Volume 9, Issue 7

Lieberman R, You M, . Corrupting the DNA damage response: a critical role for Rad52 in tumor cell survival. . 9:1647-1659. https://doi.org/10.18632/aging.101263

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                TY  - JOUR
                AU  - Lieberman, Rachel 
                AU  - You, Ming 
                TI  - Corrupting the DNA damage response: a critical role for Rad52 in tumor cell survival
                JO  - 
                JA  - 
                VL  - 9
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101263
                DO  - 10.18632/aging.101263
                SP  - 1647
                EP  - 1659
                PY  - 
                AB  - The DNA damage response enables cells to survive, maintain genome integrity, and to safeguard the transmission of high-fidelity genetic information. Upon sensing DNA damage, cells respond by activating this multi-faceted DNA damage response leading to restoration of the cell, senescence, programmed cell death, or genomic instability if the cell survives without proper repair. However, unlike normal cells, cancer cells maintain a marked level of genomic instability. Because of this enhanced propensity to accumulate DNA damage, tumor cells rely on homologous recombination repair as a means of protection from the lethal effect of both spontaneous and therapy-induced double-strand breaks (DSBs) in DNA. Thus, modulation of DNA repair pathways have important consequences for genomic instability within tumor cell biology and viability maintenance under high genotoxic stress. Efforts are underway to manipulate specific components of the DNA damage response in order to selectively induce tumor cell death by augmenting genomic instability past a viable threshold. New evidence suggests that RAD52, a component of the homologous recombination pathway, is important for the maintenance of tumor genome integrity. This review highlights recent reports indicating that reducing homologous recombination through inhibition of RAD52 may represent an important focus for cancer therapy and the specific efforts that are already demonstrating potential.
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Chemo brain or tumor brain - that is the question: the presence of extracranial tumors profoundly affects molecular processes in the prefrontal cortex of TumorGraft mice

Anna Kovalchuk, Yaroslav Ilnytskyy, Rocio Rodriguez-Juarez, Svitlana Shpyleva, Stepan Melnyk, Igor Pogribny, Amanda Katz, David Sidransky, Olga Kovalchuk, Bryan Kolb,

https://doi.org/10.18632/aging.101243 pp 1660—1676

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Kovalchuk A, Ilnytskyy Y, Rodriguez-Juarez R, Shpyleva S, Melnyk S, Pogribny I, Katz A, Sidransky D, Kovalchuk O, Kolb B, . Chemo brain or tumor brain - that is the question: the presence of extracranial tumors profoundly affects molecular processes in the prefrontal cortex of TumorGraft mice. . 9:1660-1676. https://doi.org/10.18632/aging.101243

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                TY  - JOUR
                AU  - Kovalchuk, Anna 
                AU  - Ilnytskyy, Yaroslav 
                AU  - Rodriguez-Juarez, Rocio 
                AU  - Shpyleva, Svitlana 
                AU  - Melnyk, Stepan 
                AU  - Pogribny, Igor 
                AU  - Katz, Amanda 
                AU  - Sidransky, David 
                AU  - Kovalchuk, Olga 
                AU  - Kolb, Bryan 
                TI  - Chemo brain or tumor brain - that is the question: the presence of extracranial tumors profoundly affects molecular processes in the prefrontal cortex of TumorGraft mice
                JO  - 
                JA  - 
                VL  - 9
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101243
                DO  - 10.18632/aging.101243
                SP  - 1660
                EP  - 1676
                PY  - 
                AB  - Cancer chemotherapy causes numerous persistent central nervous system complications. This condition is known as chemo brain. Cognitive impairments occur even before treatment, and hence are referred to as cancer associated cognitive changes, or tumor brain. There is much yet to be learned about the mechanisms of both chemo brain and tumor brain. The frequency and timing of chemo brain and tumor brain occurrence and persistence strongly suggest they may be epigenetic in nature and associated with altered gene expression. Here we used TumorGraftTM models wherein part of a patient’s tumor is removed and grafted into immune-deficient mice and conducted global gene expression and DNA methylation analysis. We show that malignant non-central nervous system tumor growth causes profound molecular alterations in the brain. Mice harbouring triple negative or progesterone positive breast cancer TumorGrafts exhibited altered gene expression, decreased levels of DNA methylation, increased levels of DNA hydroxymethylation, and oxidative stress in the prefrontal cortex. Interestingly, chemotherapy did not have any additional synergistic effects on the analyzed processes. The molecular changes observed in this study are known signs of neurodegeneration and brain aging. This study provides an important roadmap for future large-scale analysis of the molecular and cellular mechanisms of tumor brain.
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The Golgi-localized, gamma ear-containing, ARF-binding (GGA) protein family alters alpha synuclein (α-syn) oligomerization and secretion

