AGE最新文献

{"title":"Interspecific correlation between red blood cell mitochondrial ROS production, cardiolipin content and longevity in birds.","authors":"Jessica Delhaye,&nbsp;Nicolas Salamin,&nbsp;Alexandre Roulin,&nbsp;François Criscuolo,&nbsp;Pierre Bize,&nbsp;Philippe Christe","doi":"10.1007/s11357-016-9940-z","DOIUrl":"https://doi.org/10.1007/s11357-016-9940-z","url":null,"abstract":"<p><p>Mitochondrial respiration releases reactive oxygen species (ROS) as by-products that can damage the soma and may in turn accelerate ageing. Hence, according to \"the oxidative stress theory of ageing\", longer-lived organisms may have evolved mechanisms that improve mitochondrial function, reduce ROS production and/or increase cell resistance to oxidative damage. Cardiolipin, an important mitochondrial inner-membrane phospholipid, has these properties by binding and stabilizing mitochondrial inner-membrane proteins. Here, we investigated whether ROS production, cardiolipin content and cell membrane resistance to oxidative attack in freshly collected red blood cells (RBCs) are associated with longevity (range 5-35 years) in 21 bird species belonging to seven Orders. After controlling for phylogeny, body size and oxygen consumption, variation in maximum longevity was significantly explained by mitochondrial ROS production and cardiolipin content, but not by membrane resistance to oxidative attack. RBCs of longer-lived species produced less ROS and contained more cardiolipin than RBCs of shorter-lived species did. These results support the oxidative stress theory of ageing and shed light on mitochondrial cardiolipin as an important factor linking ROS production to longevity.</p>","PeriodicalId":7632,"journal":{"name":"AGE","volume":"38 5-6","pages":"433-443"},"PeriodicalIF":0.0,"publicationDate":"2016-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11357-016-9940-z","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34345475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pioglitazone is equally effective for diabetes prevention in older versus younger adults with impaired glucose tolerance.","authors":"Sara E Espinoza, Chen-Pin Wang, Devjit Tripathy, Stephen C Clement, Dawn C Schwenke, Mary Ann Banerji, George A Bray, Thomas A Buchanan, Robert R Henry, Abbas E Kitabchi, Sunder Mudaliar, Frankie B Stentz, Peter D Reaven, Ralph A DeFronzo, Nicolas Musi","doi":"10.1007/s11357-016-9946-6","DOIUrl":"10.1007/s11357-016-9946-6","url":null,"abstract":"<p><p>To determine the efficacy of pioglitazone to prevent type 2 diabetes in older compared to younger adults with pre-diabetes. Six hundred two participants with impaired glucose tolerance (IGT) were randomized in double blind fashion to placebo or pioglitazone for diabetes prevention in the ACT NOW study (NEJM 364:1104-1115, 2011). Cox proportional hazard regression was used to compare time to development of diabetes over a mean of 2 years between older (≥61 years) and younger participants. We compared effects of pioglitazone versus placebo on metabolic profiles, inflammatory markers, adipokines, β cell function (disposition index), insulin sensitivity (Matsuda index), and body composition by ANOVA. Diabetes incidence was reduced by 85 % in older and 69 % in younger subjects (p = 0.41). β cell function (disposition index) increased by 35.0 % in the older and 26.7 % in younger subjects (p = 0.83). Insulin sensitivity (Matsuda index) increased by 3.07 (5.2-fold) in older and by 2.54 (3.8-fold) in younger participants (p = 0.58). Pioglitazone more effectively increased adiponectin in older versus younger subjects (22.9 ± 3.2 μg/mL [2.7-fold] vs. 12.7 ± 1.4 μg/mL [2.2-fold], respectively; p = 0.04). Younger subjects tended to have a greater increase in whole body fat mass compared to older subjects (3.6 vs. 3.1 kg; p = 0.061). Younger and older subjects had similar decreases in bone mineral density (0.018 ± 0.0071 vs. 0.0138 ± 0.021 g/cm²). Younger and older pre-diabetic adults taking pioglitazone had similar reductions in conversion to diabetes and older adults had similar or greater improvements in metabolic risk factors, demonstrating that pioglitazone is useful in preventing diabetes in older adults.