy P.E. Spencer; Sandrine Thuret; Ondine van de Rest; Maurits Vandewoude; Keith Wesnes; Robert J. Williams; Robin S.B. Williams; Maria Ramirez
      Pages: 222 - 240
      Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35
      Author(s): David Vauzour, Maria Camprubi-Robles, Sophie Miquel-Kergoat, Cristina Andres-Lacueva, Diána Bánáti, Pascale Barberger-Gateau, Gene L. Bowman, Laura Caberlotto, Robert Clarke, Eef Hogervorst, Amanda J. Kiliaan, Ugo Lucca, Claudine Manach, Anne-Marie Minihane, Ellen Siobhan Mitchell, Robert Perneczky, Hugh Perry, Anne-Marie Roussel, Jeroen Schuermans, John Sijben, Jeremy P.E. Spencer, Sandrine Thuret, Ondine van de Rest, Maurits Vandewoude, Keith Wesnes, Robert J. Williams, Robin S.B. Williams, Maria Ramirez
      As people age they become increasingly susceptible to chronic and extremely debilitating brain diseases. The precise cause of the neuronal degeneration underlying these disorders, and indeed normal brain ageing remains however elusive. Considering the limits of existing preventive methods, there is a desire to develop effective and safe strategies. Growing preclinical and clinical research in healthy individuals or at the early stage of cognitive decline has demonstrated the beneficial impact of nutrition on cognitive functions. 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). The latest scientific advances specific to how dietary nutrients and non-nutrient may affect cognitive ageing are presented. Furthermore, several key points related to mechanisms contributing to brain ageing, pathological conditions affecting brain function, and brain biomarkers are also discussed. Overall, findings are inconsistent and fragmented and more research is warranted to determine the underlying mechanisms and to establish dose-response relationships for optimal brain maintenance in different population subgroups. Such approaches are likely to provide the necessary evidence to develop research portfolios that will inform about new dietary recommendations on how to prevent cognitive decline.

      PubDate: 2017-03-17T06:00:14Z
      DOI: 10.1016/j.arr.2016.09.010
      Issue No: Vol. 35 (2017)
       
  • Molecular pathology endpoints useful for aging studies
    • Authors: L.J. Niedernhofer; J.L. Kirkland; W. Ladiges
      Pages: 241 - 249
      Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35
      Author(s): L.J. Niedernhofer, J.L. Kirkland, W. Ladiges
      The first clinical trial aimed at targeting fundamental processes of aging will soon be launched (TAME: Targeting Aging with Metformin). In its wake is a robust pipeline of therapeutic interventions that have been demonstrated to extend lifespan or healthspan of preclinical models, including rapalogs, antioxidants, anti-inflammatory agents, and senolytics. This ensures that if the TAME trial is successful, numerous additional clinical trials are apt to follow. But a significant impediment to these trials remains the question of what endpoints should be measured? The design of the TAME trial very cleverly skirts around this based on the fact that there are decades of data on metformin in humans, providing unequaled clarity of what endpoints are most likely to yield a positive outcome. But for a new chemical entity, knowing what endpoints to measure remains a formidable challenge. For economy’s sake, and to achieve results in a reasonable time frame, surrogate markers of lifespan and healthy aging are desperately needed. This review provides a comprehensive analysis of molecular endpoints that are currently being used as indices of age-related phenomena (e.g., morbidity, frailty, mortality) and proposes an approach for validating and prioritizing these endpoints.

      PubDate: 2017-03-17T06:00:14Z
      DOI: 10.1016/j.arr.2016.09.012
      Issue No: Vol. 35 (2017)
       
  • Structural neuroimaging in preclinical dementia: From microstructural
           deficits and grey matter atrophy to macroscale connectomic changes
    • Authors: Elijah Mak; Silvy Gabel; Habib Mirette; Li Su; Guy B Williams; Adam Waldman; Katie Wells; Karen Ritchie; Craig Ritchie; John O’Brien
      Pages: 250 - 264
      Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35
      Author(s): Elijah Mak, Silvy Gabel, Habib Mirette, Li Su, Guy B Williams, Adam Waldman, Katie Wells, Karen Ritchie, Craig Ritchie, John O’Brien
      The last decade has witnessed a proliferation of neuroimaging studies characterising brain changes associated with Alzheimer’s disease (AD), where both widespread atrophy and ‘signature’ brain regions have been implicated. In parallel, a prolonged latency period has been established in AD, with abnormal cerebral changes beginning many years before symptom onset. This raises the possibility of early therapeutic intervention, even before symptoms, when treatments could have the greatest effect on disease-course modification. Two important prerequisites of this endeavour are (1) accurate characterisation or risk stratification and (2) monitoring of progression using neuroimaging outcomes as a surrogate biomarker in those without symptoms but who will develop AD, here referred to as preclinical AD. Structural neuroimaging modalities have been used to identify brain changes related to risk factors for AD, such as familial genetic mutations, risk genes (for example apolipoprotein epsilon-4 allele), and/or family history. In this review, we summarise structural imaging findings in preclinical AD. Overall, the literature suggests early vulnerability in characteristic regions, such as the medial temporal lobe structures and the precuneus, as well as white matter tracts in the fornix, cingulum and corpus callosum. We conclude that while structural markers are promising, more research and validation studies are needed before future secondary prevention trials can adopt structural imaging biomarkers as either stratification or surrogate biomarkers.

      PubDate: 2017-03-17T06:00:14Z
      DOI: 10.1016/j.arr.2016.10.001
      Issue No: Vol. 35 (2017)
       
  • Metal ions influx is a double edged sword for the pathogenesis of
           Alzheimer’s disease
    • Authors: Pu Wang; Zhan-You Wang
      Pages: 265 - 290
      Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35
      Author(s): Pu Wang, Zhan-You Wang
      Alzheimer’s disease (AD) is a common form of dementia in aged people, which is defined by two pathological characteristics: β-amyloid protein (Aβ) deposition and tau hyperphosphorylation. Although the mechanisms of AD development are still being debated, a series of evidence supports the idea that metals, such as copper, iron, zinc, magnesium and aluminium, are involved in the pathogenesis of the disease. In particular, the processes of Aβ deposition in senile plaques (SP) and the inclusion of phosphorylated tau in neurofibrillary tangles (NFTs) are markedly influenced by alterations in the homeostasis of the aforementioned metal ions. Moreover, the mechanisms of oxidative stress, synaptic plasticity, neurotoxicity, autophagy and apoptosis mediate the effects of metal ions-induced the aggregation state of Aβ and phosphorylated tau on AD development. More importantly, imbalance of these mechanisms finally caused cognitive decline in different experiment models. Collectively, reconstructing the signaling network that regulates AD progression by metal ions may provide novel insights for developing chelators specific for metal ions to combat AD.
      Graphical abstract image

      PubDate: 2017-03-17T06:00:14Z
      DOI: 10.1016/j.arr.2016.10.003
      Issue No: Vol. 35 (2017)
       
  • The senescence accelerated mouse prone 8 (SAMP8): A novel murine model for
           cardiac aging
    • Authors: Vengadeshprabhu Karuppagounder; Somasundaram Arumugam; Sahana Suresh Babu; Suresh S. Palaniyandi; Kenichi Watanabe; John P. Cooke; Rajarajan A. Thandavarayan
      Pages: 291 - 296
      Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35
      Author(s): Vengadeshprabhu Karuppagounder, Somasundaram Arumugam, Sahana Suresh Babu, Suresh S. Palaniyandi, Kenichi Watanabe, John P. Cooke, Rajarajan A. Thandavarayan
      Because cardiovascular disease remains the major cause of mortality and morbidity world-wide, there remains a compelling need for new insights and novel therapeutic avenues. In this regard, the senescence-accelerated mouse prone 8 (SAMP8) line is a particularly good model for studying the effects of aging on cardiovascular health. Accumulating evidence suggests that this model may shed light on age-associated cardiac and vascular dysfunction and disease. These animals manifest evidence of inflammation, oxidative stress and adverse cardiac remodeling that may recapitulate processes involved in human disease. Early alterations in oxidative damage promote endoplasmic reticulum stress to trigger apoptosis and cytokine production in this genetically susceptible mouse strain. Conversely, pharmacological treatments that reduce inflammation and oxidative stress improve cardiac function in these animals. Therefore, the SAMP8 mouse model provides an exciting opportunity to expand our knowledge of aging in cardiovascular disease and the potential identification of novel targets of treatment. Herein, we review the previous studies performed in SAMP8 mice that provide insight into age-related cardiovascular alterations.
      Graphical abstract image

      PubDate: 2017-03-17T06:00:14Z
      DOI: 10.1016/j.arr.2016.10.006
      Issue No: Vol. 35 (2017)
       
  • The origin of life at the origin of ageing?
    • Authors: Antonio Currais
      Pages: 297 - 300
      Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35
      Author(s): Antonio Currais
      At first glance, the ageing of unicellular organisms would appear to be different from the ageing of complex, multicellular organisms. In an attempt to describe the nature of ageing in diverse organisms, the intimate links between the origins of life and ageing are examined. Departing from Leslie Orgel’s initial ideas on why organisms age, it is then discussed how the potentially detrimental events characteristic of ageing are continuous, cell-autonomous and universal to all organisms. The manifestation of these alterations relies on the balance between their production and cellular renewal. Renewal is achieved not only by repair and maintenance mechanisms but, importantly, by the process of cell division such that every time cells divide ageing-associated effects are diluted.