Bjoern von Einem, Judith Eschbach, Martin Kiechle, Anke Wahler, Dietmar R. Thal, Pamela J. McLean, Jochen H. Weishaupt, Albert C. Ludolph, Christine A.F. von Arnim, Karin M. Danzer,

https://doi.org/10.18632/aging.101261 pp 1677—1697

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von Einem B, Eschbach J, Kiechle M, Wahler A, Thal DR, McLean PJ, Weishaupt JH, Ludolph AC, von Arnim CA, Danzer KM, . The Golgi-localized, gamma ear-containing, ARF-binding (GGA) protein family alters alpha synuclein (α-syn) oligomerization and secretion. . 9:1677-1697. https://doi.org/10.18632/aging.101261

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                TY  - JOUR
                AU  - von Einem, Bjoern 
                AU  - Eschbach, Judith 
                AU  - Kiechle, Martin 
                AU  - Wahler, Anke 
                AU  - Thal, Dietmar R. 
                AU  - McLean, Pamela J. 
                AU  - Weishaupt, Jochen H. 
                AU  - Ludolph, Albert C. 
                AU  - von Arnim, Christine A.F. 
                AU  - Danzer, Karin M. 
                TI  - The Golgi-localized, gamma ear-containing, ARF-binding (GGA) protein family alters alpha synuclein (α-syn) oligomerization and secretion
                JO  - 
                JA  - 
                VL  - 9
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101261
                DO  - 10.18632/aging.101261
                SP  - 1677
                EP  - 1697
                PY  - 
                AB  - Several age-related neurodegenerative disorders are associated with protein misfolding and aggregation of toxic peptides. α-synuclein (α-syn) aggregation and the resulting cytotoxicity is a hallmark of Parkinson’s disease (PD) as well as dementia with Lewy bodies. Rising evidence points to oligomeric and pre-fibrillar forms as the pathogenic species, and oligomer secretion seems to be crucial for the spreading and progression of PD pathology. Recent studies implicate that dysfunctions in endolysosomal/autophagosomal pathways increase α-syn secretion. Mutation in the retromer-complex protein VPS35, which is involved in endosome to Golgi transport, was suggested to cause familial PD. GGA proteins regulate vesicular traffic between Golgi and endosomes and might work as antagonists for retromer complex mediated transport. To investigate the role of the GGAs in the α-syn oligomerization and/or secretion process we utilized protein-fragment complementation assays (PCA). We here demonstrate that GGAs alter α-syn oligomer secretion and α-syn oligomer-mediated toxicity. Specifically, we determined that GGA3 modifies extracellular α-syn species in an exosome-independent manner. Our data suggest that GGA3 drives α-syn oligomerization in endosomal compartments and thus facilitates α-syn oligomer secretion. Preventing the early events in α-syn oligomer release may be a novel approach to halt disease spreading in PD and other synucleinopathies.
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Aging and sarcopenia associate with specific interactions between gut microbes, serum biomarkers and host physiology in rats

Jay Siddharth, Anirikh Chakrabarti, Alice Pannérec, Sonia Karaz, Delphine Morin-Rivron, Mojgan Masoodi, Jerome N. Feige, Scott James Parkinson,

https://doi.org/10.18632/aging.101262 pp 1698—1720

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Siddharth J, Chakrabarti A, Pannérec A, Karaz S, Morin-Rivron D, Masoodi M, Feige JN, Parkinson SJ, . Aging and sarcopenia associate with specific interactions between gut microbes, serum biomarkers and host physiology in rats. . 9:1698-1720. https://doi.org/10.18632/aging.101262

