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Showing 1 - 200 of 3030 Journals sorted alphabetically
AASRI Procedia     Open Access   (Followers: 15)
Academic Pediatrics     Hybrid Journal   (Followers: 20, SJR: 1.402, h-index: 51)
Academic Radiology     Hybrid Journal   (Followers: 16, SJR: 1.008, h-index: 75)
Accident Analysis & Prevention     Partially Free   (Followers: 79, SJR: 1.109, h-index: 94)
Accounting Forum     Hybrid Journal   (Followers: 22, SJR: 0.612, h-index: 27)
Accounting, Organizations and Society     Hybrid Journal   (Followers: 27, SJR: 2.515, h-index: 90)
Achievements in the Life Sciences     Open Access   (Followers: 4)
Acta Anaesthesiologica Taiwanica     Open Access   (Followers: 5, SJR: 0.338, h-index: 19)
Acta Astronautica     Hybrid Journal   (Followers: 303, SJR: 0.726, h-index: 43)
Acta Automatica Sinica     Full-text available via subscription   (Followers: 3)
Acta Biomaterialia     Hybrid Journal   (Followers: 25, SJR: 2.02, h-index: 104)
Acta Colombiana de Cuidado Intensivo     Full-text available via subscription  
Acta de Investigación Psicológica     Open Access   (Followers: 2)
Acta Ecologica Sinica     Open Access   (Followers: 8, SJR: 0.172, h-index: 29)
Acta Haematologica Polonica     Free   (SJR: 0.123, h-index: 8)
Acta Histochemica     Hybrid Journal   (Followers: 3, SJR: 0.604, h-index: 38)
Acta Materialia     Hybrid Journal   (Followers: 196, SJR: 3.683, h-index: 202)
Acta Mathematica Scientia     Full-text available via subscription   (Followers: 5, SJR: 0.615, h-index: 21)
Acta Mechanica Solida Sinica     Full-text available via subscription   (Followers: 9, SJR: 0.442, h-index: 21)
Acta Oecologica     Hybrid Journal   (Followers: 9, SJR: 0.915, h-index: 53)
Acta Otorrinolaringologica (English Edition)     Full-text available via subscription   (Followers: 1)
Acta Otorrinolaringológica Española     Full-text available via subscription   (Followers: 3, SJR: 0.311, h-index: 16)
Acta Pharmaceutica Sinica B     Open Access   (Followers: 2)
Acta Poética     Open Access   (Followers: 4)
Acta Psychologica     Hybrid Journal   (Followers: 21, SJR: 1.365, h-index: 73)
Acta Sociológica     Open Access  
Acta Tropica     Hybrid Journal   (Followers: 5, SJR: 1.059, h-index: 77)
Acta Urológica Portuguesa     Open Access  
Actas Dermo-Sifiliograficas     Full-text available via subscription   (Followers: 4)
Actas Dermo-Sifiliográficas (English Edition)     Full-text available via subscription   (Followers: 3)
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Actualites Pharmaceutiques     Full-text available via subscription   (Followers: 5, SJR: 0.141, h-index: 3)
Actualites Pharmaceutiques Hospitalieres     Full-text available via subscription   (Followers: 4, SJR: 0.112, h-index: 2)
Acupuncture and Related Therapies     Hybrid Journal   (Followers: 4)
Ad Hoc Networks     Hybrid Journal   (Followers: 11, SJR: 0.967, h-index: 57)
Addictive Behaviors     Hybrid Journal   (Followers: 15, SJR: 1.514, h-index: 92)
Addictive Behaviors Reports     Open Access   (Followers: 5)
Additive Manufacturing     Hybrid Journal   (Followers: 7, SJR: 1.039, h-index: 5)
Additives for Polymers     Full-text available via subscription   (Followers: 20)
Advanced Drug Delivery Reviews     Hybrid Journal   (Followers: 120, SJR: 5.2, h-index: 222)
Advanced Engineering Informatics     Hybrid Journal   (Followers: 11, SJR: 1.265, h-index: 53)
Advanced Powder Technology     Hybrid Journal   (Followers: 16, SJR: 0.739, h-index: 33)
Advances in Accounting     Hybrid Journal   (Followers: 8, SJR: 0.299, h-index: 15)
Advances in Agronomy     Full-text available via subscription   (Followers: 15, SJR: 2.071, h-index: 82)
Advances in Anesthesia     Full-text available via subscription   (Followers: 24, SJR: 0.169, h-index: 4)