      PubDate: 2017-03-17T06:00:14Z
      DOI: 10.1016/j.arr.2016.10.007
      Issue No: Vol. 35 (2017)
       
  • Multiple pathways of SIRT6 at the crossroads in the control of longevity,
           cancer, and cardiovascular diseases
    • Authors: Milena Vitiello; Alberto Zullo; Luigi Servillo; Francesco Paolo Mancini; Adriana Borriello; Alfonso Giovane; Fulvio Della Ragione; Nunzia D’Onofrio; Maria Luisa Balestrieri
      Pages: 301 - 311
      Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35
      Author(s): Milena Vitiello, Alberto Zullo, Luigi Servillo, Francesco Paolo Mancini, Adriana Borriello, Alfonso Giovane, Fulvio Della Ragione, Nunzia D’Onofrio, Maria Luisa Balestrieri
      Sirtuin 6 (SIRT6) is a member of the sirtuin family NAD+-dependent deacetylases with multiple roles in controlling organism homeostasis, lifespan, and diseases. Due to its complex and opposite functional roles, this sirtuin is considered a two-edged sword in health and disease. Indeed, SIRT6 improves longevity, similarly to the founding yeast member, silent information regulator-2 (Sir2), and modulates genome stability, telomere integrity, transcription, and DNA repair. Its deficiency is associated with chronic inflammation, diabetes, cardiac hypertrophy, obesity, liver dysfunction, muscle/adipocyte disorders, and cancer. Besides, pieces of evidence showed that SIRT6 is a promoter of specific oncogenic pathways, thus disclosing its dual role regarding cancer development. Collectively, these findings suggest that multiple mechanisms, to date not entirely known, underlie the intriguing roles of SIRT6. Here we provide an overview of the current molecular mechanisms through which SIRT6 controls cancer and heart diseases, and describe its recent implications in the atherosclerotic plaque development.

      PubDate: 2017-03-17T06:00:14Z
      DOI: 10.1016/j.arr.2016.10.008
      Issue No: Vol. 35 (2017)
       
  • Effects of age on force steadiness: A literature review and meta-analysis
    • Authors: Nathalie M.C.W. Oomen; Jaap H. van Dieën
      Pages: 312 - 321
      Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35
      Author(s): Nathalie M.C.W. Oomen, Jaap H. van Dieën
      The variability of force is indicative of the biological variability inherent in the human motor system. Previous literature showed inconsistent findings of the effect of age on the variability of force and hence a systematic review was performed. Twenty studies were included in this systematic review, of which twelve provided sufficient data to determine effect sizes for the effect of age. After determining the pooled effect size, the effect of sample size on dichotomized effect sizes (significant vs. non-significant) was determined. Also, the effect of possible determinants, age difference between age groups, dominance of investigated limb, muscle group, muscle location (proximal vs. distal and upper vs. lower extremity) and target force level on effect size (categorized as small, medium, or large) were investigated. A large pooled effect size of age was found (rtotal =0.67, 95% CI [0.61; 0.72]). No relation between sample size and effect size significance was found, indicative of no lack of power in the studies reviewed. No relations were found of associations between age difference, upper vs. lower extremity muscle location, and dominance and effect size. Significant relations of effect size with muscle group, proximal vs. distal muscle location and target force level were found. Also, an interaction effect of muscle group and target force level was suggested. The meta-analysis results are in line with motor unit loss as the main cause of the effect of ageing on force steadiness and this effect can partially explain decreased motor performance associated with ageing.

      PubDate: 2017-03-17T06:00:14Z
      DOI: 10.1016/j.arr.2016.11.004
      Issue No: Vol. 35 (2017)
       
  • The emerging role of ECM crosslinking in T cell mobility as a hallmark of
           immunosenescence in humans
    • Authors: Jean-Francois Moreau; Thomas Pradeu; Andrea Grignolio; Christine Nardini; Filippo Castiglione; Paolo Tieri; Miriam Capri; Stefano Salvioli; Jean-Luc Taupin; Paolo Garagnani; Claudio Franceschi
      Pages: 322 - 335
      Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35
      Author(s): Jean-Francois Moreau, Thomas Pradeu, Andrea Grignolio, Christine Nardini, Filippo Castiglione, Paolo Tieri, Miriam Capri, Stefano Salvioli, Jean-Luc Taupin, Paolo Garagnani, Claudio Franceschi
      Immunosenescence is thought to result from cellular aging and to reflect exposure to environmental stressors and antigens, including cytomegalovirus (CMV). However, not all of the features of immunosenescence are consistent with this view, and this has led to the emergence of the sister theory of “inflammaging”. The recently discovered diffuse tissue distribution of resident memory T cells (TRM) which don't recirculate, calls these theories into question. These cells account for most T cells residing in barrier epithelia which sit in and travel through the extracellular matrix (ECM). With almost all studies to date carried out on peripheral blood, the age-related changes of the ECM and their consequences for T cell mobility, which is crucial for the function of these cells, have been largely ignored. We propose an update of the theoretical framework of immunosenescence, based on a novel hypothesis: the increasing stiffness and cross-linking of the senescent ECM lead to a progressive immunodeficiency due to an age-related decrease in T cell mobility and eventually the death of these cells. A key element of this mechanism is the mechanical stress to which the cell cytoplasm and nucleus are subjected during passage through the ECM. This hypothesis is based on an “evo-devo” perspective bringing together some major characteristics of aging, to create a single interpretive framework for immunosenescence.
      Graphical abstract image

      PubDate: 2017-03-17T06:00:14Z
      DOI: 10.1016/j.arr.2016.11.005
      Issue No: Vol. 35 (2017)
       
  • Melatonin: Protection against age-related cardiac pathology
    • Authors: Gaia Favero; Lorenzo Franceschetti; Barbara Buffoli; Mohammed H. Moghadasian; Russel J. Reiter; Luigi F. Rodella; Rita Rezzani
      Pages: 336 - 349
      Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35
      Author(s): Gaia Favero, Lorenzo Franceschetti, Barbara Buffoli, Mohammed H. Moghadasian, Russel J. Reiter, Luigi F. Rodella, Rita Rezzani
      Aging is a complex and progressive process that involves physiological and metabolic deterioration in every organ and system. Cardiovascular diseases are one of the most common causes of mortality and morbidity among elderly subjects worldwide. Most age-related cardiovascular disorders can be influenced by modifiable behaviours such as a healthy diet rich in fruit and vegetables, avoidance of smoking, increased physical activity and reduced stress. The role of diet in prevention of various disorders is a well-established factor, which has an even more important role in the geriatric population. Melatonin, an indoleamine with multiple actions including antioxidant properties, has been identified in a very large number of plant species, including edible plant products and medical herbs. Among products where melatonin has been identified include wine, olive oil, tomato, beer, and others. Interestingly, consumed melatonin in plant foods or melatonin supplementation may promote health benefits by virtue of its multiple properties and it may counteract pathological conditions also related to cardiovascular disorders, carcinogenesis, neurological diseases and aging. In the present review, we summarized melatonin effects against age-related cardiac alterations and abnormalities with a special focus on heart ischemia/reperfusion (IR) injury and myocardial infarction.