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                TY  - JOUR
                AU  - Siddharth, Jay 
                AU  - Chakrabarti, Anirikh 
                AU  - Pannérec, Alice 
                AU  - Karaz, Sonia 
                AU  - Morin-Rivron, Delphine 
                AU  - Masoodi, Mojgan 
                AU  - Feige, Jerome N. 
                AU  - Parkinson, Scott James 
                TI  - Aging and sarcopenia associate with specific interactions between gut microbes, serum biomarkers and host physiology in rats
                JO  - 
                JA  - 
                VL  - 9
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101262
                DO  - 10.18632/aging.101262
                SP  - 1698
                EP  - 1720
                PY  - 
                AB  - The microbiome has been demonstrated to play an integral role in the maintenance of many aspects of health that are also associated with aging. In order to identify areas of potential exploration and intervention, we simultaneously characterized age-related alterations in gut microbiome, muscle physiology and serum proteomic and lipidomic profiles in aged rats to define an integrated signature of the aging phenotype. We demonstrate that aging skews the composition of the gut microbiome, in particular by altering the Sutterella to Barneseilla ratio, and alters the metabolic potential of intestinal bacteria. Age-related changes of the gut microbiome were associated with the physiological decline of musculoskeletal function, and with molecular markers of nutrient processing/availability, and inflammatory/immune status in aged versus adult rats. Altogether, our study highlights that aging leads to a complex interplay between the microbiome and host physiology, and provides candidate microbial species to target physical and metabolic decline during aging by modulating gut microbial ecology.
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Machine learning for predicting lifespan-extending chemical compounds

Diogo G. Barardo, Danielle Newby, Daniel Thornton, Taravat Ghafourian, João Pedro de Magalhães, Alex A. Freitas,

https://doi.org/10.18632/aging.101264 pp 1721—1737

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Barardo DG, Newby D, Thornton D, Ghafourian T, Pedro de Magalhães J, Freitas AA, . Machine learning for predicting lifespan-extending chemical compounds. . 9:1721-1737. https://doi.org/10.18632/aging.101264

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                TY  - JOUR
                AU  - Barardo, Diogo G. 
                AU  - Newby, Danielle 
                AU  - Thornton, Daniel 
                AU  - Ghafourian, Taravat 
                AU  - Pedro de Magalhães, João 
                AU  - Freitas, Alex A. 
                TI  - Machine learning for predicting lifespan-extending chemical compounds
                JO  - 
                JA  - 
                VL  - 9
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101264
                DO  - 10.18632/aging.101264
                SP  - 1721
                EP  - 1737
                PY  - 
                AB  - Increasing age is a risk factor for many diseases; therefore developing pharmacological interventions that slow down ageing and consequently postpone the onset of many age-related diseases is highly desirable. In this work we analyse data from the DrugAge database, which contains chemical compounds and their effect on the lifespan of model organisms. Predictive models were built using the machine learning method random forests to predict whether or not a chemical compound will increase Caenorhabditis elegans’ lifespan, using as features Gene Ontology (GO) terms annotated for proteins targeted by the compounds and chemical descriptors calculated from each compound’s chemical structure. The model with the best predictive accuracy used both biological and chemical features, achieving a prediction accuracy of 80%. The top 20 most important GO terms include those related to mitochondrial processes, to enzymatic and immunological processes, and terms related to metabolic and transport processes. We applied our best model to predict compounds which are more likely to increase C. elegans’ lifespan in the DGIdb database, where the effect of the compounds on an organism’s lifespan is unknown. The top hit compounds can be broadly divided into four groups: compounds affecting mitochondria, compounds for cancer treatment, anti-inflammatories, and compounds for gonadotropin-releasing hormone therapies.
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Werner syndrome: a model for sarcopenia due to accelerated aging

Masaya Yamaga, Minoru Takemoto, Mayumi Shoji, Kenichi Sakamoto, Masashi Yamamoto, Takahiro Ishikawa, Masaya Koshizaka, Yoshiro Maezawa, Kazuki Kobayashi, Koutaro Yokote,

https://doi.org/10.18632/aging.101265 pp 1738—1744

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Yamaga M, Takemoto M, Shoji M, Sakamoto K, Yamamoto M, Ishikawa T, Koshizaka M, Maezawa Y, Kobayashi K, Yokote K, . Werner syndrome: a model for sarcopenia due to accelerated aging. . 9:1738-1744. https://doi.org/10.18632/aging.101265