Advances in Antiviral Drug Design     Full-text available via subscription   (Followers: 3)
Advances in Applied Mathematics     Full-text available via subscription   (Followers: 6, SJR: 1.054, h-index: 35)
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Advances in Applied Microbiology     Full-text available via subscription   (Followers: 21, SJR: 1.286, h-index: 49)
Advances In Atomic, Molecular, and Optical Physics     Full-text available via subscription   (Followers: 16, SJR: 3.31, h-index: 42)
Advances in Biological Regulation     Hybrid Journal   (Followers: 4, SJR: 2.277, h-index: 43)
Advances in Botanical Research     Full-text available via subscription   (Followers: 3, SJR: 0.619, h-index: 48)
Advances in Cancer Research     Full-text available via subscription   (Followers: 26, SJR: 2.215, h-index: 78)
Advances in Carbohydrate Chemistry and Biochemistry     Full-text available via subscription   (Followers: 9, SJR: 0.9, h-index: 30)
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Advances in Cellular and Molecular Biology of Membranes and Organelles     Full-text available via subscription   (Followers: 12)
Advances in Chemical Engineering     Full-text available via subscription   (Followers: 24, SJR: 0.183, h-index: 23)
Advances in Child Development and Behavior     Full-text available via subscription   (Followers: 10, SJR: 0.665, h-index: 29)
Advances in Chronic Kidney Disease     Full-text available via subscription   (Followers: 8, SJR: 1.268, h-index: 45)
Advances in Clinical Chemistry     Full-text available via subscription   (Followers: 28, SJR: 0.938, h-index: 33)
Advances in Colloid and Interface Science     Full-text available via subscription   (Followers: 18, SJR: 2.314, h-index: 130)
Advances in Computers     Full-text available via subscription   (Followers: 16, SJR: 0.223, h-index: 22)
Advances in Developmental Biology     Full-text available via subscription   (Followers: 11)
Advances in Digestive Medicine     Open Access   (Followers: 4)
Advances in DNA Sequence-Specific Agents     Full-text available via subscription   (Followers: 5)
Advances in Drug Research     Full-text available via subscription   (Followers: 22)
Advances in Ecological Research     Full-text available via subscription   (Followers: 39, SJR: 3.25, h-index: 43)
Advances in Engineering Software     Hybrid Journal   (Followers: 25, SJR: 0.486, h-index: 10)
Advances in Experimental Biology     Full-text available via subscription   (Followers: 7)
Advances in Experimental Social Psychology     Full-text available via subscription   (Followers: 38, SJR: 5.465, h-index: 64)
Advances in Exploration Geophysics     Full-text available via subscription   (Followers: 3)
Advances in Fluorine Science     Full-text available via subscription   (Followers: 8)
Advances in Food and Nutrition Research     Full-text available via subscription   (Followers: 41, SJR: 0.674, h-index: 38)
Advances in Fuel Cells     Full-text available via subscription   (Followers: 14)
Advances in Genetics     Full-text available via subscription   (Followers: 15, SJR: 2.558, h-index: 54)
Advances in Genome Biology     Full-text available via subscription   (Followers: 11)
Advances in Geophysics     Full-text available via subscription   (Followers: 6, SJR: 2.325, h-index: 20)
Advances in Heat Transfer     Full-text available via subscription   (Followers: 18, SJR: 0.906, h-index: 24)
Advances in Heterocyclic Chemistry     Full-text available via subscription   (Followers: 8, SJR: 0.497, h-index: 31)
Advances in Human Factors/Ergonomics     Full-text available via subscription   (Followers: 22)
Advances in Imaging and Electron Physics     Full-text available via subscription   (Followers: 2, SJR: 0.396, h-index: 27)