      PubDate: 2017-03-17T06:00:14Z
      DOI: 10.1016/j.arr.2016.11.007
      Issue No: Vol. 35 (2017)
       
  • Are microRNAs true sensors of ageing and cellular senescence?
    • Authors: Justin Williams; Flint Smith; Subodh Kumar; Murali Vijayan; P. Hemachandra Reddy
      Pages: 350 - 363
      Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35
      Author(s): Justin Williams, Flint Smith, Subodh Kumar, Murali Vijayan, P. Hemachandra Reddy
      All living beings are programmed to death due to aging and age-related processes. Aging is a normal process of every living species. While all cells are inevitably progressing towards death, many disease processes accelerate the aging process, leading to senescence. Pathologies such as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, amyotrophic lateral sclerosis, Huntington’s disease, cardiovascular disease, cancer, and skin diseases have been associated with deregulated aging. Healthy aging can delay onset of all age-related diseases. Genetics and epigenetics are reported to play large roles in accelerating and/or delaying the onset of age-related diseases. Cellular mechanisms of aging and age-related diseases are not completely understood. However, recent molecular biology discoveries have revealed that microRNAs (miRNAs) are potential sensors of aging and cellular senescence. Due to miRNAs capability to bind to the 3′ untranslated region (UTR) of mRNA of specific genes, miRNAs can prevent the translation of specific genes. The purpose of our article is to highlight recent advancements in miRNAs and their involvement in cellular changes in aging and senescence. Our article discusses the current understanding of cellular senescence, its interplay with miRNAs regulation, and how they both contribute to disease processes.

      PubDate: 2017-03-17T06:00:14Z
      DOI: 10.1016/j.arr.2016.11.008
      Issue No: Vol. 35 (2017)
       
  • Regulation of longevity by FGF21: interaction between energy metabolism
           and stress responses
    • Abstract: Publication date: Available online 25 May 2017
      Source:Ageing Research Reviews
      Author(s): Antero Salminen, Kai Kaarniranta, Anu Kauppinen
      Fibroblast growth factor 21 (FGF21) is a hormone-like member of FGF family which controls metabolic multiorgan crosstalk enhancing energy expenditure through glucose and lipid metabolism. In addition, FGF21 acts as a stress hormone induced by endoplasmic reticulum stress and dysfunctions of mitochondria and autophagy in several tissues. FGF21 also controls stress responses and metabolism by modulating the functions of somatotropic axis and hypothalamic-pituitary-adrenal (HPA) pathway. FGF21 is a potent longevity factor coordinating interactions between energy metabolism and stress responses. Recent studies have revealed that FGF21 treatment can alleviate many age-related metabolic disorders, e.g. atherosclerosis, obesity, type 2 diabetes, and some cardiovascular diseases. In addition, transgenic mice overexpressing FGF21 have an extended lifespan. However, chronic metabolic and stress-related disorders involving inflammatory responses can provoke FGF21 resistance and thus disturb healthy aging process. First, we will describe the role of FGF21 in interorgan energy metabolism and explain how its functions as a stress hormone can improve healthspan. Next, we will examine both the induction of FGF21 expression via the integrated stress response and the molecular mechanism through which FGF21 enhances healthy aging. Finally, we postulate that FGF21 resistance, similarly to insulin resistance, jeopardizes human healthspan and accelerates the aging process.

      PubDate: 2017-05-27T23:09:24Z
       
  • Remote tissue conditioning − an emerging approach for inducing body-wide
           protection against diseases of ageing
    • Abstract: Publication date: Available online 24 May 2017
      Source:Ageing Research Reviews
      Author(s): Boaz Kim, Alice Brandli, John Mitrofanis, Jonathan Stone, Sivaraman Purushothuman, Daniel M. Johnstone
      We have long accepted that exercise is ‘good for us’; that − put more rigorously − moderate exercise is associated with not just aerobic fitness but also reduced morbidity and reduced mortality from cardiovascular disease and even malignancies. Caloric restriction (moderate hunger) and our exposure to dietary phytochemicals are also emerging as stresses which are ‘good for us’ in the same sense. This review focuses on an important extension of this concept: that stress localized within the body (e.g. in a limb) can induce resilience in tissues throughout the body. We describe evidence for the efficacy of two ‘remote’ protective interventions − remote ischemic conditioning and remote photobiomodulation − and discuss the mechanisms underlying their protective actions. While the biological phenomenon of remote tissue conditioning is only partially understood, it holds promise for protecting critical-to-life tissues while mitigating risks and practical barriers to direct conditioning of these tissues.

      PubDate: 2017-05-27T23:09:24Z
       
  • IFC: Aims and Scope
    • Abstract: Publication date: July 2017
      Source:Ageing Research Reviews, Volume 36


      PubDate: 2017-05-22T22:58:04Z
       
  • Evidence on multimorbidity from definition to intervention: an overview of
           systematic reviews
    • Authors: Xiaolin Xu; Gita D. Mishra; Mark Jones
      Abstract: Publication date: Available online 13 May 2017
      Source:Ageing Research Reviews
      Author(s): Xiaolin Xu, Gita D. Mishra, Mark Jones
      The increasing challenge of multiple chronic diseases (multimorbidity) requires more evidence-based knowledge and effective practice. In order to better understand the existing evidence on multimorbidity, we performed a systematic review of systematic reviews on multimorbidity with pre-established search strategies and exclusion criteria by searching multiple databases and grey literature. Of 8006 articles found, 53 systematic reviews (including meta-analysis and qualitative research synthesis performed in some reviews) that stated multimorbidity as the main focus were included, with 79% published during 2013 to 2016. Existing evidence on definition, measurement, prevalence, risk factors, health outcomes, clinical practice and medication (polypharmacy), and intervention and management were identified and synthesised. There were three major definitions from three perspectives. Seven studies on prevalence reported a range from 3.5% to 100%. As six studies showed, depression, hypertension, diabetes, arthritis, asthma, and osteoarthritis were prone to be comorbid with other conditions. Four groups of risk factors and eight multimorbidity associated outcomes were explored by five and six studies, respectively. 27 studies evaluated interventions, which could be categorized into either organizational or patient-oriented, the effects of these interventions were varied. We were unable to draw solid conclusions from this overview due to the heterogeneity in methodology and inconsistent findings among included reviews. As suggested by all included studies, there is a need for prospective research, especially longitudinal cohort studies and randomized control trials, to provide more definitive evidence on multimorbidity.

      PubDate: 2017-05-17T22:51:49Z
      DOI: 10.1016/j.arr.2017.05.003
       
  • The role of 5-hydroxymethylcytosine in development, aging and age-related
           diseases
    • Authors: V. López; A.F. Fernández; M.F. Fraga
      Abstract: Publication date: Available online 10 May 2017
      Source:Ageing Research Reviews
      Author(s): V. López, A.F. Fernández, M.F. Fraga
      DNA methylation at the fifth position of cytosines (5mC) represents a major epigenetic modification in mammals. The recent discovery of 5-hydroxymethylcytosine (5hmC), resulting from 5mC oxidation, is redefining our view of the epigenome, as multiple studies indicate that 5hmC is not simply an intermediate of DNA demethylation, but a genuine epigenetic mark that may play an important functional role in gene regulation. Currently, the availability of platforms that discriminates between the presence of 5mC and 5hmC at single-base resolution is starting to shed light on the functions of 5hmC. In this review, we provide an overview of the genomic distribution of 5hmC, and examine recent findings on the role of this mark and the potential consequences of its misregulation during three fundamental biological processes: cell differentiation, cancer and aging.

