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Sökning: L773:1872 6216 OR L773:0047 6374 > (2020-2024)

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1.
  • Aaseth, Jan, et al. (författare)
  • Coenzyme Q(10) supplementation - In ageing and disease
  • 2021
  • Ingår i: Mechanisms of Ageing and Development. - : Elsevier Ireland Ltd. - 0047-6374 .- 1872-6216. ; 197
  • Tidskriftsartikel (refereegranskat)abstract
    • Coenzyme Q(10) (CoQ(10)) is an essential component of the mitochondrial electron transport chain. It is also an antioxidant in cellular membranes and lipoproteins. All cells produce CoQ(10) by a specialized cytoplasmatic-mitochondrial pathway. CoQ(10) deficiency can result from genetic failure or ageing. Some drugs including statins, widely used by inter alia elderly, may inhibit endogenous CoQ(10) synthesis. There are also chronic diseases with lower levels of CoQ(10) in tissues and organs. High doses of CoQ(10) may increase both circulating and intracellular levels, but there are conflicting results regarding bioavailability. Here, we review the current knowledge of CoQ(10) biosynthesis and primary and acquired CoQ(10) deficiency, and results from clinical trials based on CoQ(10) supplementation. There are indications that supplementation positively affects mitochondrial deficiency syndrome and some of the symptoms of ageing. Cardiovascular disease and inflammation appear to be alleviated by the antioxidant effect of CoQ(10). There is a need for further studies and well-designed clinical trials, with CoQ(10) in a formulation of proven bioavailability, involving a greater number of participants undergoing longer treatments in order to assess the benefits of CoQ(10) treatment in neurodegenerative disorders, as well as in metabolic syndrome and its complications.
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  • Chaillou, Thomas, 1985-, et al. (författare)
  • Glutamine-stimulated in vitro hypertrophy is preserved in muscle cells from older women
  • 2020
  • Ingår i: Mechanisms of Ageing and Development. - : Elsevier. - 0047-6374 .- 1872-6216. ; 187
  • Tidskriftsartikel (refereegranskat)abstract
    • Age-related loss of muscle mass may result from reduced protein synthesis stimulation in response to anabolic stimuli, such as amino acid (AA) supplementation. The exact etiology of anabolic resistance to AA remains unclear. Therefore, the aim of this study was to investigate the anabolic response [cell size, protein synthesis and mechanistic target of rapamycin (mTOR) pathway] to the AA glutamine (a strong anabolic AA highly present in skeletal muscle) in myotubes obtained from 8 young (YW; 21-35 yrs) and 8 older (OW; 65-70 yrs) healthy women. This in vitro model of human primary myogenic cells explores the intrinsic behavior of muscle cells, while excluding potential influences of external factors. We showed that despite lower muscle mass, strength and cardiorespiratory fitness in OW compared to YW, myotube size (myotube diameter and area) and protein synthesis were not altered in OW, and glutamine-induced myotube hypertrophy and protein synthesis were preserved in OW. Apart from a lower glutamine-induced increase in P70S6 kinase phosphorylation in OW, no significant differences in other components of the mTOR pathway were observed between groups. Altogether, our data support the idea that the intrinsic capacity of muscle cells to respond to glutamine stimulation is preserved in healthy older women.