Advances in Immunology     Full-text available via subscription   (Followers: 33, SJR: 4.152, h-index: 85)
Advances in Inorganic Chemistry     Full-text available via subscription   (Followers: 9, SJR: 1.132, h-index: 42)
Advances in Insect Physiology     Full-text available via subscription   (Followers: 3, SJR: 1.274, h-index: 27)
Advances in Integrative Medicine     Hybrid Journal   (Followers: 4)
Advances in Intl. Accounting     Full-text available via subscription   (Followers: 4)
Advances in Life Course Research     Hybrid Journal   (Followers: 7, SJR: 0.764, h-index: 15)
Advances in Lipobiology     Full-text available via subscription   (Followers: 1)
Advances in Magnetic and Optical Resonance     Full-text available via subscription   (Followers: 8)
Advances in Marine Biology     Full-text available via subscription   (Followers: 16, SJR: 1.645, h-index: 45)
Advances in Mathematics     Full-text available via subscription   (Followers: 10, SJR: 3.261, h-index: 65)
Advances in Medical Sciences     Hybrid Journal   (Followers: 5, SJR: 0.489, h-index: 25)
Advances in Medicinal Chemistry     Full-text available via subscription   (Followers: 5)
Advances in Microbial Physiology     Full-text available via subscription   (Followers: 4, SJR: 1.44, h-index: 51)
Advances in Molecular and Cell Biology     Full-text available via subscription   (Followers: 21)
Advances in Molecular and Cellular Endocrinology     Full-text available via subscription   (Followers: 10)
Advances in Molecular Toxicology     Full-text available via subscription   (Followers: 6, SJR: 0.324, h-index: 8)
Advances in Nanoporous Materials     Full-text available via subscription   (Followers: 3)
Advances in Oncobiology     Full-text available via subscription   (Followers: 3)
Advances in Organometallic Chemistry     Full-text available via subscription   (Followers: 15, SJR: 2.885, h-index: 45)
Advances in Parallel Computing     Full-text available via subscription   (Followers: 7, SJR: 0.148, h-index: 11)
Advances in Parasitology     Full-text available via subscription   (Followers: 7, SJR: 2.37, h-index: 73)
Advances in Pediatrics     Full-text available via subscription   (Followers: 20, SJR: 0.4, h-index: 28)
Advances in Pharmaceutical Sciences     Full-text available via subscription   (Followers: 14)
Advances in Pharmacology     Full-text available via subscription   (Followers: 13, SJR: 1.718, h-index: 58)
Advances in Physical Organic Chemistry     Full-text available via subscription   (Followers: 7, SJR: 0.384, h-index: 26)
Advances in Phytomedicine     Full-text available via subscription  
Advances in Planar Lipid Bilayers and Liposomes     Full-text available via subscription   (Followers: 3, SJR: 0.248, h-index: 11)
Advances in Plant Biochemistry and Molecular Biology     Full-text available via subscription   (Followers: 8)
Advances in Plant Pathology     Full-text available via subscription   (Followers: 5)
Advances in Porous Media     Full-text available via subscription   (Followers: 4)
Advances in Protein Chemistry     Full-text available via subscription   (Followers: 18)
Advances in Protein Chemistry and Structural Biology     Full-text available via subscription   (Followers: 17, SJR: 1.5, h-index: 62)
Advances in Psychology     Full-text available via subscription   (Followers: 56)
Advances in Quantum Chemistry     Full-text available via subscription   (Followers: 5, SJR: 0.478, h-index: 32)
Advances in Radiation Oncology     Open Access  
Advances in Small Animal Medicine and Surgery     Hybrid Journal   (Followers: 1, SJR: 0.1, h-index: 2)
Advances in Space Research     Full-text available via subscription   (Followers: 332, SJR: 0.606, h-index: 65)
Advances in Structural Biology     Full-text available via subscription   (Followers: 7)