      PubDate: 2017-05-12T22:43:39Z
      DOI: 10.1016/j.arr.2017.05.002
       
  • Influence of anaerobic and aerobic exercise on age-related pathways in
           skeletal muscle
    • Authors: Ignacio Navas-Enamorado; Michel Bernier; Gloria Brea-Calvo; Rafael de Cabo
      Abstract: Publication date: Available online 6 May 2017
      Source:Ageing Research Reviews
      Author(s): Ignacio Navas-Enamorado, Michel Bernier, Gloria Brea-Calvo, Rafael de Cabo


      PubDate: 2017-05-08T00:43:42Z
      DOI: 10.1016/j.arr.2017.04.005
       
  • 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
      Abstract: Publication date: Available online 6 May 2017
      Source:Ageing Research Reviews
      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: 2017-05-08T00:43:42Z
      DOI: 10.1016/j.arr.2017.05.001
       
  • Circuit resistance training is an effective means to enhance muscle
           strength in older adults
    • Authors: Assaf Buch; Ofer Kis; Eli Carmeli; Lital Keinan-Boker; Yitshal Berner; Yael Barer; Gabi Shefer; Yonit Marcus; Naftali Stern
      Abstract: Publication date: Available online 27 April 2017
      Source:Ageing Research Reviews
      Author(s): Assaf Buch, Ofer Kis, Eli Carmeli, Lital Keinan-Boker, Yitshal Berner, Yael Barer, Gabi Shefer, Yonit Marcus, Naftali Stern
      Physical exercise, particularly resistance training (RT), is presently the only proven means 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. Here we investigate the efficacy of circuit resistance training (CRT) on muscle strength, lean mass and aerobic capacity in older adults. MEDLINE (Ovid), EMBASE, ClinicalTrials.gov, Cochrane electronic databases were systematically searched including references of pertinent articles up to August 2016. The search yielded a total of 237 articles, 106 of which did not meet the inclusion criteria. Sensitivity analysis was conducted using studies with higher likelihood for bias. Ten articles were included with a total of 362 patients (average age of 64.51±7.39 years). The intervention programs averaged 3±1.15 sessions/week and 41.78±15.89minutes/session. 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; 1.02–2.61). A subgroup analysis revealed that higher program volume (>24 sessions) positively influenced upper body strength and aerobic capacity. CRT is a valid alternative to conventional RT. Because of its shorter duration and lower intensity relative to traditional RT, it may increase adherence to training in older adults.

      PubDate: 2017-05-03T08:21:34Z
      DOI: 10.1016/j.arr.2017.04.003
       
  • Splicing regulatory factors, ageing and age-related disease
    • Authors: Eva Latorre; Lorna. W Harries
      Abstract: Publication date: Available online 26 April 2017
      Source:Ageing Research Reviews
      Author(s): Eva Latorre, Lorna. W Harries
      Alternative splicing is a co-transcriptional process, which allows for the production of multiple transcripts from a single gene and is emerging as an important control point for gene expression. Alternatively expressed isoforms often have antagonistic function and differential temporal or spatial expression patterns, yielding enormous plasticity and adaptability to cells and increasing their ability to respond to environmental challenge. The regulation of alternative splicing is critical for numerous cellular functions in both pathological and physiological conditions, and deregulated alternative splicing is a key feature of common chronic diseases. Isoform choice is controlled by a battery of splicing regulatory proteins, which include the serine arginine rich (SRSF) proteins and the heterogeneous ribonucleoprotein (hnRNP) classes of genes. These important splicing regulators have been implicated in age-related disease, and in the ageing process itself. This review will outline the important contribution of splicing regulator proteins to ageing and age-related disease.

      PubDate: 2017-05-03T08:21:34Z
      DOI: 10.1016/j.arr.2017.04.004
       
  • In vivo prion models and the disconnection between transmissibility and
           neurotoxicity
    • Authors: Matteo Senesi; Victoria Lewis; Jee H. Kim; Paul A. Adlard; David I. Finkelstein; Steven J. Collins
      Abstract: Publication date: Available online 24 April 2017
      Source:Ageing Research Reviews
      Author(s): Matteo Senesi, Victoria Lewis, Jee H. Kim, Paul A. Adlard, David I. Finkelstein, Steven J. Collins
      The primary causative event in the development of prion diseases is the misfolding of the normal prion protein (PrPC) into an ensemble of altered conformers (herein collectively denoted as PrPSc) that accumulate in the brain. Prominent amongst currently unresolved key aspects underpinning prion disease pathogenesis is whether transmission and toxicity are sub-served by different molecular species of PrPSc, which may directly impact on the development of effective targeted treatments. The use of murine models of prion disease has been of fundamental importance for probing the relationship between hypothesised “neurotoxic” and “transmissible” PrPSc and the associated kinetic profiles of their production during disease evolution, but unfortunately consensus has not been achieved. Recent in vivo studies have led to formulation of the “two-phase” hypothesis, which postulates that there is first an exponential increase in transmitting PrPSc species followed by an abrupt transition to propagation of neurotoxic PrPSc species. Such observations however, appear inconsistent with previous in vivo murine studies employing detailed time-course behavioural testing, wherein evidence of neurotoxicity could be detected early in disease progression. This review analyses the contributions of in vivo murine models attempting to provide insights into the relationship between transmitting and neurotoxic PrPSc species and explores possible refinements to the “two-phase hypothesis”, that better accommodate the available historical and recent evidence.

      PubDate: 2017-04-26T08:14:12Z
      DOI: 10.1016/j.arr.2017.03.007
       
  • Recent advances in cochlear hair cell regeneration—a promising
           opportunity for the treatment of age-related hearing loss.
    • Authors: Miren Revuelta; Francisco Santaolalla; Olatz Arteaga; Antonia Alvarez; Ana Sánchez del Rey; Enrique Hilario
      Abstract: Publication date: Available online 13 April 2017
      Source:Ageing Research Reviews
      Author(s): Miren Revuelta, Francisco Santaolalla, Olatz Arteaga, Antonia Alvarez, Ana Sánchez del Rey, Enrique Hilario
      The objective of this paper is to review current information regarding the treatment of age-related hearing loss by using cochlear hair cell regeneration. Recent advances in the regeneration of the inner ear, including the usefulness of stem cells, are also presented. Based on the current literature, cochlear cell regeneration may well be possible in the short term and cochlear gene therapy may also be useful for the treatment of hearing loss associated with ageing. The present review provide further insight into the pathogenesis of Inner Ear senescence and aged-related hearing loss and facilitate the development of therapeutic strategies to repair hair cells damaged by ageing. More research will be needed in order to translate them into an effective treatment for deafness linked to cochlear senescence in humans.

      PubDate: 2017-04-19T01:43:40Z
      DOI: 10.1016/j.arr.2017.04.002
       
  • From lymphopoiesis to plasma cells differentiation, the age-related
           modifications of B cell compartment are influenced by “Inflamm-Ageing”
           
    • Authors: Matteo Bulati; Calogero Caruso; Giuseppina Colonna-Romano
      Abstract: Publication date: Available online 7 April 2017
      Source:Ageing Research Reviews
      Author(s): Matteo Bulati, Calogero Caruso, Giuseppina Colonna-Romano
      Ageing is a complex process characterized by a general decline in physiological functions with increasing morbidity and mortality. The most important aspect of ageing is the chronic inflammatory status, named “inflamm-ageing”, strictly associated with the deterioration of the immune function, termed “immunosenescence”. Both are causes of increased susceptibility of elderly to infectious diseases, cancer, dementia, cardiovascular diseases and autoimmunity, and of a decreased response to vaccination. It has been widely demonstrated that ageing has a strong impact on the remodelling of the B cell branch of immune system. The first evident effect is the significant decrease in circulating B cells, primarily due to the reduction of new B cell coming from bone marrow (BM) progenitors, as inflammation directly impacts on B lymphopoiesis. Besides, in aged individuals, there is a shift from naïve to memory immunoglobulins production, accompanied by the impaired ability to produce high affinity protective antibodies against newly encountered antigens. This is accompanied by the increase of expanded clones of B cells, which correlates with poor health status. Age-related modifications also occur in naïve/memory B cells subsets. Indeed, in the elderly, there is a reduction of naïve B cells, accompanied by the expansion of memory B cells that show a senescence-associated phenotype. Finally, elderly show the impaired ability of memory B cells to differentiate into plasma cells. It can be concluded that inflammation is the leading cause of the age-related impairment of B cell compartment, which play certainly a key role in the development of age-related diseases. This makes study of B cells in the aged an important tool for monitoring immunosenescence, chronic inflammatory disorders and the effectiveness of vaccines or pharmacological therapies.