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                TY  - JOUR
                AU  - Yamaga, Masaya 
                AU  - Takemoto, Minoru 
                AU  - Shoji, Mayumi 
                AU  - Sakamoto, Kenichi 
                AU  - Yamamoto, Masashi 
                AU  - Ishikawa, Takahiro 
                AU  - Koshizaka, Masaya 
                AU  - Maezawa, Yoshiro 
                AU  - Kobayashi, Kazuki 
                AU  - Yokote, Koutaro 
                TI  - Werner syndrome: a model for sarcopenia due to accelerated aging
                JO  - 
                JA  - 
                VL  - 9
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101265
                DO  - 10.18632/aging.101265
                SP  - 1738
                EP  - 1744
                PY  - 
                AB  - Werner syndrome (WS) is a rare inheritable progeroid syndrome caused by a mutation in the WRN gene. Although WS has been described as a characteristic appearance of very slender extremities with a stocky trunk, few studies have investigated the loss of muscle mass, fat mass distribution (body composition), and mobility according to age and sex. Therefore, the aim of this study was to precisely describe the body composition in WS. Nine Japanese patients with WS (four males and five females; mean age 48±8.8 years) were recruited. Body composition was examined by dual-energy X-ray absorptiometry and computed tomography (CT). The hand grip strength and mobility were evaluated using the two-step test, stand-up test and 25-question geriatric locomotive function scale (GLFS). The mean skeletal muscle index (SMI) was 4.0±0.6 kg/m2. SMI of all patients met the criteria of sarcopenia, even though some patients were aged &lt; 40 years. All patients also showed deceased mobility. In conclusion, these results indicate that all patients with WS, even those aged &lt; 40 years, had already lost muscle mass to the level of sarcopenia. Continued research on sarcopenia in WS might facilitate the discovery of novel mechanisms and development of new treatment strategies for sarcopenia.
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HIF-1–dependent regulation of lifespan in Caenorhabditis elegans by the acyl-CoA–binding protein MAA-1

Mehrnaz Shamalnasab, Manel Dhaoui, Manjunatha Thondamal, Eva Bang Harvald, Nils J. Færgeman, Hugo Aguilaniu, Paola Fabrizio,

https://doi.org/10.18632/aging.101267 pp 1745—1769

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Shamalnasab M, Dhaoui M, Thondamal M, Harvald EB, Færgeman NJ, Aguilaniu H, Fabrizio P, . HIF-1–dependent regulation of lifespan in Caenorhabditis elegans by the acyl-CoA–binding protein MAA-1. . 9:1745-1769. https://doi.org/10.18632/aging.101267

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 TY - JOUR
 AU - Shamalnasab, Mehrnaz 
 AU - Dhaoui, Manel 
 AU - Thondamal, Manjunatha 
 AU - Harvald, Eva Bang 
 AU - Færgeman, Nils J. 
 AU - Aguilaniu, Hugo 
 AU - Fabrizio, Paola 
 TI - HIF-1–dependent regulation of lifespan in Caenorhabditis elegans by the acyl-CoA–binding protein MAA-1
 JO - 
 JA - 
 VL - 9
 IS - 7
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101267
 DO - 10.18632/aging.101267
 SP - 1745
 EP - 1769
 PY - 
 AB - In yeast, the broadly conserved acyl-CoA–binding protein (ACBP) is a negative regulator of stress resistance and longevity. Here, we have turned to the nematode C. elegans as a model organism in which to determine whether ACBPs play similar roles in multicellular organisms. We systematically inactivated each of the seven C. elegans ACBP paralogs and found that one of them, maa-1 (which encodes membrane-associated ACBP 1), is indeed involved in the regulation of longevity. In fact, loss of maa-1 promotes lifespan extension and resistance to different types of stress. Through genetic and gene expression studies we have demonstrated that HIF-1, a master transcriptional regulator of adaptation to hypoxia, plays a central role in orchestrating the anti-aging response induced by MAA-1 deficiency. This response relies on the activation of molecular chaperones known to contribute to maintenance of the proteome. Our work extends to C. elegans the role of ACBP in aging, implicates HIF-1 in the increase of lifespan of maa-1–deficient worms, and sheds light on the anti-aging function of HIF-1. Given that both ACBP and HIF-1 are highly conserved, our results suggest the possible involvement of these proteins in the age-associated decline in proteostasis in mammals.
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The effects of graded levels of calorie restriction: XI. Evaluation of the main hypotheses underpinning the life extension effects of CR using the hepatic transcriptome