Advances in Surgery     Full-text available via subscription   (Followers: 6, SJR: 0.823, h-index: 27)
Advances in the Study of Behavior     Full-text available via subscription   (Followers: 28, SJR: 1.321, h-index: 56)
Advances in Veterinary Medicine     Full-text available via subscription   (Followers: 14)
Advances in Veterinary Science and Comparative Medicine     Full-text available via subscription   (Followers: 12)
Advances in Virus Research     Full-text available via subscription   (Followers: 5, SJR: 1.878, h-index: 68)
Advances in Water Resources     Hybrid Journal   (Followers: 42, SJR: 2.408, h-index: 94)
Aeolian Research     Hybrid Journal   (Followers: 5, SJR: 0.973, h-index: 22)
Aerospace Science and Technology     Hybrid Journal   (Followers: 304, SJR: 0.816, h-index: 49)
AEU - Intl. J. of Electronics and Communications     Hybrid Journal   (Followers: 8, SJR: 0.318, h-index: 36)
African J. of Emergency Medicine     Open Access   (Followers: 4, SJR: 0.344, h-index: 6)
Ageing Research Reviews     Hybrid Journal   (Followers: 7, SJR: 3.289, h-index: 78)
Aggression and Violent Behavior     Hybrid Journal   (Followers: 390, SJR: 1.385, h-index: 72)
Agri Gene     Hybrid Journal  
Agricultural and Forest Meteorology     Hybrid Journal   (Followers: 15, SJR: 2.18, h-index: 116)
Agricultural Systems     Hybrid Journal   (Followers: 29, SJR: 1.275, h-index: 74)
Agricultural Water Management     Hybrid Journal   (Followers: 36, SJR: 1.546, h-index: 79)
Agriculture and Agricultural Science Procedia     Open Access  
Agriculture and Natural Resources     Open Access   (Followers: 1)
Agriculture, Ecosystems & Environment     Hybrid Journal   (Followers: 48, SJR: 1.879, h-index: 120)
Ain Shams Engineering J.     Open Access   (Followers: 5, SJR: 0.434, h-index: 14)
Air Medical J.     Hybrid Journal   (Followers: 3, SJR: 0.234, h-index: 18)
AKCE Intl. J. of Graphs and Combinatorics     Open Access   (SJR: 0.285, h-index: 3)
Alcohol     Hybrid Journal   (Followers: 9, SJR: 0.922, h-index: 66)
Alcoholism and Drug Addiction     Open Access   (Followers: 5)
Alergologia Polska : Polish J. of Allergology     Full-text available via subscription   (Followers: 1)
Alexandria Engineering J.     Open Access   (Followers: 1, SJR: 0.436, h-index: 12)
Alexandria J. of Medicine     Open Access  
Algal Research     Partially Free   (Followers: 7, SJR: 2.05, h-index: 20)
Alkaloids: Chemical and Biological Perspectives     Full-text available via subscription   (Followers: 3)
Allergologia et Immunopathologia     Full-text available via subscription   (Followers: 1, SJR: 0.46, h-index: 29)
Allergology Intl.     Open Access   (Followers: 5, SJR: 0.776, h-index: 35)
ALTER - European J. of Disability Research / Revue Européenne de Recherche sur le Handicap     Full-text available via subscription   (Followers: 6, SJR: 0.158, h-index: 9)
Alzheimer's & Dementia     Hybrid Journal   (Followers: 45, SJR: 4.289, h-index: 64)
Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring     Open Access   (Followers: 5)
Alzheimer's & Dementia: Translational Research & Clinical Interventions     Open Access   (Followers: 3)
American Heart J.     Hybrid Journal   (Followers: 45, SJR: 3.157, h-index: 153)
American J. of Cardiology     Hybrid Journal   (Followers: 47, SJR: 2.063, h-index: 186)
American J. of Emergency Medicine     Hybrid Journal   (Followers: 34, SJR: 0.574, h-index: 65)
American J. of Geriatric Pharmacotherapy     Full-text available via subscription   (Followers: 6, SJR: 1.091, h-index: 45)
American J. of Geriatric Psychiatry     Hybrid Journal   (Followers: 14, SJR: 1.653, h-index: 93)
American J. of Human Genetics     Hybrid Journal   (Followers: 32, SJR: 8.769, h-index: 256)