      PubDate: 2017-04-11T23:58:26Z
      DOI: 10.1016/j.arr.2017.04.001
       
  • Aging and cancer: The role of macrophages and neutrophils
    • Authors: Connie Jackaman; Federica Tomay; Lelinh Duong; Norbaini Bintu Abdol Razak; Fiona J. Pixley; Pat Metharom; Delia J. Nelson
      Abstract: Publication date: Available online 6 April 2017
      Source:Ageing Research Reviews
      Author(s): Connie Jackaman, Federica Tomay, Lelinh Duong, Norbaini Bintu Abdol Razak, Fiona J. Pixley, Pat Metharom, Delia J. Nelson
      Impaired immune function has been implicated in the declining health and higher incidence of cancer in the elderly. However, age-related changes to immunity are not completely understood. Neutrophils and macrophages represent the first line of defence yet their ability to phagocytose pathogens decreases with aging. Cytotoxic T lymphocytes are critical in eliminating tumors, but T cell function is also compromised with aging. T cell responses can be regulated by macrophages and may depend on the functional phenotype macrophages adopt in response to microenvironmental signals. This can range from pro-inflammatory, anti-tumorigenic M1 to anti-inflammatory, pro-tumorigenic M2 macrophages. Macrophages in healthy elderly adipose and hepatic tissue exhibit a more pro-inflammatory M1 phenotype compared to young hosts whilst immunosuppressive M2 macrophages increase in elderly lymphoid tissues, lung and muscle. These M2-like macrophages demonstrate altered responses to stimuli. Recent studies suggest that neutrophils also regulate T cell function and, like macrophages, neutrophil function is modulated with aging. It is possible that age-modified tissue-specific macrophages and neutrophils contribute to chronic low-grade inflammation that is associated with dysregulated macrophage-mediated immunosuppression, which together are responsible for development of multiple pathologies, including cancer. This review discusses recent advances in macrophage and neutrophil biology in healthy aging and cancer.

      PubDate: 2017-04-11T23:58:26Z
      DOI: 10.1016/j.arr.2017.03.008
       
  • DNA damage response and autophagy in the degeneration of retinal pigment
           epithelial cells – Implications for age-related macular degeneration
           (AMD)
    • Authors: Juha M.T. Hyttinen; Janusz Błasiak; Minna Niittykoski; Kati Kinnunen; Anu Kauppinen; Antero Salminen; Kai Kaarniranta
      Abstract: Publication date: Available online 27 March 2017
      Source:Ageing Research Reviews
      Author(s): Juha M.T. Hyttinen, Janusz Błasiak, Minna Niittykoski, Kati Kinnunen, Anu Kauppinen, Antero Salminen, Kai Kaarniranta
      In this review we will discuss the links between autophagy, a mechanism involved in the maintenance of cellular homeostasis and controlling cellular waste management, and the DNA damage response (DDR), comprising various mechanisms preserving the integrity and stability of the genome. A reduced autophagy capacity in retinal pigment epithelium has been shown to be connected in the pathogenesis of age-related macular degeneration (AMD), an eye disease. This degenerative disease is a major and increasing cause of vision loss in the elderly in developed countries, primarily due to the profound accumulation of intra- and extracellular waste: lipofuscin and drusen. An abundance of reactive oxygen species is produced in the retina since this tissue has a high oxygen demand and contains mitochondria-rich cells. The retina is exposed to light and it also houses many photoactive molecules. These factors are clearly reflected in both the autophagy and DNA damage rates, and in both nuclear and mitochondrial genomes. It remains to be revealed whether DNA damage and DDR capacity have a more direct role in the development of AMD.

      PubDate: 2017-03-28T23:26:06Z
      DOI: 10.1016/j.arr.2017.03.006
       
  • FUNCTIONAL NEUROIMAGING FINDINGS IN HEALTHY MIDDLE-AGED ADULTS AT RISK OF
           ALZHEIMER’s DISEASE
    • Authors: Mirette Habib; Elijah Mak; Silvy Gabel; Li Su; Guy Williams; Adam Waldman; Katie Wells; Karen Ritchie; Craig Ritchie; John T. O’Brien
      Abstract: Publication date: Available online 22 March 2017
      Source:Ageing Research Reviews
      Author(s): Mirette Habib, Elijah Mak, Silvy Gabel, Li Su, Guy Williams, Adam Waldman, Katie Wells, Karen Ritchie, Craig Ritchie, John T. O’Brien
      It is well established that the neurodegenerative process of Alzheimer's disease (AD) begins many years before symptom onset. This preclinical phase provides a crucial time-window for therapeutic intervention, though this requires biomarkers that could evaluate the efficacy of future disease-modification treatments in asymptomatic individuals. The last decade has witnessed a proliferation of studies characterizing the temporal sequence of the earliest functional and structural brain imaging changes in AD. These efforts have focused on studying individuals who are highly vulnerable to develop AD, such as those with familial genetic mutations, susceptibility genes (i.e. apolipoprotein epsilon-4 allele), and/or a positive family history of AD. In this paper, we review the rapidly growing literature of functional imaging changes in cognitively intact individuals who are middle-aged: positron emission tomography (PET) studies of amyloid deposition, glucose metabolism, as well as arterial spin labeling (ASL), task-dependent, resting-state functional magnetic resonance imaging (fMRI) and magnetic resonance spectroscopy (MRS) studies. The prevailing evidence points to early brain functional changes in the relative absence of cognitive impairment and structural atrophy, although there is marked variability in the directionality of the changes, which could, in turn, be related to antagonistic pleiotropy early in life. A common theme across studies relates to the spatial extent of these changes, most of which overlap with brain regions that are implicated in established AD. Notwithstanding several methodological caveats, functional imaging techniques could be preferentially sensitive to the earliest events of AD pathology prior to macroscopic grey matter loss and clinical manifestations of AD. We conclude that while these techniques have great potential to serve as biomarkers to identify at-risk individuals, more longitudinal studies with greater sample size and robust correction for multiple comparisons are still warranted to establish their utility.

      PubDate: 2017-03-28T23:26:06Z
      DOI: 10.1016/j.arr.2017.03.004
       
  • The relevance of α-KLOTHO to the central nervous system: Some key
           questions
    • Authors: Marina Minto Lopes-Cararo; Caio Henrique Yokoyama Mazucanti; Cristoforo Scavone; Elisa Mitiko Kawamoto; Daniel Charles Berwick
      Abstract: Publication date: Available online 18 March 2017
      Source:Ageing Research Reviews
      Author(s): Marina Minto Lopes-Cararo, Caio Henrique Yokoyama Mazucanti, Cristoforo Scavone, Elisa Mitiko Kawamoto, Daniel Charles Berwick
      α-Klotho is well described as an anti-aging protein, with critical roles in kidney function as a transmembrane co-receptor for FGF23, and as a soluble factor in serum. α-Klotho is also expressed in the choroid plexus, where it is released into the cerebrospinal fluid. Nonetheless, α-Klotho is also expressed in the brain parenchyma. Accumulating evidence indicates that this pool of α-Klotho, which we define as brain α-Klotho, may play important roles as a neuroprotective factor and in promoting myelination, thereby supporting healthy brain aging. Here we summarize what is known about brain α-Klotho before focusing on the outstanding scientific questions related to its function. We believe there is a need for in vitro studies designed to distinguish between brain α-Klotho and other pools of α-Klotho, and for a greater understanding of the basic function of soluble α-Klotho. The mechanism by which the human KL-VS variant affects cognition also requires further elucidation. To help address these questions we suggest some experimental approaches that other laboratories might consider. In short, we hope to stimulate fresh ideas and encourage new research approaches that will allow the importance of α-Klotho for the aging brain to become clear.