Davina Derous, Sharon E. Mitchell, Lu Wang, Cara L. Green, Yingchun Wang, Luonan Chen, Jing-Dong J. Han, Daniel E.L. Promislow, David Lusseau, Alex Douglas, John R. Speakman,

https://doi.org/10.18632/aging.101269 pp 1770—1824

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Derous D, Mitchell SE, Wang L, Green CL, Wang Y, Chen L, Han JJ, Promislow DE, Lusseau D, Douglas A, Speakman JR, . The effects of graded levels of calorie restriction: XI. Evaluation of the main hypotheses underpinning the life extension effects of CR using the hepatic transcriptome. . 9:1770-1824. https://doi.org/10.18632/aging.101269

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                TY  - JOUR
                AU  - Derous, Davina 
                AU  - Mitchell, Sharon E. 
                AU  - Wang, Lu 
                AU  - Green, Cara L. 
                AU  - Wang, Yingchun 
                AU  - Chen, Luonan 
                AU  - Han, Jing-Dong J. 
                AU  - Promislow, Daniel E.L. 
                AU  - Lusseau, David 
                AU  - Douglas, Alex 
                AU  - Speakman, John R. 
                TI  - The effects of graded levels of calorie restriction: XI. Evaluation of the main hypotheses underpinning the life extension effects of CR using the hepatic transcriptome
                JO  - 
                JA  - 
                VL  - 9
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101269
                DO  - 10.18632/aging.101269
                SP  - 1770
                EP  - 1824
                PY  - 
                AB  - Calorie restriction (CR) may extend longevity by modulating the mechanisms involved in aging. Different hypotheses have been proposed for its main mode of action. We quantified hepatic transcripts of male C57BL/6 mice exposed to graded levels of CR (0% to 40% CR) for three months, and evaluated the responses relative to these various hypotheses. Of the four main signaling pathways implied to be linked to the impact of CR on lifespan (insulin/insulin like growth factor 1 (IGF-1), nuclear factor-kappa beta (NF-ĸB), mechanistic target of rapamycin (mTOR) and sirtuins (SIRTs)), all the pathways except SIRT were altered in a manner consistent with increased lifespan. However, the expression levels of SIRT4 and SIRT7 were decreased with increasing levels of CR. Changes consistent with altered fuel utilization under CR may reduce reactive oxygen species production, which was paralleled by reduced protection. Downregulated major urinary protein (MUP) transcription suggested reduced reproductive investment. Graded CR had a positive effect on autophagy and xenobiotic metabolism, and was protective with respect to cancer signaling. CR had no significant effect on fibroblast growth factor-21 (FGF21) transcription but affected transcription in the hydrogen sulfide production pathway. Responses to CR were consistent with several different hypotheses, and the benefits of CR on lifespan likely reflect the combined impact on multiple aging related processes.
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Aging and calorie restriction regulate the expression of miR-125a-5p and its target genes Stat3, Casp2 and Stard13

Kuldeep Makwana, Sonal Arvind Patel, Nikkhil Velingkaar, Jey Sabith Ebron, Girish C. Shukla, Roman V. Kondratov,

https://doi.org/10.18632/aging.101270 pp 1825—1843

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Makwana K, Patel SA, Velingkaar N, Ebron JS, Shukla GC, Kondratov RV, . Aging and calorie restriction regulate the expression of miR-125a-5p and its target genes Stat3, Casp2 and Stard13. . 9:1825-1843. https://doi.org/10.18632/aging.101270