</p>","PeriodicalId":7632,"journal":{"name":"AGE","volume":"38 5-6","pages":"485-493"},"PeriodicalIF":0.0,"publicationDate":"2016-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5266219/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34701033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Basal body temperature as a biomarker of healthy aging","authors":"E. Simonsick, H. Meier, N. C. Shaffer, S. Studenski, L. Ferrucci","doi":"10.1007/s11357-016-9952-8","DOIUrl":"https://doi.org/10.1007/s11357-016-9952-8","url":null,"abstract":"","PeriodicalId":7632,"journal":{"name":"AGE","volume":"244 1","pages":"445 - 454"},"PeriodicalIF":0.0,"publicationDate":"2016-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78938170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural brain changes and all-cause mortality in the elderly population—the mediating role of inflammation","authors":"U. Hanning, A. Roesler, A. Peters, K. Berger, B. Baune","doi":"10.1007/s11357-016-9951-9","DOIUrl":"https://doi.org/10.1007/s11357-016-9951-9","url":null,"abstract":"","PeriodicalId":7632,"journal":{"name":"AGE","volume":"348 1","pages":"455 - 464"},"PeriodicalIF":0.0,"publicationDate":"2016-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77626000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum to: Effects of aging on human leukocytes (part II): immunophenotyping of adaptive immune B and T cell subsets","authors":"U. Stervbo, Cecilia Bozzetti, U. Baron, K. Jürchott, Sarah Meier, J. Mälzer, M. Nienen, S. Olek, D. Rachwalik, A. Schulz, A. Neumann, N. Babel, A. Grützkau, A. Thiel","doi":"10.1007/s11357-016-9928-8","DOIUrl":"https://doi.org/10.1007/s11357-016-9928-8","url":null,"abstract":"","PeriodicalId":7632,"journal":{"name":"AGE","volume":"143 1","pages":"535 - 536"},"PeriodicalIF":0.0,"publicationDate":"2016-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77318390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Apolipoproteins and HDL cholesterol do not associate with the risk of future dementia and Alzheimer’s disease: the National Finnish population study (FINRISK)","authors":"Juho Tynkkynen, J. Hernesniemi, T. Laatikainen, A. Havulinna, J. Sundvall, J. Leiviskä, P. Salo, V. Salomaa","doi":"10.1007/s11357-016-9950-x","DOIUrl":"https://doi.org/10.1007/s11357-016-9950-x","url":null,"abstract":"","PeriodicalId":7632,"journal":{"name":"AGE","volume":"81 1","pages":"465 - 473"},"PeriodicalIF":0.0,"publicationDate":"2016-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75380807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Age at menarche and age at natural menopause in East Asian women: a genome-wide association study","authors":"Jiajun Shi, Ben Zhang, Ji-Yeob Choi, Yuxue Gao, Huaixing Li, W. Lu, J. Long, D. Kang, Y. Xiang, W. Wen, Sue-Kyung Park, X. Ye, D. Noh, Ying Zheng, Yiqin Wang, Seokang Chung, Xu Lin, Q. Cai, X. Shu","doi":"10.1007/s11357-016-9939-5","DOIUrl":"https://doi.org/10.1007/s11357-016-9939-5","url":null,"abstract":"","PeriodicalId":7632,"journal":{"name":"AGE","volume":"24 1","pages":"513 - 523"},"PeriodicalIF":0.0,"publicationDate":"2016-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77673279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Accelerated reduction of serum thyroxine and hippocampal histone acetylation links to exacerbation of spatial memory impairment in aged CD-1 mice pubertally exposed to bisphenol-a","authors":"Wei Jiang, Lei Cao, Fang Wang, Hai Ge, Peng Wu, Xue-wei Li, Gui-Hai Chen","doi":"10.1007/s11357-016-9947-5","DOIUrl":"https://doi.org/10.1007/s11357-016-9947-5","url":null,"abstract":"","PeriodicalId":7632,"journal":{"name":"AGE","volume":"150 1","pages":"405 - 418"},"PeriodicalIF":0.0,"publicationDate":"2016-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82497039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating IGF-1 deficiency exacerbates hypertension-induced microvascular rarefaction in the mouse hippocampus and retrosplenial cortex: implications for cerebromicrovascular and brain aging.","authors":"Stefano Tarantini, Zsuzsanna Tucsek, M Noa Valcarcel-Ares, Peter Toth, Tripti Gautam, Cory B Giles, Praveen Ballabh, Jeanne Y Wei, Jonathan D Wren, Nicole M Ashpole, William E Sonntag, Zoltan Ungvari, Anna Csiszar","doi":"10.1007/s11357-016-9931-0","DOIUrl":"10.1007/s11357-016-9931-0","url":null,"abstract":"<p><p>Strong epidemiological and experimental evidence indicate that both age and hypertension lead to significant functional and structural impairment of the cerebral microcirculation, predisposing to the development of vascular cognitive impairment (VCI) and Alzheimer's disease. Preclinical studies establish a causal link between cognitive decline and microvascular rarefaction in the hippocampus, an