Showing papers in "Ageing Research Reviews in 2018"
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TL;DR: This work provides a comprehensive and critical overview of the current clinical, neuropathological, and genetic understanding of genetic forms of Parkinson disease and discusses advances in screening for genetic PD-related risk factors.
335 citations
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TL;DR: Loss of muscle mass with age is due to atrophy and loss of individual muscle fibres, and anabolic resistance is fundamental in age-related fibre atrophy.
323 citations
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TL;DR: Biomarker panels for frailty would be of high value and better than single markers.
267 citations
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TL;DR: In this review, recent findings regarding alterations and the role of gut microbiota and microbial metabolites in PD are summarized, and potential molecular mechanisms and microbiota-targeted interventions inPD are discussed.
228 citations
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TL;DR: Short telomeres are associated with increased all-cause mortality risk in the general population, however, TL measurement techniques and age at measurement contribute to the heterogeneity of effect estimation.
177 citations
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TL;DR: A plethora of pathological cascades triggered by gluco- and lipotoxicity are dissected, converging on candidate phenomena possibly explaining the enduring pro-inflammatory program observed in diabetic tissues, i.e. persistent immune-system stimulation, accumulation of senescent cells, epigenetic rearrangements, and alterations in microbiota composition.
163 citations
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TL;DR: It is concluded that both fasting and CR have a role in the upregulation of autophagy, the evidence overwhelmingly suggesting thatAutophagy is induced in a wide variety of tissues and organs in response to food deprivation.
163 citations
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TL;DR: Conceptualising the distinct similarity between tumorigenesis and cellular reprogramming, this review provides a perspective discussion on involvement of SIRT1 in improving efficiency in the induction and maintenance of pluripotent state.
154 citations
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TL;DR: An overview of the research to date concerning senescence immunosurviellance is provided, including a focused discussion on the mechanisms by which macrophages may recognise senescent cells, and strategies as an alternative to senolytics for the removal ofsenescent cells are discussed.
153 citations
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TL;DR: The basic functions of the enzymes involved in NAD synthesis and degradation, as well as the outcomes of their dysregulation in various aging processes are summarized and a particular focus is given on the role of NAD metabolism in the longevity of various organisms.
149 citations
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TL;DR: Current knowledge regarding cellular plasticity in chondrocytes and OA is highlighted to enable better comprehension of the mechanisms involved in these processes and to understand the molecular pathways that promote abnormal repair and cartilage degradation in OA.
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TL;DR: An overview of the current state of scientific knowledge on the occurrence of AGEs in foods and the daily uptake, contribution to endogenous levels and the effect on health-/disease-related biomarkers in humans is given.
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TL;DR: The beneficial effects of polyphenol-rich foods in relation to the Mediterranean diet and the dietary habits of long-lived individuals are discussed, and their ability to modulate bacterial genera in the gut is examined.
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University of Leeds1, Radboud University Nijmegen2, University of North Carolina at Pembroke3, International Life Sciences Institute4, University of Catania5, Uppsala University6, University College Cork7, University of Amsterdam8, Institut national de la recherche agronomique9, University of Antwerp10, University of California, Davis11, DSM12, Karolinska Institutet13, University of Reading14, King's College London15, University of East Anglia16, University of Exeter17, University of Dundee18, London School of Economics and Political Science19
TL;DR: Coupling studies of cognitive ageing with studies investigating the effect of nutrition and dietary interventions as strategies targeting specific mechanisms, such as neurogenesis, protein clearance, inflammation, and non-coding and microRNAs is of high value.
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TL;DR: It is proposed that exercise will attenuate cortical atrophy and synaptic loss inherent to neurodegenerative disorders - many of which also exhibit aberrant down-regulation of BDNF - and have critical therapeutic implications for the prevention and amelioration of memory loss and cognitive impairment in Alzheimer's disease and associated dementias.
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TL;DR: It is suggested that nutritional and pharmaceutical compounds can significantly reduce established biomarkers of systemic inflammation in middle-age and older adults, and should be interpreted with caution, however, due to the evidence of heterogeneity across the studies.
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TL;DR: It is concluded that understanding Nrf2 regulatory mechanisms is essential to develop a rational strategy to prevent the loss of cellular protection response during aging.
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TL;DR: Four categories of melatonin's protective effects on ageing-induced molecular and structural alterations are depicted, including an antioxidant, immunomodulatory, antiproliferative, oncostatic, and endocrine-modulatory molecule.
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TL;DR: The information reviewed here should be significant for understanding the roles of FOXO 1/3 in fibrosis and should contribute to the design of further studies related to FOXO1/3 and the fibrotic response and shed light on a potential treatment for fibrosis.
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TL;DR: There is no consensus on the definition of cognitive frailty for use in clinical and community settings or on which measures to be used for detecting cognitive impairment, and further study is required to formulate effective preventive strategies for disability in the elderly.
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TL;DR: The recent findings on the molecular involvement of melatonin in the regeneration of various tissues including the nervous system, liver, bone, kidney, bladder, skin, and muscle are discussed.
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TL;DR: The epidemiological data linking metformin to ARD prevention is summarized, the deeply studied mechanisms of action explaining its antihyperglycemic effect and the putative mechanisms supporting its anti-ageing properties are dissected, and it is hypothesized that the molecular observations obtained in different models with met formin could be indirectly mediated by its effect on gut flora.
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TL;DR: It seems that proinflammatory changes in tissues with aging stimulate the myelopoietic production of MDSCs which subsequently induces immunosenescence and maintains the chronic inflammaging process.
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TL;DR: This review highlights recent progress in research on the involvement of PGC-1α in certain major neurodegenerative disorders (NDDs), including Alzheimer’s disease, Parkinson's disease, Huntington's Disease, and amyotrophic lateral sclerosis.
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TL;DR: This review summarizes studies investigating the modulation of neural activity and structural brain integrity in response to interventions involving cognitive training, physical exercise and non-invasive brain stimulation in healthy elderly and cognitively impaired subjects.
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TL;DR: The lysosomal-mitochondrial axis is proposed to serve a potential function as an inducer of senescence alleviation and should represent an important research directive for developing therapeutics toward ageing-related disease as well as the aging process itself.
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TL;DR: A framework needs to be developed to better understand the mediating effects of physical capacity and cognitive function on I ADL and to design MCTs that effectively improve IADL.
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TL;DR: Advances in neuroimaging, genetics, neuroscience and the availability of large well characterized biobanks will facilitate research exploring the role of IGF-1 in both normal ageing and age-related cognitive decline.
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TL;DR: Despite advancing age, this review suggests that chronic exercise training preserves physical function, muscular strength and body fat levels similar to that of young, healthy individuals in an exercise mode-specific manner.
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TL;DR: According to recent data, the organism seems to respond to the enhancement of aging-related toxicity by forming a new homeostatic set point and further research will focus on understanding the properties of the new set point, the general nature of this phenomenon and the limits of brains' adaptivity.