Volume 8, Issue 9

Hasegawa T, Ukai W, . Targeting therapy for homocysteic acid in the blood represents a potential recovery treatment for cognition in Alzheimer’s disease patients. . 8:1838-1843. https://doi.org/10.18632/aging.101046

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                TY  - JOUR
                AU  - Hasegawa, Tohru 
                AU  - Ukai, Wataru 
                TI  - Targeting therapy for homocysteic acid in the blood represents a potential recovery treatment for cognition in Alzheimer’s disease patients
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101046
                DO  - 10.18632/aging.101046
                SP  - 1838
                EP  - 1843
                PY  - 
                AB  - At present, we have no reliable means of recovering cognitive impairment in Alzheimer’s disease (AD) patients. We hypothesized that homocysteic acid (HA) in the blood might represent one such pathogen that could be excreted into the urine. Since DHA is known to reduce circulating levels of homocysteine, and since exercise attenuates this effect, it follows that supplementation of the diet with DHA, along with increased levels of physical activity, may help to reduce cognitive impairment in AD patients. Our hypothesis was proven to be correct because memory problems in 3xTg- AD mice (a model for AD in which animals develop amyloid pathology), and in a mouse model of familial AD, were recovered following treatment with an anti-HA antibody and not by amyloid treatment. Interestingly, 3xTg-AD mice with amyloid pathology showed increased levels of HA level. This could perhaps be explained by the fact that amyloid precursor protein and/or presenilin increases calcium influx, which could then increase levels of superoxide and consequently increase levels of HA from homocysteine or methionine. Our hypothesis is also partially supported by an open clinical trial of certain dietary supplements that has shown impressive results. Also there are other treatments hypothesis which would be possible for the effective therapies, such as ribonucleoprotein therapy, a β-secretase inhibitor treatment and the metabolic enhancement treatment.
                ER  -

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DNA methylation-based measures of biological age: meta-analysis predicting time to death

Brian H. Chen, Riccardo E. Marioni, Elena Colicino, Marjolein J. Peters, Cavin K. Ward-Caviness, Pei-Chien Tsai, Nicholas S. Roetker, Allan C. Just, Ellen W. Demerath, Weihua Guan, Jan Bressler, Myriam Fornage, Stephanie Studenski, Amy R. Vandiver, Ann Zenobia Moore, Toshiko Tanaka, Douglas P. Kiel, Liming Liang, Pantel Vokonas, Joel Schwartz, Kathryn L. Lunetta, Joanne M. Murabito, Stefania Bandinelli, Dena G. Hernandez, David Melzer, Michael Nalls, Luke C. Pilling, Timothy R. Price, Andrew B. Singleton, Christian Gieger, Rolf Holle, Anja Kretschmer, Florian Kronenberg, Sonja Kunze, Jakob Linseisen, Christine Meisinger, Wolfgang Rathmann, Melanie Waldenberger, Peter M. Visscher, Sonia Shah, Naomi R. Wray, Allan F. McRae, Oscar H. Franco, Albert Hofman, André G. Uitterlinden, Devin Absher, Themistocles Assimes, Morgan E. Levine, Ake T. Lu, Philip S. Tsao, Lifang Hou, JoAnn E. Manson, Cara L. Carty, Andrea Z. LaCroix, Alexander P. Reiner, Tim D. Spector, Andrew P. Feinberg, Daniel Levy, Andrea Baccarelli, Joyce van Meurs, Jordana T. Bell, Annette Peters, Ian J. Deary, James S. Pankow, Luigi Ferrucci, Steve Horvath,

https://doi.org/10.18632/aging.101020 pp 1844—1865

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Chen BH, Marioni RE, Colicino E, Peters MJ, Ward-Caviness CK, Tsai P, Roetker NS, Just AC, Demerath EW, Guan W, Bressler J, Fornage M, Studenski S, et al, . DNA methylation-based measures of biological age: meta-analysis predicting time to death. . 8:1844-1865. https://doi.org/10.18632/aging.101020