area of brain important for learning and memory. Age-related decline in circulating IGF-1 levels results in functional impairment of the cerebral microvessels; however, the mechanistic role of IGF-1 deficiency in impaired hippocampal microvascularization remains elusive. The present study was designed to characterize the additive/synergistic effects of IGF-1 deficiency and hypertension on microvascular density and expression of genes involved in angiogenesis and microvascular regression in the hippocampus. To achieve that goal, we induced hypertension in control and IGF-1 deficient mice (Igf1 ^f/f  + TBG-Cre-AAV8) by chronic infusion of angiotensin II. We found that circulating IGF-1 deficiency is associated with decreased microvascular density and exacerbates hypertension-induced microvascular rarefaction both in the hippocampus and the neocortex. The anti-angiogenic hippocampal gene expression signature observed in hypertensive IGF-1 deficient mice in the present study provides important clues for subsequent studies to elucidate mechanisms by which hypertension may contribute to the pathogenesis and clinical manifestation of VCI. In conclusion, adult-onset, isolated endocrine IGF-1 deficiency exerts deleterious effects on the cerebral microcirculation, leading to a significant decline in cortical and hippocampal capillarity and exacerbating hypertension-induced cerebromicrovascular rarefaction. The morphological impairment of the cerebral microvasculature induced by IGF-1 deficiency and hypertension reported here, in combination with neurovascular uncoupling, increased blood-brain barrier disruption and neuroinflammation reported in previous studies likely contribute to the pathogenesis of vascular cognitive impairment in elderly hypertensive humans.</p>","PeriodicalId":7632,"journal":{"name":"AGE","volume":" ","pages":"273-289"},"PeriodicalIF":0.0,"publicationDate":"2016-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5061685/pdf/11357_2016_Article_9931.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34377566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of the antioxidant enzyme CuZnSOD (Sod1) mimics an age-related increase in absolute mitochondrial DNA copy number in the skeletal muscle.","authors":"Dustin R Masser,&nbsp;Nicholas W Clark,&nbsp;Holly Van Remmen,&nbsp;Willard M Freeman","doi":"10.1007/s11357-016-9930-1","DOIUrl":"https://doi.org/10.1007/s11357-016-9930-1","url":null,"abstract":"<p><p>Mitochondria contain multiple copies of the circular mitochondrial genome (mtDNA) that encodes ribosomal RNAs and proteins locally translated for oxidative phosphorylation. Loss of mtDNA integrity, both altered copy number and increased mutations, is implicated in cellular dysfunction with aging. Published data on mtDNA copy number and aging is discordant which may be due to methodological limitations for quantifying mtDNA copy number. Existing quantitative PCR (qPCR) mtDNA copy number quantification methods provide only relative abundances and are problematic to normalize to different template input amounts and across tissues/sample types. As well, existing methods cannot quantify mtDNA copy number in subcellular isolates, such as isolated mitochondria and neuronal synaptic terminals, which lack nuclear genomic DNA for normalization. We have developed and validated a novel absolute mtDNA copy number quantitation method that uses chip-based digital polymerase chain reaction (dPCR) to count the number of copies of mtDNA and used this novel method to assess the literature discrepancy in which there is no clear consensus whether mtDNA numbers change with aging in skeletal muscle. Skeletal muscle in old mice was found to have increased absolute mtDNA numbers compared to young controls. Furthermore, young Sod1 ^-/- mice were assessed and show an age-mimicking increase in skeletal muscle mtDNA. These findings reproduce a number of previous studies that demonstrate age-related increases in mtDNA. This simple and cost effective dPCR approach should enable precise and accurate mtDNA copy number quantitation in mitochondrial studies, eliminating contradictory studies of mitochondrial DNA content with aging.</p>","PeriodicalId":7632,"journal":{"name":"AGE","volume":" ","pages":"323-333"},"PeriodicalIF":0.0,"publicationDate":"2016-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11357-016-9930-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34752356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}