      PubDate: 2017-03-21T21:04:32Z
      DOI: 10.1016/j.arr.2017.03.003
       
  • IFC: Aims and Scope
    • Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35


      PubDate: 2017-03-17T06:00:14Z
       
  • in vivo tau PET imaging in dementia: pathophysiology, radiotracer
           quantification, and a systematic review of clinical findings
    • Authors: Benjamin Hall; Elijah Mak; Simon Cervenka; Franklin I. Aigbirhio; James B. Rowe; John T. O’Brien
      Abstract: Publication date: Available online 15 March 2017
      Source:Ageing Research Reviews
      Author(s): Benjamin Hall, Elijah Mak, Simon Cervenka, Franklin I. Aigbirhio, James B. Rowe, John T. O’Brien
      In addition to the deposition of β-amyloid plaques, neurofibrillary tangles composed of aggregated hyperphosphorylated tau are one of the pathological hallmarks of Alzheimer’s disease and other neurodegenerative disorders. Until now, our understanding about the natural history and topography of tau deposition has only been based on post-mortem and cerebrospinal fluid studies, and evidence continues to implicate tau as a central driver of downstream neurodegenerative processes and cognitive decline. Recently, it has become possible to assess the regional distribution and severity of tau burden in vivo with the development of novel radiotracers for positron emission tomography (PET) imaging. In this article, we provide a comprehensive discussion of tau pathophysiology, its quantification with novel PET radiotracers, as well as a systematic review of tau PET imaging in normal aging and various dementia conditions: mild cognitive impairment, Alzheimer’s disease, frontotemporal dementia, progressive supranuclear palsy, and Lewy body dementia. We discuss the main findings in relation to group differences, clinical-cognitive correlations of tau PET, and multi-modal relationships among tau PET and other pathological markers. Collectively, the small but growing literature of tau PET has yielded consistent anatomical patterns of tau accumulation that recapitulate post-mortem distribution of neurofibrillary tangles which correlate with cognitive functions and other markers of pathology. In general, AD is characterised by increased tracer retention in the inferior temporal lobe, extending into the frontal and parietal regions in more severe cases. It is also noted that the spatial topography of tau accumulation is markedly distinct to that of amyloid burden in aging and AD. Tau PET imaging has also revealed characteristic spatial patterns among various non-AD tauopathies, supporting its potential role for differential diagnosis. Finally, we propose novel directions for future tau research, including (a) longitudinal imaging in preclinical dementia, (b) multi-modal mapping of tau pathology onto other pathological processes such as neuroinflammation, and (c) the need for more validation studies against post-mortem samples of the same subjects.

      PubDate: 2017-03-17T06:00:14Z
      DOI: 10.1016/j.arr.2017.03.002
       
  • Cognitive functioning of individuals aged 90 years and older without
           dementia: a systematic review
    • Authors: N. Legdeur; T.T. Binnekade; R.H. Otten; M. Badissi; P. Scheltens; P.J. Visser; A.B. Maier
      Abstract: Publication date: Available online 8 March 2017
      Source:Ageing Research Reviews
      Author(s): N. Legdeur, T.T. Binnekade, R.H. Otten, M. Badissi, P. Scheltens, P.J. Visser, A.B. Maier
      INTRODUCTION Reference values to define cognitive impairment in individuals aged 90 years and older are lacking. We systematically reviewed the literature to determine the level of cognitive functioning of individuals aged 90 years and older without dementia. METHODS The search identified 3972 articles of which 20 articles were included in the review. We calculated mean cognitive test scores and cut-off scores for cognitive tests published in two or more articles. RESULTS The mean cognitive test scores (SD)/cut-off scores for individuals aged 90 years and older without dementia of the five most commonly used cognitive tests were: MMSE: 26.6 (2.6)/23.3 points, Digit Span forward: 5.9 (1.8)/3.6 digits, Digit Span backward: 4.4 (1.6)/2.4 digits, TMT-A: 85.8 (42.5)/140.2seconds and TMT-B: 220.3 (99.2)/347.3seconds. DISCUSSION We provided mean cognitive test scores and cut-off scores that will improve the diagnostic process of cognitive impairment in individuals aged 90 years and older.

      PubDate: 2017-03-09T18:42:03Z
      DOI: 10.1016/j.arr.2017.02.006
       
  • Theoretical and practical aspects of using fetal fibroblasts for skin
           regeneration
    • Authors: Meirong Li; Yali Zhao; Haojie Hao; Weidong Han; Xiaobing Fu
      Abstract: Publication date: Available online 24 February 2017
      Source:Ageing Research Reviews
      Author(s): Meirong Li, Yali Zhao, Haojie Hao, Weidong Han, Xiaobing Fu
      Cutaneous wounding in late-gestational fetal or postnatal humans results in scar formation without any skin appendages. Early or mid- gestational skin healing in humans is characterized by the absence of scaring in a process resembling regeneration. Tremendous cellular and molecular mechanisms contribute to this distinction, and fibroblasts play critical roles in scar or scarless wound healing. This review discussed the different repair mechanisms involved in wound healing of fibroblasts at different developmental stages and further confirmed that fetal fibroblast transplantation resulted in reduced scar healing in vivo. We also discussed the possible problem in fetal fibroblast transplantation for wound repair. We proposed the use of small molecules to improve the regenerative potential of repairing cells in the wound given that remodeling of the wound microenvironment into a regenerative microenvironment in adults might improve skin regeneration.

      PubDate: 2017-02-25T01:56:12Z
      DOI: 10.1016/j.arr.2017.02.005
       
  • Suspected Non Alzheimer’s Pathology – Is it
           non-Alzheimer’s or non-Amyloid?
    • Authors: M. Dani; D.J. Brooks; P. Edison
      Abstract: Publication date: Available online 21 February 2017
      Source:Ageing Research Reviews
      Author(s): M. Dani, D.J. Brooks, P. Edison
      Neurodegeneration, the progressive loss of neurons, is a major process involved in dementia and age-related cognitive impairment. It can be detected clinically using currently available biomarker tests. Suspected Non Alzheimer Pathology (SNAP) is a biomarker-based concept that encompasses a group of individuals with neurodegeneration, but no evidence of amyloid deposition (thereby distinguishing it from Alzheimer’s disease (AD)). These individuals may often have a clinical diagnosis of AD, but their clinical features, genetic susceptibility and progression can differ significantly, carrying crucial implications for precise diagnostics, clinical management, and efficacy of clinical drug trials. SNAP has caused wide interest in the dementia research community, because it is still unclear whether it represents distinct pathology separate from AD, or whether in some individuals, it could represent the earliest stage of AD. This debate has raised pertinent questions about the pathways to AD, the need for biomarkers, and the sensitivity of current biomarker tests. In this review, we discuss the biomarker and imaging trials that first recognized SNAP. We describe the pathological correlates of SNAP and comment on the different causes of neurodegeneration. Finally, we discuss the debate around the concept of SNAP, and further unanswered questions that are emerging.

      PubDate: 2017-02-25T01:56:12Z
      DOI: 10.1016/j.arr.2017.02.003
       
  • Targeting the TLR4 signaling pathway by polyphenol: A novel therapeutic
           strategy for neuroinflammation
    • Authors: Mahban Rahimifard; Faheem Maqbool; Shermineh Moeini-Nodeh; Kamal Niaz; Mohammad Abdollahi; Nady Braidy; Seyed Mohammad Nabavi; Seyed Fazel Nabavi
      Abstract: Publication date: Available online 21 February 2017
      Source:Ageing Research Reviews
      Author(s): Mahban Rahimifard, Faheem Maqbool, Shermineh Moeini-Nodeh, Kamal Niaz, Mohammad Abdollahi, Nady Braidy, Seyed Mohammad Nabavi, Seyed Fazel Nabavi
      A wide array of cell signaling mediators and their interactions play vital roles in neuroinflammation associated with ischemia, brain trauma, developmental disorders and age-related neurodegeneration. Along with neurons, microglia and astrocytes are also affected by the inflammatory cascade by releasing pro-inflammatory cytokines, chemokines and reactive oxygen species. The release of pro-inflammatory mediators in response to neural dysfunction may be helpful, neutral or even deleterious to normal cellular survival. Moreover, the important role of NF-κB factors in the central nervous system (CNS) through toll-like receptor (TLR) activation has been well established. This review demonstrates recent findings regarding therapeutic aspects of polyphenolic compounds for the treatment of neuroinflammation, with the aim of regulating TLR4. Polyphenols including flavonoids, phenolic acids, phenolic alcohols, stilbenes and lignans, can target TLR4 signaling pathways in multiple ways. Toll interacting protein expression could be modulated by epigallocatechin-3-gallate. Resveratrol may also exert neuroprotective effects via the TLR4/NF-κB/STAT signaling cascade. Its role in activation of cascade via interfering with TLR4 oligomerization upon receptor stimulation has also been reported. Curcumin, another polyphenol, can suppress overexpression of inflammatory mediators via inhibiting the TLR4-MAPK/NF-κB pathway. It can also reduce neuronal apoptosis via a mechanism concerning the TLR4/MyD88/NF-κB signaling pathway in microglia/macrophages. Despite a symphony of in vivo and in vitro studies, many molecular and pharmacological aspects of neuroinflammation remain unclear. It is proposed that natural compounds targeting TLR4 may serve as important pharmacophores for the development of potent drugs for the treatment of neurological disorders.