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Provider: 
 TY - JOUR
 AU - Makwana, Kuldeep 
 AU - Patel, Sonal Arvind 
 AU - Velingkaar, Nikkhil 
 AU - Ebron, Jey Sabith 
 AU - Shukla, Girish C. 
 AU - Kondratov, Roman V. 
 TI - Aging and calorie restriction regulate the expression of miR-125a-5p and its target genes Stat3, Casp2 and Stard13
 JO - 
 JA - 
 VL - 9
 IS - 7
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101270
 DO - 10.18632/aging.101270
 SP - 1825
 EP - 1843
 PY - 
 AB - Calorie restriction (CR) is a dietary intervention known to delay aging. In order, to understand molecular mechanisms of CR, we analyzed the expression of 983 MicroRNAs (miRNAs) in the liver of female mice after 2 years of 30% CR using micro-array. 16 miRNAs demonstrated significant changes in their expression upon CR in comparison with age-matched control. mmu-miR-125a-5p (miR-125a-5p) was significantly upregulated upon CR, and in agreement with this, the expression of mRNAs for its three predicted target genes: Stat3, Casp2, and Stard13 was significantly downregulated in the liver of CR animals. The expression of precursor miRNA for miR-125a-5p was also upregulated upon CR, which suggests its regulation at the level of transcription. Upon aging miR-125a-5p expression was downregulated while the expression of its target genes was upregulated. Thus, CR prevented age-associated changes in the expression of miR-125a-5p and its targets. We propose that miR-125a-5p dependent downregulation of Stat3, Casp2, and Stard13 contributes to the calorie restriction-mediated delay of aging.
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Correction: The complex genetics of gait speed: genome-wide meta-analysis approach

Dan Ben-Avraham, David Karasik, Joe Verghese, Kathryn L. Lunetta, Jennifer A. Smith, John D. Eicher, Rotem Vered, Joris Deelen, Alice M. Arnold, Aron S. Buchman, Toshiko Tanaka, Jessica D. Faul, Maria Nethander, Myriam Fornage, Hieab H. Adams, Amy M. Matteini, Michele L. Callisaya, Albert V. Smith, Lei Yu, Philip L. De Jager, Denis A. Evans, Vilmundur Gudnason, Albert Hofman, Alison Pattie, Janie Corley, Lenore J. Launer, Davis S. Knopman, Neeta Parimi, Stephen T. Turner, Stefania Bandinelli, Marian Beekman, Danielle Gutman, Lital Sharvit, Simon P. Mooijaart, David C. Liewald, Jeanine J. Houwing-Duistermaat, Claes Ohlsson, Matthijs Moed, Vincent J. Verlinden, Dan Mellström, Jos N. van der Geest, Magnus Karlsson, Dena Hernandez, Rebekah McWhirter, Yongmei Liu, Russell Thomson, Gregory J. Tranah, Andre G. Uitterlinden, David R. Weir, Wei Zhao, John M. Starr, Andrew D. Johnson, M. Arfan Ikram, David A. Bennett, Steven R. Cummings, Ian J. Deary, Tamara B. Harris, Sharon L. R. Kardia, Thomas H. Mosley, Velandai K. Srikanth, Beverly G. Windham, Ann B. Newman, Jeremy D. Walston, Gail Davies, Daniel S. Evans, Eline P. Slagboom, Luigi Ferrucci, Douglas P. Kiel, Joanne M. Murabito, Gil Atzmon,

https://doi.org/10.18632/aging.101260 pp 1844—1846

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Ben-Avraham D, Karasik D, Verghese J, Lunetta KL, Smith JA, Eicher JD, Vered R, Deelen J, Arnold AM, Buchman AS, Tanaka T, Faul JD, Nethander M, et al, . Correction: The complex genetics of gait speed: genome-wide meta-analysis approach. . 9:1844-1846. https://doi.org/10.18632/aging.101260