American J. of Infection Control     Hybrid Journal   (Followers: 25, SJR: 1.259, h-index: 81)
American J. of Kidney Diseases     Hybrid Journal   (Followers: 31, SJR: 2.313, h-index: 172)
American J. of Medicine     Hybrid Journal   (Followers: 48, SJR: 2.023, h-index: 189)
American J. of Medicine Supplements     Full-text available via subscription   (Followers: 3)
American J. of Obstetrics and Gynecology     Hybrid Journal   (Followers: 174, SJR: 2.255, h-index: 171)
American J. of Ophthalmology     Hybrid Journal   (Followers: 51, SJR: 2.803, h-index: 148)
American J. of Ophthalmology Case Reports     Open Access   (Followers: 2)
American J. of Orthodontics and Dentofacial Orthopedics     Full-text available via subscription   (Followers: 6, SJR: 1.249, h-index: 88)
American J. of Otolaryngology     Hybrid Journal   (Followers: 22, SJR: 0.59, h-index: 45)
American J. of Pathology     Hybrid Journal   (Followers: 23, SJR: 2.653, h-index: 228)
American J. of Preventive Medicine     Hybrid Journal   (Followers: 21, SJR: 2.764, h-index: 154)
American J. of Surgery     Hybrid Journal   (Followers: 32, SJR: 1.286, h-index: 125)
American J. of the Medical Sciences     Hybrid Journal   (Followers: 13, SJR: 0.653, h-index: 70)
Ampersand : An Intl. J. of General and Applied Linguistics     Open Access   (Followers: 5)
Anaerobe     Hybrid Journal   (Followers: 4, SJR: 1.066, h-index: 51)
Anaesthesia & Intensive Care Medicine     Full-text available via subscription   (Followers: 52, SJR: 0.124, h-index: 9)
Anaesthesia Critical Care & Pain Medicine     Full-text available via subscription   (Followers: 3)
Anales de Cirugia Vascular     Full-text available via subscription  
Anales de Pediatría     Full-text available via subscription   (Followers: 2, SJR: 0.209, h-index: 27)
Anales de Pediatría (English Edition)     Full-text available via subscription  
Anales de Pediatría Continuada     Full-text available via subscription   (SJR: 0.104, h-index: 3)
Analytic Methods in Accident Research     Hybrid Journal   (Followers: 2, SJR: 2.577, h-index: 7)
Analytica Chimica Acta     Hybrid Journal   (Followers: 38, SJR: 1.548, h-index: 152)
Analytical Biochemistry     Hybrid Journal   (Followers: 154, SJR: 0.725, h-index: 154)
Analytical Chemistry Research     Open Access   (Followers: 7, SJR: 0.18, h-index: 2)
Analytical Spectroscopy Library     Full-text available via subscription   (Followers: 10)
Anesthésie & Réanimation     Full-text available via subscription  
Anesthesiology Clinics     Full-text available via subscription   (Followers: 21, SJR: 0.421, h-index: 40)
Angiología     Full-text available via subscription   (SJR: 0.124, h-index: 9)
Angiologia e Cirurgia Vascular     Open Access  
Animal Behaviour     Hybrid Journal   (Followers: 143, SJR: 1.907, h-index: 126)
Animal Feed Science and Technology     Hybrid Journal   (Followers: 5, SJR: 1.151, h-index: 83)
Animal Reproduction Science     Hybrid Journal   (Followers: 5, SJR: 0.711, h-index: 78)
Annales d'Endocrinologie     Full-text available via subscription   (SJR: 0.394, h-index: 30)
Annales d'Urologie     Full-text available via subscription  
Annales de Cardiologie et d'Angéiologie     Full-text available via subscription   (SJR: 0.177, h-index: 13)
Annales de Chirurgie de la Main et du Membre Supérieur     Full-text available via subscription  
Annales de Chirurgie Plastique Esthétique     Full-text available via subscription   (Followers: 2, SJR: 0.354, h-index: 22)
Annales de Chirurgie Vasculaire     Full-text available via subscription   (Followers: 1)

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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  [3030 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
    • 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.
