early aging
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Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1868
Author(s):  
Derek G. Epiney ◽  
Charlotte Salameh ◽  
Deirdre Cassidy ◽  
Luhan T. Zhou ◽  
Joshua Kruithof ◽  
...  

As organisms age, their resistance to stress decreases while their risk of disease increases. This can be shown in patients with Werner syndrome (WS), which is a genetic disease characterized by accelerated aging along with increased risk of cancer and metabolic disease. WS is caused by mutations in WRN, a gene involved in DNA replication and repair. Recent research has shown that WRN mutations contribute to multiple hallmarks of aging including genomic instability, telomere attrition, and mitochondrial dysfunction. However, questions remain regarding the onset and effect of stress on early aging. We used a fly model of WS (WRNexoΔ) to investigate stress response during different life stages and found that stress sensitivity varies according to age and stressor. While larvae and young WRNexoΔ adults are not sensitive to exogenous oxidative stress, high antioxidant activity suggests high levels of endogenous oxidative stress. WRNexoΔ adults are sensitive to stress caused by elevated temperature and starvation suggesting abnormalities in energy storage and a possible link to metabolic dysfunction in WS patients. We also observed higher levels of sleep in aged WRNexoΔ adults suggesting an additional adaptive mechanism to protect against age-related stress. We suggest that stress response in WRNexoΔ is multifaceted and evokes a systemic physiological response to protect against cellular damage. These data further validate WRNexoΔ flies as a WS model with which to study mechanisms of early aging and provide a foundation for development of treatments for WS and similar diseases.


Author(s):  
Alessia Remigante ◽  
Sara Spinelli ◽  
Vincenzo Trichilo ◽  
Saverio Loddo ◽  
Antonio Sarikas ◽  
...  

Author(s):  
Ugo Carraro ◽  
Helmut Kern ◽  
Giovanna Albertin

Paolo Gava, (Conegliano, Treviso, September 1, 1946 – Stra, Venezia, Italy, July 19, 2021) was a sustainable resources engineer, who worked in Italy, France and England, leading research programs well before the current international interest in countering global warming. Passionate about Tango, Paolo kept himself in shape for many decades by running or pedaling or roller-skating, after years of training as a semi-professional athlete, competing and winning Italian and European short distance races in the Master classes. Then, Paolo applied his engineering skills to optimize comparisons between the results of the different Classes of Master Athletes, questioning the rules used by Italian and World Master Sports Associations. Friendly discussing during an after-dinner, he shocked us claiming that, in absence of diseases and trauma (Early Aging), the aging decay is a linear process from 30 to 110 years. Under our friendly pressure he was able to publish his first biomedical article, detailing his mathematical approaches and results in a 2015 issue of Experimental Aging Research, titled: Age-associated power decline from running, jumping and throwing male master world records. To honor his other legacies during his last six years of life, we add here further examples of Paolo's scientific studies and his relationships with senior colleagues and young students of sports and aging sciences.


Cancers ◽  
2021 ◽  
Vol 13 (20) ◽  
pp. 5214
Author(s):  
Silvia Ravera ◽  
Tiziana Vigliarolo ◽  
Silvia Bruno ◽  
Fabio Morandi ◽  
Danilo Marimpietri ◽  
...  

Survival rates of childhood cancer patients have improved over the past four decades, although cancer treatments increase the risk of developing chronic diseases typical of aging. Thus, we aimed to identify molecular/metabolic cellular alterations responsible for early aging in childhood cancer survivors (CCS). Biochemical, proteomic, and molecular biology analyses were conducted on mononuclear cells (MNCs) isolated from peripheral blood of 196 CCS, the results being compared with those obtained on MNCs of 154 healthy subjects. CCS-MNCs showed inefficient oxidative phosphorylation associated with low energy status, and increased lipid peroxidation and lactate fermentation compared with age-matched normal controls. According to a mathematical model based on biochemical parameters, CCS-MNCs showed significantly higher metabolic ages than their real ages. The dysfunctional metabolism of CCS-MNCs is associated with lower expression levels of genes and proteins involved in mitochondrial biogenesis and metabolism regulation, such as CLUH, PGC1-alpha, and SIRT6 in CCS, not observed in the age-matched healthy or elderly subjects. In conclusion, our study identified some biochemical and molecular alterations possibly contributing to the pathophysiology of aging and metabolic deficiencies in CCS. These results identify new targets for pharmacological interventions to restore mitochondrial function, slowing down the aging-associated pathologies in CCS.


Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3139
Author(s):  
Marta Ferrari ◽  
Stefano Stagi

Oxidative stress is the result of an imbalance in the redox state in a cell or a tissue. When the production of free radicals, which are physiologically essential for signaling, exceeds the antioxidant capability, pathological outcomes including oxidative damage to macromolecules, aberrant signaling, and inflammation can occur. Down syndrome (DS) and Williams-Beuren syndrome (WBS) are well-known and common genetic conditions with multi-systemic involvement. Their etiology is linked to oxidative stress with important causative genes, such as SOD-1 and NCF-1, respectively, of the diseases being primarily involved in the regulation of the redox state. Early aging, dementia, autoimmunity, and chronic inflammation are some of the main characteristics of these conditions that can be associated with oxidative stress. In recent decades, there has been a growing interest in the possible role of oxidative stress and inflammation in the pathology of these conditions. However, at present, few studies have investigated these correlations. We provide an overview of the current literature concerning the role of oxidative stress and oxidative damage in genetic syndromes with a focus on Down syndrome and WBS. We hope to provide new insights to improve the management of complications related to these diseases.


2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Kendall Zaleski ◽  
Stephen Ives ◽  
Cheyanne Slocum ◽  
Gabriel O'Brien ◽  
Lauren Gorstein ◽  
...  

2021 ◽  
Author(s):  
Silvia Ravera ◽  
Tiziana Vigliarolo ◽  
Silvia Bruno ◽  
Fabio Morandi ◽  
Danilo Marimpietri ◽  
...  

ABSTRACTPurposeSurvival rates of Childhood Cancer Patients have improved tremendously over the past four decades. However, cancer treatments are associated with an increased risk of developing an anticipated onset of chronic diseases typical of aging. Thus, we aimed to identify molecular/metabolic cellular alterations responsible for early aging in Childhood Cancer Survivors (CCS).Patients and MethodsBiochemical, proteomic and molecular biology analyses were conducted on mononuclear cells (MNCs) isolated from peripheral blood of 196 CCS, comparing the results with those obtained on MNCs of 154 healthy subjects.ResultsData demonstrate that CCS-MNCs show: i) inefficient oxidative phosphorylation associated with low energy status and a metabolic switch to lactate fermentation compared with age-matched normal controls; ii) increment of lipid peroxidation due to an unbalance among the oxidative stress production and the activation of the antioxidant defenses; (iii) significantly lower expression of genes and proteins involved in mitochondrial biogenesis and metabolism regulation, such as CLUH, PGC1-α, and SIRT6 in CCS, not observed in the age-matched healthy or elderly subjects. The application of a mathematical model based on biochemical parameters predicts that CCS have a biological age significantly increased by decades compared to the chronological age. Overall, the results show that the impact of chemo/chemoradiotherapy on mitochondria efficiency in 196 CCS was rather homogeneous, irrespective of cancer type, treatment protocols, and time elapsed from the end of the curative period.ConclusionsOur study identifies some biochemical and molecular alterations possibly contributing to the pathophysiology of anticipated aging and metabolic deficiency described in CCS. These results may be useful in identifying approaches to restore the mitochondrial function, slowing down the aging and the associated pathological conditions in CCS.


2021 ◽  
Vol 99 (S265) ◽  
Author(s):  
José A. Fernández‐Albarral ◽  
Elena Salobrar‐Garcia ◽  
Inés López‐Cuenca ◽  
María Pilar Rojas Lozano ◽  
Juan José Salazar Corral ◽  
...  
Keyword(s):  

2021 ◽  
Vol 99 (S265) ◽  
Author(s):  
José A. Fernández‐Albarral ◽  
Inés López‐Cuenca ◽  
Elena Salobrar‐Garcia ◽  
María Pilar Rojas Lozano ◽  
Ana I. Ramírez ◽  
...  

2021 ◽  
Author(s):  
Yu Han ◽  
Lauren Z Li ◽  
Nikhitha L. Kastury ◽  
Cody T. Thomas ◽  
Maggie P. Y. Lam ◽  
...  

We performed total RNA sequencing and multi-omics analysis comparing skeletal muscle and cardiac muscle in young adult (4 months) vs. early aging (20 months) mice to examine the molecular mechanisms...


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