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                TY  - JOUR
                AU  - Chen, Brian H. 
                AU  - Marioni, Riccardo E. 
                AU  - Colicino, Elena 
                AU  - Peters, Marjolein J. 
                AU  - Ward-Caviness, Cavin K. 
                AU  - Tsai, Pei-Chien 
                AU  - Roetker, Nicholas S. 
                AU  - Just, Allan C. 
                AU  - Demerath, Ellen W. 
                AU  - Guan, Weihua 
                AU  - Bressler, Jan 
                AU  - Fornage, Myriam 
                AU  - Studenski, Stephanie 
                AU  - Vandiver, Amy R. 
                AU  - Moore, Ann Zenobia 
                AU  - Tanaka, Toshiko 
                AU  - Kiel, Douglas P. 
                AU  - Liang, Liming 
                AU  - Vokonas, Pantel 
                AU  - Schwartz, Joel 
                AU  - Lunetta, Kathryn L. 
                AU  - Murabito, Joanne M. 
                AU  - Bandinelli, Stefania 
                AU  - Hernandez, Dena G. 
                AU  - Melzer, David 
                AU  - Nalls, Michael 
                AU  - Pilling, Luke C. 
                AU  - Price, Timothy R. 
                AU  - Singleton, Andrew B. 
                AU  - Gieger, Christian 
                AU  - Holle, Rolf 
                AU  - Kretschmer, Anja 
                AU  - Kronenberg, Florian 
                AU  - Kunze, Sonja 
                AU  - Linseisen, Jakob 
                AU  - Meisinger, Christine 
                AU  - Rathmann, Wolfgang 
                AU  - Waldenberger, Melanie 
                AU  - Visscher, Peter M. 
                AU  - Shah, Sonia 
                AU  - Wray, Naomi R. 
                AU  - McRae, Allan F. 
                AU  - Franco, Oscar H. 
                AU  - Hofman, Albert 
                AU  - Uitterlinden, André G. 
                AU  - Absher, Devin 
                AU  - Assimes, Themistocles 
                AU  - Levine, Morgan E. 
                AU  - Lu, Ake T. 
                AU  - Tsao, Philip S. 
                AU  - Hou, Lifang 
                AU  - Manson, JoAnn E. 
                AU  - Carty, Cara L. 
                AU  - LaCroix, Andrea Z. 
                AU  - Reiner, Alexander P. 
                AU  - Spector, Tim D. 
                AU  - Feinberg, Andrew P. 
                AU  - Levy, Daniel 
                AU  - Baccarelli, Andrea 
                AU  - van Meurs, Joyce 
                AU  - Bell, Jordana T. 
                AU  - Peters, Annette 
                AU  - Deary, Ian J. 
                AU  - Pankow, James S. 
                AU  - Ferrucci, Luigi 
                AU  - Horvath, Steve 
                TI  - DNA methylation-based measures of biological age: meta-analysis predicting time to death
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101020
                DO  - 10.18632/aging.101020
                SP  - 1844
                EP  - 1865
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Chen, Brian H. 
                AU  - Marioni, Riccardo E. 
                AU  - Colicino, Elena 
                AU  - Peters, Marjolein J. 
                AU  - Ward-Caviness, Cavin K. 
                AU  - Tsai, Pei-Chien 
                AU  - Roetker, Nicholas S. 
                AU  - Just, Allan C. 
                AU  - Demerath, Ellen W. 
                AU  - Guan, Weihua 
                AU  - Bressler, Jan 
                AU  - Fornage, Myriam 
                AU  - Studenski, Stephanie 
                AU  - Vandiver, Amy R. 
                AU  - Moore, Ann Zenobia 
                AU  - Tanaka, Toshiko 
                AU  - Kiel, Douglas P. 
