Translational Medicine of Aging最新文献_第7页

Role of hematopoietic aging in cognitive decline 造血老化在认知能力下降中的作用

Translational Medicine of Aging Pub Date : 2020-01-01 DOI: 10.1016/j.tma.2020.07.003

Helen S. Goodridge

引用次数: 1

Mitochondrial hyperactivity as a potential therapeutic target in Parkinson’s disease 线粒体多活性作为帕金森病的潜在治疗靶点

Translational Medicine of Aging Pub Date : 2020-01-01 DOI: 10.1016/j.tma.2020.07.007

Danielle E. Mor, Coleen T. Murphy

{"title":"Mitochondrial hyperactivity as a potential therapeutic target in Parkinson’s disease","authors":"Danielle E. Mor, Coleen T. Murphy","doi":"10.1016/j.tma.2020.07.007","DOIUrl":"10.1016/j.tma.2020.07.007","url":null,"abstract":"<div>Mitochondrial dysfunction is thought to contribute to neurodegeneration in Parkinson’s disease (PD), yet the cellular events that lead to mitochondrial disruption remain unclear. Post-mortem studies of PD patient brains and the use of complex I inhibitors to model the disease previously suggested a reduction in mitochondrial activity as a causative factor in PD, but this may represent an endpoint in the disease process. In our recent studies, we identified a novel link between branched-chain amino acid metabolism and PD, and uncovered mitochondrial hyperactivity as a potential alternative mechanism of PD pathogenesis. Increased mitochondrial activity may occur in a subset of PD patients, or may be a more common early event that precedes the ultimate loss of mitochondrial function. Therefore, it may be that any imbalance in mitochondrial activity, either increased or decreased, could cause a loss of mitochondrial homeostasis that leads to disease. An effective therapeutic strategy may be to target specific imbalances in activity at selective stages of PD or in specific patients, with any efforts to reduce mitochondrial activity constituting a surprising new avenue for PD treatment.</div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"4 ","pages":"Pages 117-120"},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tma.2020.07.007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38697666","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}

引用次数: 6

Remote but not isolated 偏远但不孤立

Translational Medicine of Aging Pub Date : 2020-01-01 DOI: 10.1016/j.tma.2020.06.001

William B. Mair

引用次数: 1

The heat shock transcription factor HSF-1 protects Caenorhabditis elegans from peroxide stress 热休克转录因子HSF-1保护秀丽隐杆线虫免受过氧化应激

Translational Medicine of Aging Pub Date : 2020-01-01 DOI: 10.1016/j.tma.2020.07.002

Francesco A. Servello, Javier Apfeld

引用次数: 0

SPOCK, an R based package for high-throughput analysis of growth rate, survival, and chronological lifespan in yeast SPOCK，一个基于R的软件包，用于酵母的高通量生长速率，存活率和按时间顺序的寿命分析

Translational Medicine of Aging Pub Date : 2020-01-01 DOI: 10.1016/j.tma.2020.08.003

Eric M. Small , Daniel P. Felker , Olivia C. Heath , Ryla J. Cantergiani , Christine E. Robbins , Mary Ann Osley , Mark A. McCormick

引用次数: 8

Aging Science Talks: The role of miR-181a in age-related loss of muscle mass and function 衰老科学讲座:miR-181a在年龄相关的肌肉质量和功能损失中的作用

Translational Medicine of Aging Pub Date : 2020-01-01 DOI: 10.1016/j.tma.2020.07.001

Maria Borja-Gonzalez , Jose C. Casas-Martinez , Brian McDonagh , Katarzyna Goljanek-Whysall

引用次数: 5

ELOVL2: Not just a biomarker of aging ELOVL2:不仅仅是衰老的生物标志物

Translational Medicine of Aging Pub Date : 2020-01-01 DOI: 10.1016/j.tma.2020.06.004

Daniel L. Chao , Dorota Skowronska-Krawczyk

引用次数: 13

A high throughput drug screening paradigm using transgenic Caenorhabditis elegans model of Alzheimer’s disease 利用转基因秀丽隐杆线虫模型对阿尔茨海默病进行高通量药物筛选

Translational Medicine of Aging Pub Date : 2020-01-01 DOI: 10.1016/j.tma.2019.12.002