      PubDate: 2017-02-25T01:56:12Z
      DOI: 10.1016/j.arr.2017.02.004
       
  • Handgrip Strength as a Means of Monitoring Progression of Cognitive
           Decline – A Scoping Review
    • Authors: Nora E. Fritz; Caitlin J. McCarthy; Diane E. Adamo
      Abstract: Publication date: Available online 8 February 2017
      Source:Ageing Research Reviews
      Author(s): Nora E. Fritz, Caitlin J. McCarthy, Diane E. Adamo
      Cognitive decline in older adults contributes to reduced ability to perform daily tasks and continued disuse leads to muscle weakness and potentiates functional loss. Despite explicit links between the motor and cognitive systems, few health care providers assess motor function when addressing the needs of individuals with cognitive loss. Early and easy measurable biomarkers of cognitive decline have the potential to improve care for individuals with dementia and mild cognitive impairment. The aim of this study was to conduct a systematic search to determine the relationship among handgrip strength, as a measure of global muscle strength, and cognitive decline over time. Fifteen prospective, cohort, longitudinal studies of adults >60years old who were healthy or at risk of cognitive decline at study onset were included in the review. Studies that investigated changes in cognition relative to baseline grip strength and, those that investigated changes in grip strength relative to cognitive function were revealed. Findings here support the use of handgrip strength as a way to monitor cognitive changes and show that reduced handgrip strength over time may serve as a predictor of cognitive loss with advancing age.

      PubDate: 2017-02-12T15:09:13Z
      DOI: 10.1016/j.arr.2017.01.004
       
  • Pain perception in Parkinson’s disease: A systematic review and
           meta-analysis of experimental studies
    • Authors: Trevor Thompson; Katy Gallop; Christoph U. Correll; Andre F. Carvalho; Nicola Veronese; Ellen Wright; Brendon Stubbs
      Abstract: Publication date: Available online 4 February 2017
      Source:Ageing Research Reviews
      Author(s): Trevor Thompson, Katy Gallop, Christoph U. Correll, Andre F. Carvalho, Nicola Veronese, Ellen Wright, Brendon Stubbs
      While hyperalgesia (increased pain sensitivity) has been suggested to contribute to the increased prevalence of clinical pain in Parkinson’s disease (PD), experimental research is equivocal and mechanisms are poorly understood. We conducted a meta-analysis of studies comparing PD patients to healthy controls (HCs) in their response to experimental pain stimuli. Articles were acquired through systematic searches of major databases from inception until 10/2016. Twenty-six studies met inclusion criteria, comprising 1,292 participants (PD=739, HCs=553). Random effects meta-analysis of standardized mean differences (SMD) revealed lower pain threshold (indicating hyperalgesia) in PD patients during unmedicated OFF states (SMD =0.51) which was attenuated during dopamine-medicated ON states (SMD =0.23), but unaffected by age, PD duration or PD severity. Analysis of 6 studies employing suprathreshold stimulation paradigms indicated greater pain in PD patients, just failing to reach significance (SMD =0.30, p=.06). These findings (a) support the existence of hyperalgesia in PD, which could contribute to the onset/intensity of clinical pain, and (b) implicate dopamine deficiency as a potential underlying mechanism, which may present opportunities for the development of novel analgesic strategies.

      PubDate: 2017-02-04T14:43:45Z
      DOI: 10.1016/j.arr.2017.01.005
       
  • RISK OF CARDIOVASCULAR DISEASE MORBIDITY AND MORTALITY IN FRAIL AND
           PRE-FRAIL OLDER ADULTS: RESULTS FROM A META-ANALYSIS AND EXPLORATORY
           META-REGRESSION ANALYSIS
    • Authors: Nicola Veronese; Emanuele Cereda; Brendon Stubbs; Marco Solmi; Claudio Luchini; Enzo Manzato; Giuseppe Sergi; Peter Manu; Tamara Harris; Luigi Fontana; Timo Strandberg; Helene Amieva; Julien Dumurgier; Alexis Elbaz; Christophe Tzourio; Monika Eicholzer; Sabine Rohrmann; Claudio Moretti; Fabrizio D’Ascenzo; Giorgio Quadri; Alessandro Polidoro; Roberto Alves Lourenço; Virgilio Garcia Moreira; Juan Sanchis; Valeria Scotti; Stefania Maggi; Christoph U. Correll
      Abstract: Publication date: Available online 28 January 2017
      Source:Ageing Research Reviews
      Author(s): Nicola Veronese, Emanuele Cereda, Brendon Stubbs, Marco Solmi, Claudio Luchini, Enzo Manzato, Giuseppe Sergi, Peter Manu, Tamara Harris, Luigi Fontana, Timo Strandberg, Helene Amieva, Julien Dumurgier, Alexis Elbaz, Christophe Tzourio, Monika Eicholzer, Sabine Rohrmann, Claudio Moretti, Fabrizio D’Ascenzo, Giorgio Quadri, Alessandro Polidoro, Roberto Alves Lourenço, Virgilio Garcia Moreira, Juan Sanchis, Valeria Scotti, Stefania Maggi, Christoph U. Correll
      Frailty is common and associated with poorer outcomes in the elderly, but its role as potential cardiovascular disease (CVD) risk factor requires clarification. We thus aimed to meta-analytically evaluate the evidence of frailty and pre-frailty as risk factors for CVD. Two reviewers selected all studies comparing data about CVD prevalence or incidence rates between frail/pre-frail vs. robust. The association between frailty status and CVD in cross-sectional studies was explored by calculating and pooling crude and adjusted odds ratios (ORs) ±95% confidence intervals (CIs); the data from longitudinal studies were pooled using the adjusted hazard ratios (HRs). Eighteen cohorts with a total of 31,343 participants were meta-analyzed. Using estimates from 10 cross-sectional cohorts, both frailty and pre-frailty were associated with higher odds of CVD than robust participants. Longitudinal data were obtained from 6 prospective cohort studies. After a median follow-up of 4.4 years, we identified an increased risk for faster onset of any-type CVD in the frail (HR=1.70 [95%CI, 1.18-2.45]; I2 =66%) and pre-frail (HR=1.23 [95%CI, 1.07-1.36]; I2 =67%) vs. robust groups. Similar results were apparent for time to CVD mortality in the frail and pre-frail groups. In conclusion, frailty and pre-frailty constitute addressable and independent risk factors for CVD in older adults.

      PubDate: 2017-01-29T14:36:39Z
      DOI: 10.1016/j.arr.2017.01.003
       
  • Understanding quasi-apoptosis of the most numerous enucleated components
           of blood needs detailed molecular autopsy
    • Authors: Gennadii Petrovich Gusev; Rukmini Govekar; Nikhil Gadewal; Natalia Ivanovna Agalakova
      Abstract: Publication date: Available online 18 January 2017
      Source:Ageing Research Reviews
      Author(s): Gennadii Petrovich Gusev, Rukmini Govekar, Nikhil Gadewal, Natalia Ivanovna Agalakova
      Erythrocytes are the most numerous cells in human body and their function of oxygen transport is pivotal to human physiology. However, being enucleated, they are often referred to as a sac of molecules and their cellularity is challenged. Interestingly, their programmed death stands a testimony to their cell-hood. They are capable of self-execution after a defined life span by both cell-specific mechanism and that resembling the cytoplasmic events in apoptosis of nucleated cells. Since the execution process lacks the nuclear and mitochondrial events in apoptosis, it has been referred to as quasi-apoptosis or eryptosis. Several studies on molecular mechanisms underlying death of erythrocytes have been reported. The data has generated a non-cohesive sketch of the process. The lacunae in the present knowledge need to be filled to gain deeper insight into the mechanism of physiological ageing and death of erythrocytes, as well as the effect of age of organism on RBCs survival. This would entail how the most numerous cells in the human body die and enable a better understanding of signaling mechanisms of their senescence and premature eryptosis observed in individuals of advanced age.