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  • Davidy, Tal, et al. (författare)
  • A feasibility study of the combination of intranasal insulin with oral semaglutide for cognition in older adults with metabolic syndrome at high dementia risk- Study rationale and design
  • 2024
  • Ingår i: Mechanisms of Ageing and Development. - 0047-6374 .- 1872-6216. ; 218
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: We present the rationale and design of a double-blind placebo-controlled feasibility trial combining intranasal insulin (INI) with semaglutide, a GLP-1 receptor agonist, to improve cognition in older adults with metabolic syndrome (MetS) and mild cognitive impairment (MCI). Since both INI and dulaglutide have beneficial effects on the cerebrovascular disease (CVD), we anticipate that improved CVD will underlie the hypothesized cognitive benefits. Methods: This 12-months trial will include 80 older adults aged > 60 with MetS and MCI, randomized to 4 groups: INI/oral semaglutide, intranasal placebo/oral semaglutide, INI/oral placebo, and intranasal placebo/oral placebo. Feasibility of combining INI with semaglutide will be tested by examining the ease of use of INI (20IU, twice/day) with semaglutide (14 once daily), adherence, and safety profile are the efficacy of combination therapy on global cognition and neurobiological markers: cerebral blood flow, cerebral glucose utilization, white matter hyperintensities, Alzheimer's related blood biomarkers and expression of insulin signaling proteins measured in brain-derived exosomes. Efficacy will be assessed for the intent-to-treat sample. Discussion: This feasibility study is anticipated to provide the basis for a multi-center large-scale randomized clinical trial (RCT) of the cognitive benefits of the combination of INI with semaglutide in individuals enriched for CVD and at high dementia risk.
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  • Onder, Graziano, et al. (författare)
  • Facing multimorbidity in the precision medicine era
  • 2020
  • Ingår i: Mechanisms of Ageing and Development. - : Elsevier BV. - 0047-6374 .- 1872-6216. ; 190
  • Tidskriftsartikel (refereegranskat)abstract
    • The clinical picture of multimorbidity is heterogeneous and it is characterized by great complexity. Precision medicine is an innovative approach to provide personalized care focused on individual characteristics and to deliver the right treatments, at the right time, to the right person. The precision medicine approach, which represents an epochal change in the field of chronic diseases, has been poorly implemented in patients with multimorbidity. Several factors can limit this application. First, the precision medicine approach has been successfully applied in the treatment of mono-factorial diseases while multimorbidity is multifactorial. Second, there is lack of understanding of risk factors in the development and evolution of multimorbidity. Third, precision medicine is mainly focused on understanding genetic aspects of diseases and neglects other characteristics contributing to the definition of individual profiles. Finally, individual pathways may lead to the development of different multimorbidity phenotypes. A possible solution to simplify the application of precision medicine to this condition is to reduce its complexity and to find homogeneous patterns of chronic diseases that may work as targets of preventive and therapeutic strategies. This approach can lead to better understanding how these factors interact at individual level and to define interventions that might target multimorbidity.
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  • Pentinmikko, N, et al. (författare)
  • The role of stem cell niche in intestinal aging
  • 2020
  • Ingår i: Mechanisms of ageing and development. - : Elsevier BV. - 1872-6216 .- 0047-6374. ; 191, s. 111330-
  • Tidskriftsartikel (refereegranskat)
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  • Triolo, Federico, et al. (författare)
  • The complex interplay between depression and multimorbidity in late life : risks and pathways
  • 2020
  • Ingår i: Mechanisms of Ageing and Development. - : Elsevier BV. - 0047-6374 .- 1872-6216. ; 192
  • Tidskriftsartikel (refereegranskat)abstract
    • Multimorbidity and depression are complex multifactorial conditions with major implications for older individuals, their families, and healthcare providers. In this scoping review, we aimed to 1) review findings from longitudinal epidemiological studies investigating the association between multimorbidity and depression; 2) identify potential mechanisms linking multimorbidity and depression; 3) discuss challenges to advance the research field. Overall, evidence emerging from longitudinal studies supports a bidirectional association between the two conditions, although studies are methodologically heterogeneous in terms of design, inclusion criteria, measurement of multimorbidity and depression, and length of follow-up. A variety of biological, psychosocial, and care-related drivers may regulate the transition from multimorbidity to depression, and the other way around, although these mechanisms are yet to be explicitly verified. Further research is required to unravel the intricate interplay between multimorbidity, depression, their common drivers, and precipitating factors underlying the relationship between the two conditions. Understanding these processes will inform strategies aimed at promoting mental and physical health during aging.
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