                AU  - Liang, Liming 
                AU  - Vokonas, Pantel 
                AU  - Schwartz, Joel 
                AU  - Lunetta, Kathryn L. 
                AU  - Murabito, Joanne M. 
                AU  - Bandinelli, Stefania 
                AU  - Hernandez, Dena G. 
                AU  - Melzer, David 
                AU  - Nalls, Michael 
                AU  - Pilling, Luke C. 
                AU  - Price, Timothy R. 
                AU  - Singleton, Andrew B. 
                AU  - Gieger, Christian 
                AU  - Holle, Rolf 
                AU  - Kretschmer, Anja 
                AU  - Kronenberg, Florian 
                AU  - Kunze, Sonja 
                AU  - Linseisen, Jakob 
                AU  - Meisinger, Christine 
                AU  - Rathmann, Wolfgang 
                AU  - Waldenberger, Melanie 
                AU  - Visscher, Peter M. 
                AU  - Shah, Sonia 
                AU  - Wray, Naomi R. 
                AU  - McRae, Allan F. 
                AU  - Franco, Oscar H. 
                AU  - Hofman, Albert 
                AU  - Uitterlinden, André G. 
                AU  - Absher, Devin 
                AU  - Assimes, Themistocles 
                AU  - Levine, Morgan E. 
                AU  - Lu, Ake T. 
                AU  - Tsao, Philip S. 
                AU  - Hou, Lifang 
                AU  - Manson, JoAnn E. 
                AU  - Carty, Cara L. 
                AU  - LaCroix, Andrea Z. 
                AU  - Reiner, Alexander P. 
                AU  - Spector, Tim D. 
                AU  - Feinberg, Andrew P. 
                AU  - Levy, Daniel 
                AU  - Baccarelli, Andrea 
                AU  - van Meurs, Joyce 
                AU  - Bell, Jordana T. 
                AU  - Peters, Annette 
                AU  - Deary, Ian J. 
                AU  - Pankow, James S. 
                AU  - Ferrucci, Luigi 
                AU  - Horvath, Steve 
                TI  - DNA methylation-based measures of biological age: meta-analysis predicting time to death
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101020
                DO  - 10.18632/aging.101020
                SP  - 1844
                EP  - 1865
                PY  - 
                AB  - Estimates of biological age based on DNA methylation patterns, often referred to as "epigenetic age", "DNAm age", have been shown to be robust biomarkers of age in humans. We previously demonstrated that independent of chronological age, epigenetic age assessed in blood predicted all-cause mortality in four human cohorts. Here, we expanded our original observation to 13 different cohorts for a total sample size of 13,089 individuals, including three racial/ethnic groups. In addition, we examined whether incorporating information on blood cell composition into the epigenetic age metrics improves their predictive power for mortality. All considered measures of epigenetic age acceleration were predictive of mortality (p≤8.2x10-9), independent of chronological age, even after adjusting for additional risk factors (p&lt;5.4x10-4), and within the racial/ethnic groups that we examined (non-Hispanic whites, Hispanics, African Americans). Epigenetic age estimates that incorporated information on blood cell composition led to the smallest p-values for time to death (p=7.5x10-43). Overall, this study a) strengthens the evidence that epigenetic age predicts all-cause mortality above and beyond chronological age and traditional risk factors, and b) demonstrates that epigenetic age estimates that incorporate information on blood cell counts lead to highly significant associations with all-cause mortality.
                ER  -