      PubDate: 2017-01-22T14:21:57Z
      DOI: 10.1016/j.arr.2017.01.002
       
  • ‘Tagging’ along memories in aging: Synaptic tagging and capture
           mechanisms in the aged hippocampus
    • Authors: Mahesh Shivarama Shetty; Sreedharan Sajikumar
      Abstract: Publication date: Available online 5 January 2017
      Source:Ageing Research Reviews
      Author(s): Mahesh Shivarama Shetty, Sreedharan Sajikumar
      Aging is accompanied by a general decline in the physiological functions of the body with the deteriorating organ systems. Brain is no exception to this and deficits in cognitive functions are quite common in advanced aging. Though a variety of age-related alterations are observed in the structure and function throughout the brain, certain regions show selective vulnerability. Medial temporal lobe, especially the hippocampus, is one such preferentially vulnerable region and is a crucial structure involved in the learning and long-term memory functions. Hippocampal synaptic plasticity, such as long-term potentiation (LTP) and depression (LTD), are candidate cellular correlates of learning and memory and alterations in these properties have been well documented in aging. A related phenomenon called synaptic tagging and capture (STC) has been proposed as a mechanism for cellular memory consolidation and to account for temporal association of memories. Mounting evidences from behavioral settings suggest that STC could be a physiological phenomenon. In this article, we review the recent data concerning STC and provide a framework for how alterations in STC-related mechanisms could contribute to the age-associated memory impairments. The enormity of impairment in learning and memory functions demands an understanding of age-associated memory deficits at the fundamental level given its impact in the everyday tasks, thereby in the quality of life. Such an understanding is also crucial for designing interventions and preventive measures for successful brain aging.

      PubDate: 2017-01-08T01:29:56Z
      DOI: 10.1016/j.arr.2016.12.008
       
  • Does music therapy enhance behavioral and cognitive function in elderly
           dementia patients? A systematic review and meta-analysis
    • Authors: Yingshi Zhang; Jiayi Cai; Li An; Fuhai Hui; Tianshu Ren; Hongda Ma; Qingchun Zhao
      Pages: 1 - 11
      Abstract: Publication date: May 2017
      Source:Ageing Research Reviews, Volume 35
      Author(s): Yingshi Zhang, Jiayi Cai, Li An, Fuhai Hui, Tianshu Ren, Hongda Ma, Qingchun Zhao
      Demographic aging is a worldwide phenomenon, cognitive and behavioral impairment is becoming global burden of nerve damage. However, the effect of pharmacological treatment is not satisfying. Therefore, we analyzed the efficacy of music therapy in elderly dementia patients, and if so, whether music therapy can be used as first-line non-pharmacological treatment. A comprehensive literature search was performed on PubMed, EMbase and the Cochrane Library from inception to September 2016. A total of 34 studies (42 analyses, 1757 subjects) were included; all of them had an acceptable quality based on the PEDro and CASP scale scores. Studies based on any type of dementia patient were combined and analyzed by subgroup. The standardized mean difference was −0.42 (-0.74 to −0.11) for disruptive behavior and 0.20 (-0.09 to 0.49) for cognitive function as primary outcomes in random effect models using controls as the comparator; the secondary outcomes were depressive score, anxiety and quality of life. No evidence of publication bias was found based on Begg’s and Egger’s test. The meta-analysis confirmed that the baseline differences between the two groups were balanced. Subgroup analyses showed that disease sub-type, intervention method, comparator, subject location, trial design, trial period and outcome measure instrument made little difference in outcomes. The meta-regression may have identified the causes of heterogeneity as the intervention method, comparator and trial design. Music therapy was effective when patients received interactive therapy with a compared group. There was positive evidence to support the use of music therapy to treat disruptive behavior and anxiety; there were positive trends supporting the use of music therapy for the treatment of cognitive function, depression and quality of life. This study is registered with PROSPERO, number CRD42016036153.

      PubDate: 2016-12-30T01:27:04Z
      DOI: 10.1016/j.arr.2016.12.003
      Issue No: Vol. 35 (2016)
       
  • Aberrant spontaneous low-frequency brain activity in amnestic mild
           cognitive impairment: A meta-analysis of resting-state fMRI studies
    • Authors: PingLei Pan; Lin Zhu TingTing HaiCun Shi Bing Zhang Ruomeng
      Abstract: Publication date: Available online 23 December 2016
      Source:Ageing Research Reviews
      Author(s): PingLei Pan, Lin Zhu, TingTing Yu, HaiCun Shi, Bing Zhang, Ruomeng Qin, Xiaolei Zhu, Lai Qian, Hui Zhao, Hong Zhou, Yun Xu
      Recent resting-state functional magnetic resonance imaging (rs-fMRI) studies have provided strong evidence of abnormal spontaneous brain activity in amnestic mild cognitive impairment (aMCI). However, the conclusions have been inconsistent. A meta-analysis of whole-brain rs-fMRI studies that measured differences in the amplitude of low-frequency fluctuations (ALFF) between aMCI patients and healthy controls was conducted using the Seed-based d Mapping software package. Twelve studies reporting 14 datasets were included in the meta-analysis. Compared to healthy controls, patients with aMCI showed decreased ALFFs in the bilateral precuneus/posterior cingulate cortices, bilateral frontoinsular cortices, left occipitotemporal cortex, and right supramarginal gyrus and increased ALFFs in the right lingual gyrus, left middle occipital gyrus, left hippocampus, and left inferior temporal gyrus. A meta-regression analysis demonstrated that the increased severity of cognitive impairment in aMCI patients was associated with greater decreases in ALFFs in the cuneus/precuneus cortices. Our comprehensive meta-analysis suggests that aMCI is associated with widespread aberrant regional spontaneous brain activity, predominantly involving the default mode, salience, and visual networks, which contributes to understanding its pathophysiology.

      PubDate: 2016-12-30T01:27:04Z
       
  • Biomarkers associated with sedentary behaviour in older adults: a
           systematic review
    • Authors: Katharina Wirth; Jochen Klenk; Simone Brefka; Dhayana Dallmeier; Kathrin Faehling; Marta Roqué i Figuls; Mark A Tully; Maria Giné-Garriga; Paolo Caserotti; Antoni Salvà; Dietrich Rothenbacher; Michael Denkinger; Brendon Stubbs
      Abstract: Publication date: Available online 23 December 2016
      Source:Ageing Research Reviews
      Author(s): Katharina Wirth, Jochen Klenk, Simone Brefka, Dhayana Dallmeier, Kathrin Faehling, Marta Roqué i Figuls, Mark A Tully, Maria Giné-Garriga, Paolo Caserotti, Antoni Salvà, Dietrich Rothenbacher, Michael Denkinger, Brendon Stubbs
      Objective Pathomechanisms of sedentary behavior (SB) are unclear. We conducted a systematic review to investigate the associations between SB and various biomarkers in older adults. Methods Electronic databases were searched (MEDLINE, EMBASE, CINAHL, AMED) up to July 2015 to identify studies with objective or subjective measures of SB, sample size≥50, mean age≥60years and accelerometer wear time ≥3 days. Methodological quality was appraised with the CASP tool. The protocol was pre-specified (PROSPERO CRD42015023731). Results 12701 abstracts were retrieved, 275 full text articles further explored, from which 249 were excluded. In the final sample (26 articles) a total of 63 biomarkers were detected. Most investigated markers were: body mass index (BMI, n=15), waist circumference (WC, n=15), blood pressure (n=11), triglycerides (n=12) and high density lipoprotein (HDL, n=15). Some inflammation markers were identified such as interleukin-6, C-reactive protein or tumor necrosis factor alpha. There was a lack of renal, muscle or bone biomarkers. Randomized controlled trials found a positive correlation for SB with BMI, neck circumference, fat mass, HbA1C, cholesterol and insulin levels, cohort studies additionally for WC, leptin, C-peptide, ApoA1 and Low density lipoprotein and a negative correlation for HDL. Conclusion Most studied biomarkers associated with SB were of cardiovascular or metabolic origin. There is a suggestion of a negative impact of SB on biomarkers but still a paucity of high quality investigations exist. Longitudinal studies with objectively measured SB are needed to further elucidate the pathophysiological pathways and possible associations of unexplored biomarkers.

      PubDate: 2016-12-30T01:27:04Z
      DOI: 10.1016/j.arr.2016.12.002
       
 
 
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