@article{MaBalazadehMuellerRoeber2019,
  author    = {Ma, Xuemin and Balazadeh, Salma and Mueller-Roeber, Bernd},
  title     = {Tomato fruit ripening factor NOR controls leaf senescence},
  series = {Journal of experimental botany},
  volume    = {70},
  journal   = {Journal of experimental botany},
  number    = {10},
  publisher = {Oxford Univ. Press},
  address   = {Oxford},
  issn      = {0022-0957},
  doi       = {10.1093/jxb/erz098},
  pages     = {2727 -- 2740},
  year      = {2019},
  abstract  = {NAC transcription factors (TFs) are important regulators of expressional reprogramming during plant development, stress responses, and leaf senescence. NAC TFs also play important roles in fruit ripening. In tomato (Solanum lycopersicum), one of the best characterized NACs involved in fruit ripening is NON-RIPENING (NOR), and the non-ripening (nor) mutation has been widely used to extend fruit shelf life in elite varieties. Here, we show that NOR additionally controls leaf senescence. Expression of NOR increases with leaf age, and developmental as well as dark-induced senescence are delayed in the nor mutant, while overexpression of NOR promotes leaf senescence. Genes associated with chlorophyll degradation as well as senescence-associated genes (SAGs) show reduced and elevated expression, respectively, in nor mutants and NOR overexpressors. Overexpression of NOR also stimulates leaf senescence in Arabidopsis thaliana. In tomato, NOR supports senescence by directly and positively regulating the expression of several senescence-associated genes including, besides others, SlSAG15 and SlSAG113, SlSGR1, and SlYLS4. Finally, we find that another senescence control NAC TF, namely SlNAP2, acts upstream of NOR to regulate its expression. Our data support a model whereby NAC TFs have often been recruited by higher plants for both the control of leaf senescence and fruit ripening.},
  language  = {en}
}
@article{HortobagyiVetrovskyBalbimetal.2022,
  author    = {Hortob{\´a}gyi, Tibor and Vetrovsky, Tomas and Balbim, Guilherme Moraes and Sorte Silva, Narlon Cassio Boa and Manca, Andrea and Deriu, Franca and Kolmos, Mia and Kruuse, Christina and Liu-Ambrose, Teresa and Radak, Zsolt and Vaczi, Mark and Johansson, Hanna and Rocha dos Santos, Paulo Cezar and Franzen, Erika and Granacher, Urs},
  title     = {The impact of aerobic and resistance training intensity on markers of neuroplasticity in health and disease},
  series = {Ageing research reviews : ARR},
  volume    = {80},
  journal   = {Ageing research reviews : ARR},
  publisher = {Elsevier},
  address   = {Clare},
  issn      = {1568-1637},
  doi       = {10.1016/j.arr.2022.101698},
  pages     = {18},
  year      = {2022},
  abstract  = {Objective: To determine the effects of low- vs. high-intensity aerobic and resistance training on motor and cognitive function, brain activation, brain structure, and neurochemical markers of neuroplasticity and the association thereof in healthy young and older adults and in patients with multiple sclerosis, Parkinson's disease, and stroke. Design: Systematic review and robust variance estimation meta-analysis with meta-regression. Data sources: Systematic search of MEDLINE, Web of Science, and CINAHL databases. Results: Fifty studies with 60 intervention arms and 2283 in-analyses participants were included. Due to the low number of studies, the three patient groups were combined and analyzed as a single group. Overall, low- (g=0.19, p = 0.024) and high-intensity exercise (g=0.40, p = 0.001) improved neuroplasticity. Exercise intensity scaled with neuroplasticity only in healthy young adults but not in healthy older adults or patient groups. Exercise-induced improvements in neuroplasticity were associated with changes in motor but not cognitive outcomes. Conclusion: Exercise intensity is an important variable to dose and individualize the exercise stimulus for healthy young individuals but not necessarily for healthy older adults and neurological patients. This conclusion warrants caution because studies are needed that directly compare the effects of low- vs. high-intensity exercise on neuroplasticity to determine if such changes are mechanistically and incrementally linked to improved cognition and motor function.},
  language  = {en}
}
@article{HortobagyiUematsuSandersetal.2018,
  author    = {Hortobagyi, Tibor and Uematsu, Azusa and Sanders, Lianne and Kliegl, Reinhold and Tollar, Jozsef and Moraes, Renato and Granacher, Urs},
  title     = {Beam Walking to Assess Dynamic Balance in Health and Disease},
  series = {Gerontology},
  volume    = {65},
  journal   = {Gerontology},
  number    = {4},
  publisher = {Karger},
  address   = {Basel},
  issn      = {0304-324X},
  doi       = {10.1159/000493360},
  pages     = {332 -- 339},
  year      = {2018},