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      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)
  • Introduction to special issue: Neurovascular aging—A driving force for
           neurological dysfunction in stroke and neurodegenerative diseases
    • Authors: Steven H. Graham
      Pages: 1 - 2
      Abstract: Publication date: March 2017
      Source:Ageing Research Reviews, Volume 34
      Author(s): Steven H. Graham

      PubDate: 2017-01-22T14:21:57Z
      DOI: 10.1016/j.arr.2016.10.002
      Issue No: Vol. 34 (2017)
  • ER stress and impaired autophagy flux in neuronal degeneration and brain
    • Authors: Yan Yin; George Sun; Eric Li; Kirill Kiselyov; Dandan Sun
      Pages: 3 - 14
      Abstract: Publication date: March 2017
      Source:Ageing Research Reviews, Volume 34
      Author(s): Yan Yin, George Sun, Eric Li, Kirill Kiselyov, Dandan Sun
      Autophagy is a highly controlled lysosome-mediated function in eukaryotic cells to eliminate damaged or aged long-lived proteins and organelles. It is required for restoring cellular homeostasis in cell survival under multiple stresses. Autophagy is known to be a double-edged sword because too much activation or inhibition of autophagy can disrupt homeostatic degradation of protein and organelles within the brain and play a role in neuronal cell death. Many factors affect autophagy flux function in the brain, including endoplasmic reticulum (ER) stress, oxidative stress, and aging. Newly emerged research indicates that altered autophagy flux functionality is involved in neurodegeneration of the aged brain, chronic neurological diseases, and after traumatic and ischemic brain injuries. In search to identify neuroprotective agents that may reduce oxidative stress and stimulate autophagy, one particular neuroprotective agent docosahexaenoic acid (DHA) presents unique functions in reducing ER and oxidative stress and modulating autophagy. This review will summarize the recent findings on changes of autophagy in aging, neurodegenerative diseases, and brain injury after trauma or ischemic strokes. Discussion of DHA functions is focused on modulating ER stress and autophagy in regard to its neuroprotection and anti-tumor functions.
      Graphical abstract image

      PubDate: 2017-01-22T14:21:57Z
      DOI: 10.1016/j.arr.2016.08.008
      Issue No: Vol. 34 (2017)
  • The impact of cerebrovascular aging on vascular cognitive impairment and
    • Authors: Tuo Yang; Yang Sun; Zhengyu Lu; Rehana K. Leak; Feng Zhang
      Pages: 15 - 29
      Abstract: Publication date: March 2017
      Source:Ageing Research Reviews, Volume 34
      Author(s): Tuo Yang, Yang Sun, Zhengyu Lu, Rehana K. Leak, Feng Zhang
      As human life expectancy rises, the aged population will increase. Aging is accompanied by changes in tissue structure, often resulting in functional decline. For example, aging within blood vessels contributes to a decrease in blood flow to important organs, potentially leading to organ atrophy and loss of function. In the central nervous system, cerebral vascular aging can lead to loss of the integrity of the blood-brain barrier, eventually resulting in cognitive and sensorimotor decline. One of the major of types of cognitive dysfunction due to chronic cerebral hypoperfusion is vascular cognitive impairment and dementia (VCID). In spite of recent progress in clinical and experimental VCID research, our understanding of vascular contributions to the pathogenesis of VCID is still very limited. In this review, we summarize recent findings on VCID, with a focus on vascular age-related pathologies and their contribution to the development of this condition.