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Polyphenolic drug composition based on benzenepolycarboxylic acids (BP-C3) increases life span and inhibits spontaneous tumorigenesis in female SHR mice

Vladimir N. Anisimov, Irina G. Popovich, Mark A. Zabezhinski, Maria N. Yurova, Margarita L. Tyndyk, Ivan V. Anikin, Peter A. Egormin, Irina A. Baldueva, Elena I. Fedoros, Sergey E. Pigarev, Andrey V. Panchenko,

https://doi.org/10.18632/aging.101024 pp 1866—1875

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Anisimov VN, Popovich IG, Zabezhinski MA, Yurova MN, Tyndyk ML, Anikin IV, Egormin PA, Baldueva IA, Fedoros EI, Pigarev SE, Panchenko AV, . Polyphenolic drug composition based on benzenepolycarboxylic acids (BP-C3) increases life span and inhibits spontaneous tumorigenesis in female SHR mice. . 8:1866-1875. https://doi.org/10.18632/aging.101024

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                TY  - JOUR
                AU  - Anisimov, Vladimir N.
                AU  - Popovich, Irina G.
                AU  - Zabezhinski, Mark A.
                AU  - Yurova, Maria N.
                AU  - Tyndyk, Margarita L.
                AU  - Anikin, Ivan V.
                AU  - Egormin, Peter A.
                AU  - Baldueva, Irina A.
                AU  - Fedoros, Elena I.
                AU  - Pigarev, Sergey E.
                AU  - Panchenko, Andrey V.
                TI  - Polyphenolic drug composition based on benzenepolycarboxylic acids (BP-C3) increases life span and inhibits spontaneous tumorigenesis in female SHR mice
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101024
                DO  - 10.18632/aging.101024
                SP  - 1866
                EP  - 1875
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Anisimov, Vladimir N.
                AU  - Popovich, Irina G.
                AU  - Zabezhinski, Mark A.
                AU  - Yurova, Maria N.
                AU  - Tyndyk, Margarita L.
                AU  - Anikin, Ivan V.
                AU  - Egormin, Peter A.
                AU  - Baldueva, Irina A.
                AU  - Fedoros, Elena I.
                AU  - Pigarev, Sergey E.
                AU  - Panchenko, Andrey V.
                TI  - Polyphenolic drug composition based on benzenepolycarboxylic acids (BP-C3) increases life span and inhibits spontaneous tumorigenesis in female SHR mice
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101024
                DO  - 10.18632/aging.101024
                SP  - 1866
                EP  - 1875
                PY  - 
                AB  - Effects of long-term application of novel polyphenolic composition BP-C3, containing polyphenolic benzenepolycarboxylic acids, vitamins and minerals on some biomarkers of aging, life span and spontaneous tumorigenesis has been studied in female SHR mice. Administration of BP-C3 with drinking water (0.005%) did not exert any toxic effect (did not have effect on general condition of animals, weight dynamics and consumption of food), postponed age-related switch-off of estrous function, caused slight reduction of body temperature. An increased survival was observed in mice treated with BP-C3 (p=0.00164, log rank test). BP-C3 increased mean lifespan – by 8.4%, lifespan of the last 10% of animals – by 12.4%, and life span of tumor-free mice – by 11.6%. A tendency in ability of BP-C3 to inhibit development of spontaneous tumors in mice was detected, though it did not reach the level of statistical significance (p=0.166, log rank test). The number of malignant mammary tumors was 1.5 times less and total number of tumors of various localizations was 1.6 times less in BP-C3 treated animals. Multiple tumors were registered in 8% of mice in the сontrol group and no cases – in BP-C3 treated group. Thus, BP-C3 demonstrated some anti-carcinogenic and a pronounced geroprotective activity.
                ER  -

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Crosstalk of clock gene expression and autophagy in aging

Faiza Kalfalah, Linda Janke, Alfonso Schiavi, Julia Tigges, Alexander Ix, Natascia Ventura, Fritz Boege, Hans Reinke,

https://doi.org/10.18632/aging.101018 pp 1876—1895

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Kalfalah F, Janke L, Schiavi A, Tigges J, Ix A, Ventura N, Boege F, Reinke H, . Crosstalk of clock gene expression and autophagy in aging. . 8:1876-1895. https://doi.org/10.18632/aging.101018

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                TY  - JOUR
                AU  - Kalfalah, Faiza 
                AU  - Janke, Linda 
                AU  - Schiavi, Alfonso 
                AU  - Tigges, Julia 
                AU  - Ix, Alexander 
                AU  - Ventura, Natascia 
                AU  - Boege, Fritz 
                AU  - Reinke, Hans 
                TI  - Crosstalk of clock gene expression and autophagy in aging
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101018
                DO  - 10.18632/aging.101018
                SP  - 1876
                EP  - 1895
                PY  - 
                AB  - Autophagy and the circadian clock counteract tissue degeneration and support longevity in many organisms. Accumulating evidence indicates that aging compromises both the circadian clock and autophagy but the mechanisms involved are unknown. Here we show that the expression levels of transcriptional repressor components of the circadian oscillator, most prominently the human Period homologue PER2, are strongly reduced in primary dermal fibroblasts from aged humans, while raising the expression of PER2 in the same cells partially restores diminished autophagy levels. The link between clock gene expression and autophagy is corroborated by the finding that the circadian clock drives cell-autonomous, rhythmic autophagy levels in immortalized murine fibroblasts, and that siRNA-mediated downregulation of PER2 decreases autophagy levels while leaving core clock oscillations intact. Moreover, the Period homologue lin-42 regulates autophagy and life span in the nematode Caenorhabditis elegans, suggesting an evolutionarily conserved role for Period proteins in autophagy control and aging. Taken together, this study identifies circadian clock proteins as set-point regulators of autophagy and puts forward a model, in which age-related changes of clock gene expression promote declining autophagy levels.
                ER  -

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Analysis of the machinery and intermediates of the 5hmC-mediated DNA demethylation pathway in aging on samples from the MARK-AGE Study