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                TY  - JOUR
                AU  - Ben-Avraham, Dan 
                AU  - Karasik, David 
                AU  - Verghese, Joe 
                AU  - Lunetta, Kathryn L. 
                AU  - Smith, Jennifer A. 
                AU  - Eicher, John D. 
                AU  - Vered, Rotem 
                AU  - Deelen, Joris 
                AU  - Arnold, Alice M. 
                AU  - Buchman, Aron S. 
                AU  - Tanaka, Toshiko 
                AU  - Faul, Jessica D. 
                AU  - Nethander, Maria 
                AU  - Fornage, Myriam 
                AU  - Adams, Hieab H. 
                AU  - Matteini, Amy M. 
                AU  - Callisaya, Michele L. 
                AU  - Smith, Albert V. 
                AU  - Yu, Lei 
                AU  - De Jager, Philip L. 
                AU  - Evans, Denis A. 
                AU  - Gudnason, Vilmundur 
                AU  - Hofman, Albert 
                AU  - Pattie, Alison 
                AU  - Corley, Janie 
                AU  - Launer, Lenore J. 
                AU  - Knopman, Davis S. 
                AU  - Parimi, Neeta 
                AU  - Turner, Stephen T. 
                AU  - Bandinelli, Stefania 
                AU  - Beekman, Marian 
                AU  - Gutman, Danielle 
                AU  - Sharvit, Lital 
                AU  - Mooijaart, Simon P. 
                AU  - Liewald, David C. 
                AU  - Houwing-Duistermaat, Jeanine J. 
                AU  - Ohlsson, Claes 
                AU  - Moed, Matthijs 
                AU  - Verlinden, Vincent J. 
                AU  - Mellström, Dan 
                AU  - van der Geest, Jos N. 
                AU  - Karlsson, Magnus 
                AU  - Hernandez, Dena 
                AU  - McWhirter, Rebekah 
                AU  - Liu, Yongmei 
                AU  - Thomson, Russell 
                AU  - Tranah, Gregory J. 
                AU  - Uitterlinden, Andre G. 
                AU  - Weir, David R. 
                AU  - Zhao, Wei 
                AU  - Starr, John M. 
                AU  - Johnson, Andrew D. 
                AU  - Ikram, M. Arfan 
                AU  - Bennett, David A. 
                AU  - Cummings, Steven R. 
                AU  - Deary, Ian J. 
                AU  - Harris, Tamara B. 
                AU  - Kardia, Sharon L. R. 
                AU  - Mosley, Thomas H. 
                AU  - Srikanth, Velandai K. 
                AU  - Windham, Beverly G. 
                AU  - Newman, Ann B. 
                AU  - Walston, Jeremy D. 
                AU  - Davies, Gail 
                AU  - Evans, Daniel S. 
                AU  - Slagboom, Eline P. 
                AU  - Ferrucci, Luigi 
                AU  - Kiel, Douglas P. 
                AU  - Murabito, Joanne M. 
                AU  - Atzmon, Gil 
                TI  - Correction: The complex genetics of gait speed: genome-wide meta-analysis approach
                JO  - 
                JA  - 
                VL  - 9
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101260
                DO  - 10.18632/aging.101260
                SP  - 1844
                EP  - 1846
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Ben-Avraham, Dan 
                AU  - Karasik, David 
                AU  - Verghese, Joe 
                AU  - Lunetta, Kathryn L. 
                AU  - Smith, Jennifer A. 
                AU  - Eicher, John D. 
                AU  - Vered, Rotem 
                AU  - Deelen, Joris 
                AU  - Arnold, Alice M. 
                AU  - Buchman, Aron S. 
                AU  - Tanaka, Toshiko 
                AU  - Faul, Jessica D. 
                AU  - Nethander, Maria 
                AU  - Fornage, Myriam 
                AU  - Adams, Hieab H. 
                AU  - Matteini, Amy M. 
                AU  - Callisaya, Michele L. 
                AU  - Smith, Albert V. 
                AU  - Yu, Lei 
                AU  - De Jager, Philip L. 
                AU  - Evans, Denis A. 
                AU  - Gudnason, Vilmundur 
                AU  - Hofman, Albert 
                AU  - Pattie, Alison 
                AU  - Corley, Janie 
                AU  - Launer, Lenore J. 
                AU  - Knopman, Davis S. 
                AU  - Parimi, Neeta 
                AU  - Turner, Stephen T. 
                AU  - Bandinelli, Stefania 
                AU  - Beekman, Marian 
                AU  - Gutman, Danielle 
                AU  - Sharvit, Lital 
                AU  - Mooijaart, Simon P. 
                AU  - Liewald, David C. 
                AU  - Houwing-Duistermaat, Jeanine J. 
                AU  - Ohlsson, Claes 
                AU  - Moed, Matthijs 
                AU  - Verlinden, Vincent J. 
                AU  - Mellström, Dan 
                AU  - van der Geest, Jos N. 
                AU  - Karlsson, Magnus 
                AU  - Hernandez, Dena 
                AU  - McWhirter, Rebekah 
                AU  - Liu, Yongmei 
                AU  - Thomson, Russell 
                AU  - Tranah, Gregory J. 
                AU  - Uitterlinden, Andre G. 
                AU  - Weir, David R. 
                AU  - Zhao, Wei 
                AU  - Starr, John M. 
                AU  - Johnson, Andrew D. 
                AU  - Ikram, M. Arfan 
                AU  - Bennett, David A. 
                AU  - Cummings, Steven R. 
                AU  - Deary, Ian J. 
                AU  - Harris, Tamara B. 
                AU  - Kardia, Sharon L. R. 
                AU  - Mosley, Thomas H. 
                AU  - Srikanth, Velandai K. 
                AU  - Windham, Beverly G. 
                AU  - Newman, Ann B. 
                AU  - Walston, Jeremy D. 
                AU  - Davies, Gail 
                AU  - Evans, Daniel S. 
                AU  - Slagboom, Eline P. 
                AU  - Ferrucci, Luigi 
                AU  - Kiel, Douglas P. 
                AU  - Murabito, Joanne M. 
                AU  - Atzmon, Gil 
                TI  - Correction: The complex genetics of gait speed: genome-wide meta-analysis approach
                JO  - 
                JA  - 
                VL  - 9
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101260
                DO  - 10.18632/aging.101260
                SP  - 1844
                EP  - 1846
                PY  - 
                AB  - 
                ER  -