      PubDate: 2017-01-22T14:21:57Z
      DOI: 10.1016/j.arr.2016.09.007
      Issue No: Vol. 34 (2017)
  • Life and death in the trash heap: The ubiquitin proteasome pathway and
           UCHL1 in brain aging, neurodegenerative disease and cerebral Ischemia
    • Authors: Steven H. Graham; Hao Liu
      Pages: 30 - 38
      Abstract: Publication date: March 2017
      Source:Ageing Research Reviews, Volume 34
      Author(s): Steven H. Graham, Hao Liu
      The ubiquitin proteasome pathway (UPP) is essential for removing abnormal proteins and preventing accumulation of potentially toxic proteins within the neuron. UPP dysfunction occurs with normal aging and is associated with abnormal accumulation of protein aggregates within neurons in neurodegenerative diseases. Ischemia disrupts UPP function and thus may contribute to UPP dysfunction seen in the aging brain and in neurodegenerative diseases. Ubiquitin carboxy-terminal hydrolase L1 (UCHL1), an important component of the UPP in the neuron, is covalently modified and its activity inhibited by reactive lipids produced after ischemia. As a result, degradation of toxic proteins is impaired which may exacerbate neuronal function and cell death in stroke and neurodegenerative diseases. Preserving or restoring UCHL1 activity may be an effective therapeutic strategy in stroke and neurodegenerative diseases.

      PubDate: 2017-01-22T14:21:57Z
      DOI: 10.1016/j.arr.2016.09.011
      Issue No: Vol. 34 (2017)
  • In vivo prion models and the disconnection between transmissibility and
    • 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
    • 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
    • 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
    • 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
  • Dietary protein, aging and nutritional geometry
    • Authors: Stephen J. Simpson; David G. Le Couteur; David Raubenheimer; Samantha M. Solon-Biet; Gregory J. Cooney; Victoria C. Cogger; Luigi Fontana
      Abstract: Publication date: Available online 6 March 2017
      Source:Ageing Research Reviews
      Author(s): Stephen J. Simpson, David G. Le Couteur, David Raubenheimer, Samantha M. Solon-Biet, Gregory J. Cooney, Victoria C. Cogger, Luigi Fontana
      Nearly a century of research has shown that nutritional interventions can delay aging and age- related diseases in many animal models and possibly humans. The most robust and widely studied intervention is caloric restriction, while protein restriction and restriction of various amino acids (methionine, tryptophan) have also been shown to delay aging. However, there is still debate over whether the major impact on aging is secondary to caloric intake, protein intake or specific amino acids. Nutritional geometry provides new perspectives on the relationship between nutrition and aging by focusing on calories, macronutrients and their interactions across a landscape of diets, and taking into account compensatory feeding in ad libitum-fed experiments. Nutritional geometry is a state-space modelling approach that explores how animals respond to and balance changes in nutrient availability. Such studies in insects and mice have shown that low protein, high carbohydrate diets are associated with longest lifespan in ad libitum fed animals suggesting that the interaction between macronutrients may be as important as their total intake.

      PubDate: 2017-03-09T18:42:03Z
      DOI: 10.1016/j.arr.2017.03.001
  • Theoretical and practical aspects of using fetal fibroblasts for skin
    • 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
    • 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
  • IFC: Aims and Scope
    • Abstract: Publication date: March 2017
      Source:Ageing Research Reviews, Volume 34

      PubDate: 2017-01-22T14:21:57Z
  • 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
  • Corrigendum to “Inflammation and frailty in the elderly: A systematic
           review and meta-analysis” [Ageing Res Rev. 31 (2016) 1–8]
    • Authors: Pinar Soysal; Brendon Stubbs; Paola Lucato; Claudio Luchini; Marco Solmi; Roberto Peluso; Giuseppe Sergi; Ahmet Turan Isik; Enzo Manzato; Stefania Maggi; Marcello Maggio; A. Matthew Prina; Theodore D. Cosco; Yu-Tzu Wu; Nicola Veronese
      Abstract: Publication date: Available online 13 January 2017
      Source:Ageing Research Reviews