Elisabetta Valentini, Michele Zampieri, Marco Malavolta, Maria Giulia Bacalini, Roberta Calabrese, Tiziana Guastafierro, Anna Reale, Claudio Franceschi, Antti Hervonen, Bernhard Koller, Jürgen Bernhardt, P. Eline Slagboom, Olivier Toussaint, Ewa Sikora, Efstathios S. Gonos, Nicolle Breusing, Tilman Grune, Eugène Jansen, Martijn E.T. Dollé, María Moreno-Villanueva, Thilo Sindlinger, Alexander Bürkle, Fabio Ciccarone, Paola Caiafa,

https://doi.org/10.18632/aging.101022 pp 1896—1922

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Valentini E, Zampieri M, Malavolta M, Bacalini MG, Calabrese R, Guastafierro T, Reale A, Franceschi C, Hervonen A, Koller B, Bernhardt J, Slagboom PE, Toussaint O, et al, . Analysis of the machinery and intermediates of the 5hmC-mediated DNA demethylation pathway in aging on samples from the MARK-AGE Study. . 8:1896-1922. https://doi.org/10.18632/aging.101022

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                TY  - JOUR
                AU  - Valentini, Elisabetta 
                AU  - Zampieri, Michele 
                AU  - Malavolta, Marco 
                AU  - Bacalini, Maria Giulia
                AU  - Calabrese, Roberta 
                AU  - Guastafierro, Tiziana 
                AU  - Reale, Anna 
                AU  - Franceschi, Claudio 
                AU  - Hervonen, Antti 
                AU  - Koller, Bernhard 
                AU  - Bernhardt, Jürgen 
                AU  - Slagboom, P. Eline 
                AU  - Toussaint, Olivier 
                AU  - Sikora, Ewa 
                AU  - Gonos, Efstathios S.
                AU  - Breusing, Nicolle 
                AU  - Grune, Tilman 
                AU  - Jansen, Eugène 
                AU  - Dollé, Martijn E.T.
                AU  - Moreno-Villanueva, María 
                AU  - Sindlinger, Thilo 
                AU  - Bürkle, Alexander 
                AU  - Ciccarone, Fabio 
                AU  - Caiafa, Paola 
                TI  - Analysis of the machinery and intermediates of the 5hmC-mediated DNA demethylation pathway in aging on samples from the MARK-AGE Study
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101022
                DO  - 10.18632/aging.101022
                SP  - 1896
                EP  - 1922
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Valentini, Elisabetta 
                AU  - Zampieri, Michele 
                AU  - Malavolta, Marco 
                AU  - Bacalini, Maria Giulia
                AU  - Calabrese, Roberta 
                AU  - Guastafierro, Tiziana 
                AU  - Reale, Anna 
                AU  - Franceschi, Claudio 
                AU  - Hervonen, Antti 
                AU  - Koller, Bernhard 
                AU  - Bernhardt, Jürgen 
                AU  - Slagboom, P. Eline 
                AU  - Toussaint, Olivier 
                AU  - Sikora, Ewa 
                AU  - Gonos, Efstathios S.
                AU  - Breusing, Nicolle 
                AU  - Grune, Tilman 
                AU  - Jansen, Eugène 
                AU  - Dollé, Martijn E.T.
                AU  - Moreno-Villanueva, María 
                AU  - Sindlinger, Thilo 
                AU  - Bürkle, Alexander 
                AU  - Ciccarone, Fabio 
                AU  - Caiafa, Paola 
                TI  - Analysis of the machinery and intermediates of the 5hmC-mediated DNA demethylation pathway in aging on samples from the MARK-AGE Study
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101022
                DO  - 10.18632/aging.101022
                SP  - 1896
                EP  - 1922
                PY  - 
                AB  - Gradual changes in the DNA methylation landscape occur throughout aging virtually in all human tissues. A widespread reduction of 5-methylcytosine (5mC), associated with highly reproducible site-specific hypermethylation, characterizes the genome in aging. Therefore, an equilibrium seems to exist between general and directional deregulating events concerning DNA methylation controllers, which may underpin the age-related epigenetic changes. In this context, 5mC-hydroxylases (TET enzymes) are new potential players. In fact, TETs catalyze the stepwise oxidation of 5mC to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC), driving the DNA demethylation process based on thymine DNA glycosylase (TDG)-mediated DNA repair pathway. The present paper reports the expression of DNA hydroxymethylation components, the levels of 5hmC and of its derivatives in peripheral blood mononuclear cells of age-stratified donors recruited in several European countries in the context of the EU Project ‘MARK-AGE’. The results provide evidence for an age-related decline of TET1, TET3 and TDG gene expression along with a decrease of 5hmC and an accumulation of 5caC. These associations were independent of confounding variables, including recruitment center, gender and leukocyte composition. The observed impairment of 5hmC-mediated DNA demethylation pathway in blood cells may lead to aberrant transcriptional programs in the elderly.
                ER  -