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Volume 9, Issue 7

About the Cover

Editorials

Amino acid metabolites, mTORC1 and aging

Henri Antikainen, Khoosheh Khayati, Radek Dobrowolski,

Synergistic SNGI-TKI combination against LSCs

Xiaoyan Jiang,

Enhancing ER stress in myeloma

Craig T. Wallington-Beddoe, Stuart M. Pitson,

Review

Corrupting the DNA damage response: a critical role for Rad52 in tumor cell survival

Rachel Lieberman, Ming You,

Research Papers

Chemo brain or tumor brain - that is the question: the presence of extracranial tumors profoundly affects molecular processes in the prefrontal cortex of TumorGraft mice

Anna Kovalchuk, Yaroslav Ilnytskyy, Rocio Rodriguez-Juarez, Svitlana Shpyleva, Stepan Melnyk, Igor Pogribny, Amanda Katz, David Sidransky, Olga Kovalchuk, Bryan Kolb,

The Golgi-localized, gamma ear-containing, ARF-binding (GGA) protein family alters alpha synuclein (α-syn) oligomerization and secretion

Bjoern von Einem, Judith Eschbach, Martin Kiechle, Anke Wahler, Dietmar R. Thal, Pamela J. McLean, Jochen H. Weishaupt, Albert C. Ludolph, Christine A.F. von Arnim, Karin M. Danzer,

Aging and sarcopenia associate with specific interactions between gut microbes, serum biomarkers and host physiology in rats

Jay Siddharth, Anirikh Chakrabarti, Alice Pannérec, Sonia Karaz, Delphine Morin-Rivron, Mojgan Masoodi, Jerome N. Feige, Scott James Parkinson,

Machine learning for predicting lifespan-extending chemical compounds

Diogo G. Barardo, Danielle Newby, Daniel Thornton, Taravat Ghafourian, João Pedro de Magalhães, Alex A. Freitas,

Werner syndrome: a model for sarcopenia due to accelerated aging

Masaya Yamaga, Minoru Takemoto, Mayumi Shoji, Kenichi Sakamoto, Masashi Yamamoto, Takahiro Ishikawa, Masaya Koshizaka, Yoshiro Maezawa, Kazuki Kobayashi, Koutaro Yokote,

HIF-1–dependent regulation of lifespan in Caenorhabditis elegans by the acyl-CoA–binding protein MAA-1

Mehrnaz Shamalnasab, Manel Dhaoui, Manjunatha Thondamal, Eva Bang Harvald, Nils J. Færgeman, Hugo Aguilaniu, Paola Fabrizio,

The effects of graded levels of calorie restriction: XI. Evaluation of the main hypotheses underpinning the life extension effects of CR using the hepatic transcriptome

Davina Derous, Sharon E. Mitchell, Lu Wang, Cara L. Green, Yingchun Wang, Luonan Chen, Jing-Dong J. Han, Daniel E.L. Promislow, David Lusseau, Alex Douglas, John R. Speakman,

Aging and calorie restriction regulate the expression of miR-125a-5p and its target genes Stat3, Casp2 and Stard13

Kuldeep Makwana, Sonal Arvind Patel, Nikkhil Velingkaar, Jey Sabith Ebron, Girish C. Shukla, Roman V. Kondratov,

Correction

Correction: The complex genetics of gait speed: genome-wide meta-analysis approach

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