      Author(s): Pinar Soysal, Brendon Stubbs, Paola Lucato, Claudio Luchini, Marco Solmi, Roberto Peluso, Giuseppe Sergi, Ahmet Turan Isik, Enzo Manzato, Stefania Maggi, Marcello Maggio, A. Matthew Prina, Theodore D. Cosco, Yu-Tzu Wu, Nicola Veronese

      PubDate: 2017-01-16T01:41:42Z
      DOI: 10.1016/j.arr.2016.12.007
  • ‘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
  • Stem cell therapies in age-related neurodegenerative diseases and stroke
    • Authors: Yuan Wang; Xunming Ji; Rehana K. Leak; Fenghua Chen; Guodong Cao
      Abstract: Publication date: Available online 19 November 2016
      Source:Ageing Research Reviews
      Author(s): Yuan Wang, Xunming Ji, Rehana K. Leak, Fenghua Chen, Guodong Cao
      Aging, a complex process associated with various structural, functional and metabolic changes in the brain, is an important risk factor for neurodegenerative diseases and stroke. These diseases share similar neuropathological changes, such as the formation of misfolded proteins, oxidative stress, loss of neurons and synapses, dysfunction of the neurovascular unit (NVU), reduction of self-repair capacity, and motor and/or cognitive deficiencies. In addition to gray matter dysfunction, the plasticity and repair capacity of white matter also decrease with aging and contribute to neurodegenerative diseases. Aging not only renders patients more susceptible to these disorders, but also attenuates their self-repair capabilities. In addition, low drug responsiveness and intolerable side effects are major challenges in the prevention and treatment of senile diseases. Thus, stem cell therapies—characterized by cellular plasticity and the ability to self-renew—may be a promising strategy for aging-related brain disorders. Here, we review the common pathophysiological changes, treatments, and the promises and limitations of stem cell therapies in age-related neurodegenerative diseases and stroke.

      PubDate: 2016-11-23T14:44:22Z
      DOI: 10.1016/j.arr.2016.11.002
  • Disordered APP metabolism in trauma and aging: Dual risk for chronic
           neurodegenerative disorders
    • Authors: Milos D. Ikonomovic; Zhiping Mi; Eric E. Abrahamson
      Abstract: Publication date: Available online 6 November 2016
      Source:Ageing Research Reviews
      Author(s): Milos D. Ikonomovic, Zhiping Mi, Eric E. Abrahamson
      Traumatic brain injury (TBI), advanced age, and cerebral vascular disease are factors conferring increased risk for late onset Alzheimer’s disease (AD). These conditions are also related pathologically through multiple interacting mechanisms. The hallmark pathology of AD consists of pathological aggregates of amyloid-β (Aβ) peptides and tau proteins. These molecules are also involved in neuropathology of several other chronic neurodegenerative diseases, and are under intense investigation in the aftermath of TBI as potential contributors to the risk for developing AD and chronic traumatic encephalopathy (CTE). The pathology of TBI is complex and dependent on injury severity, age-at-injury, and length of time between injury and neuropathological evaluation. In addition, the mechanisms influencing pathology and recovery after TBI likely involve genetic/epigenetic factors as well as additional disorders or comorbid states related to age and central and peripheral vascular health. In this regard, dysfunction of the aging neurovascular system could be an important link between TBI and chronic neurodegenerative diseases, either as a precipitating event or related to accumulation of AD-like pathology which is amplified in the context of aging. Thus with advanced age and vascular dysfunction, TBI can trigger self-propagating cycles of neuronal injury, pathological protein aggregation, and synaptic loss resulting in chronic neurodegenerative disease. In this review we discuss evidence supporting TBI and aging as dual, interacting risk factors for AD, and the role of Aβ and cerebral vascular dysfunction in this relationship. Evidence is discussed that Aβ is involved in cyto- and synapto-toxicity after severe TBI, and that its chronic effects are potentiated by aging and impaired cerebral vascular function. From a therapeutic perspective, we emphasize that in the fields of TBI- and aging-related neurodegeneration protective strategies should include preservation of neurovascular function.

      PubDate: 2016-11-09T14:18:30Z
      DOI: 10.1016/j.arr.2016.11.003
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