Emelyne Teo , Soon Yew John Lim , Sheng Fong , Anis Larbi , Graham D. Wright , Nicholas Tolwinski , Jan Gruber

{"title":"A high throughput drug screening paradigm using transgenic Caenorhabditis elegans model of Alzheimer’s disease","authors":"Emelyne Teo , Soon Yew John Lim , Sheng Fong , Anis Larbi , Graham D. Wright , Nicholas Tolwinski , Jan Gruber","doi":"10.1016/j.tma.2019.12.002","DOIUrl":"10.1016/j.tma.2019.12.002","url":null,"abstract":"<div>Alzheimer’s disease (AD), characterized by memory loss and cognitive decline, is one of the diseases with the highest attrition rate in drug development. As with other neurodegenerative diseases, AD manifests on several scales (molecular, cellular and organismal), resulting in an organismal phenotype that is difficult to replicate and exploit for screening in vitro. Development of high-throughput drug screening platforms using invertebrate organisms may therefore facilitate drug discovery in AD, at least for compounds that target mechanisms that can be modelled in invertebrates, such as metabolic defects and mitochondrial toxicity. Here we present a potentially high-throughput screening platform against AD in Caenorhabditis elegans (C. elegans). The system is based on our transgenic AD model strain (GRU102) that expresses a pathogenic human amyloid-beta peptide (Aβ1-42) specifically in neurons and we use this approach to identify Metformin, Lithium and Curcumin as potential “hits”. We find that the ability to rescue the swim-exhaustion phenotype correlates well with lifespan and healthspan improvements in GRU102. Importantly, several other drugs, such as Thioflavin T that have been reported previously to extend lifespan, modify aspects of ageing or for which protective effects in AD model might be suspected did not rescue the swim performance nor lifespan of GRU102. This illustrates the predictive value of the screening assay and confirms that not all compounds targeting ageing are capable of compensating for the toxic effects of Aβ1-42 in GRU102. Together, these findings demonstrate the utility of our screen towards the Aβ-induced defects in GRU102.</div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"4 ","pages":"Pages 11-21"},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tma.2019.12.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55175703","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}

引用次数: 5

Automation of C. elegans lifespan measurement. 秀丽隐杆线虫寿命测量自动化。

Translational Medicine of Aging Pub Date : 2020-01-01 Epub Date: 2019-12-07

Daniel P Felker, Christine E Robbins, Mark A McCormick

{"title":"Automation of C. elegans lifespan measurement.","authors":"Daniel P Felker, Christine E Robbins, Mark A McCormick","doi":"","DOIUrl":"","url":null,"abstract":"Aging is a fundamental biological process that is still not fully understood. As many of the most significant human diseases have aging as their greatest risk factor, a better understanding of aging potentially has enormous practical implications in treating these diseases. The nematode C. elegans is an exceptionally useful genetic model organism that had been used with great success to shed light on many genes and pathways that are involved in aging. Many of these pathways and mechanisms have been shown to be conserved through mammals. The standard methods for assaying survival in C. elegans to measure changes in lifespan are tedious and time consuming. This limits the throughput and productivity of C. elegans aging researchers. In recent years, many inroads have been made into automating various facets of the collection and analysis of C. elegans lifespan experimental data. The advances described in this review all work to ameliorate some of the hurdles that come with manual worm lifespan scoring, by automating or eliminating some of the most time consuming aspects of the assay. By greatly increasing the throughput of lifespan assays, these methods will enable types of experiments (e.g., drug library screens) whose scale is currently impractical. These methods have already proved exceptionally useful, and some of them are likely to be the predecessors of even more refined methods that could lead to breakthroughs in the ability to study lifespan in C. elegans. This could in turn potentially revolutionize our understanding of the basic biology of aging, and one day lead to treatments that could offset or delay age-related diseases in humans.","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"4 ","pages":"1-10"},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7597742/pdf/nihms-1619620.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38556341","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}

引用次数: 0

Nanocarriers targeting senescent cells 靶向衰老细胞的纳米载体

Translational Medicine of Aging Pub Date : 2019-01-01 DOI: 10.1016/j.tma.2019.01.001

Daniel Muñoz-Espín

引用次数: 15