  abstract  = {Background: Dynamic balance keeps the vertical projection of the center of mass within the base of support while walking. Dynamic balance tests are used to predict the risks of falls and eventual falls. The psychometric properties of most dynamic balance tests are unsatisfactory and do not comprise an actual loss of balance while walking. Objectives: Using beam walking distance as a measure of dynamic balance, the BEAM consortium will determine the psychometric properties, lifespan and patient reference values, the relationship with selected "dynamic balance tests," and the accuracy of beam walking distance to predict falls. Methods: This cross-sectional observational study will examine healthy adults in 7 decades (n = 432) at 4 centers. Center 5 will examine patients (n = 100) diagnosed with Parkinson's disease, multiple sclerosis, stroke, and balance disorders. In test 1, all participants will be measured for demographics, medical history, muscle strength, gait, static balance, dynamic balance using beam walking under single (beam walking only) and dual task conditions (beam walking while concurrently performing an arithmetic task), and several cognitive functions. Patients and healthy participants age 50 years or older will be additionally measured for fear of falling, history of falls, miniBESTest, functional reach on a force platform, timed up and go, and reactive balance. All participants age 50 years or older will be recalled to report fear of falling and fall history 6 and 12 months after test 1. In test 2, seven to ten days after test 1, healthy young adults and age 50 years or older (n = 40) will be retested for reliability of beam walking performance. Conclusion: We expect to find that beam walking performance vis-{\`a}-vis the traditionally used balance outcomes predicts more accurately fall risks and falls. Clinical Trial Registration Number: NCT03532984.},
  language  = {en}
}
@article{NowotnyCastroHugoetal.2018,
  author    = {Nowotny, Kerstin and Castro, Jose Pedro and Hugo, Martin and Braune, Sabine and Weber, Daniela and Pignitter, Marc and Somoza, Veronika and Bornhorst, Julia and Schwerdtle, Tanja and Grune, Tilman},
  title     = {Oxidants produced by methylglyoxal-modified collagen trigger ER stress and apoptosis in skin fibroblasts},
  series = {Free radical biology and medicine : the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research},
  volume    = {120},
  journal   = {Free radical biology and medicine : the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research},
  publisher = {Elsevier},
  address   = {New York},
  issn      = {0891-5849},
  doi       = {10.1016/j.freeradbiomed.2018.03.022},
  pages     = {102 -- 113},
  year      = {2018},
  abstract  = {Methylglyoxal (MG), a highly reactive dicarbonyl, interacts with proteins to form advanced glycation end products (AGEs). AGEs include a variety of compounds which were shown to have damaging potential and to accumulate in the course of different conditions such as diabetes mellitus and aging. After confirming collagen as a main target for MG modifications in vivo within the extracellular matrix, we show here that MG-collagen disrupts fibroblast redox homeostasis and induces endoplasmic reticulum (ER) stress and apoptosis. In particular, MG-collagen-induced apoptosis is associated with the activation of the PERK-eIF2 alpha pathway and caspase-12. MG-collagen contributes to altered redox homeostasis by directly generating hydrogen peroxide and oxygen-derived free radicals. The induction of ER stress in human fibroblasts was confirmed using collagen extracts isolated from old mice in which MG-derived AGEs were enriched. In conclusion, MG-derived AGEs represent one factor contributing to diminished fibroblast function during aging.},
  language  = {en}
}
@article{FernandoDrescherNowotnyetal.2018,
  author    = {Fernando, Raquel and Drescher, Cathleen and Nowotny, Kerstin and Grune, Tilman and Castro, Jose Pedro},
  title     = {Impaired proteostasis during skeletal muscle aging},
  series = {Free radical biology and medicine : the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research},
  volume    = {132},
  journal   = {Free radical biology and medicine : the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research},
  publisher = {Elsevier},
  address   = {New York},
  issn      = {0891-5849},
  doi       = {10.1016/j.freeradbiomed.2018.08.037},
  pages     = {58 -- 66},
  year      = {2018},
  abstract  = {Aging is a complex phenomenon that has detrimental effects on tissue homeostasis. The skeletal muscle is one of the earliest tissues to be affected and to manifest age-related changes such as functional impairment and the loss of mass. Common to these alterations and to most of tissues during aging is the disruption of the proteostasis network by detrimental changes in the ubiquitin-proteasomal system (UPS) and the autophagy-lysosomal system (ALS). In fact, during aging the accumulation of protein aggregates, a process mainly driven by increased levels of oxidative stress, has been observed, clearly demonstrating UPS and ALS dysregulation. Since the UPS and ALS are the two most important pathways for the removal of misfolded and aggregated proteins and also of damaged organelles, we provide here an overview on the current knowledge regarding the connection between the loss of proteostasis and skeletal muscle functional impairment and also how redox regulation can play a role during aging. Therefore, this review serves for a better understanding of skeletal muscle aging in regard to the loss of proteostasis and how redox regulation can impact its function and maintenance.},
  language  = {en}
}