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Disruption of mechanical stress in extracellular matrix is related to Stanford type A aortic dissection through down-regulation of Yes-associated protein

Wen-Jian Jiang, Wei-Hong Ren, Xu-Jie Liu, Yan Liu, Fu-Jian Wu, Li-Zhong Sun, Feng Lan, Jie Du, Hong-Jia Zhang,

https://doi.org/10.18632/aging.101033 pp 1923—1939

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Jiang W, Ren W, Liu X, Liu Y, Wu F, Sun L, Lan F, Du J, Zhang H, . Disruption of mechanical stress in extracellular matrix is related to Stanford type A aortic dissection through down-regulation of Yes-associated protein. . 8:1923-1939. https://doi.org/10.18632/aging.101033

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                TY  - JOUR
                AU  - Jiang, Wen-Jian 
                AU  - Ren, Wei-Hong 
                AU  - Liu, Xu-Jie 
                AU  - Liu, Yan 
                AU  - Wu, Fu-Jian 
                AU  - Sun, Li-Zhong 
                AU  - Lan, Feng 
                AU  - Du, Jie 
                AU  - Zhang, Hong-Jia 
                TI  - Disruption of mechanical stress in extracellular matrix is related to Stanford type A aortic dissection through down-regulation of Yes-associated protein
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101033
                DO  - 10.18632/aging.101033
                SP  - 1923
                EP  - 1939
                PY  - 
                AB  - In this study, we assessed whether the down-regulation of Yes-associated protein (YAP) is involved in the pathogenesis of extracellular matrix (ECM) mechanical stress-induced Stanford type A aortic dissection (STAAD). Human aortic samples were obtained from heart transplantation donors as normal controls and from STAAD patients undergoing surgical replacement of the ascending aorta. Decreased maximum aortic wall velocity, ECM disorders, increased VSMC apoptosis, and YAP down-regulation were identified in STAAD samples. In a mouse model of STAAD, YAP was down-regulated over time during the development of ECM damage, and increased VSMC apoptosis was also observed. YAP knockdown induced VSMC apoptosis under static conditions in vitro, and the change in mechanical stress induced YAP down-regulation and VSMC apoptosis. This study provides evidence that YAP down-regulation caused by the disruption of mechanical stress is associated with the development of STAAD via the induction of apoptosis in aortic VSMCs. As STAAD is among the most elusive and life-threatening vascular diseases, better understanding of the molecular pathogenesis of STAAD is critical to improve clinical outcome.
                ER  -

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Higher expression of somatic repair genes in long-lived ant queens than workers

Eric R. Lucas, Eyal Privman, Laurent Keller,

https://doi.org/10.18632/aging.101027 pp 1940—1951

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Lucas ER, Privman E, Keller L, . Higher expression of somatic repair genes in long-lived ant queens than workers. . 8:1940-1951. https://doi.org/10.18632/aging.101027

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                TY  - JOUR
                AU  - Lucas, Eric R.
                AU  - Privman, Eyal 
                AU  - Keller, Laurent 
                TI  - Higher expression of somatic repair genes in long-lived ant queens than workers
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101027
                DO  - 10.18632/aging.101027
                SP  - 1940
                EP  - 1951
                PY  - 
                AB  - Understanding why organisms senesce is a fundamental question in biology. One common explanation is that senescence results from an increase in macromolecular damage with age. The tremendous variation in lifespan between genetically identical queen and worker ants, ranging over an order of magnitude, provides a unique system to study how investment into processes of somatic maintenance and macromolecular repair influence lifespan. Here we use RNAseq to compare patterns of expression of genes involved in DNA and protein repair of age-matched queens and workers. There was no difference between queens and workers in 1-day-old individuals, but the level of expression of these genes increased with age and this up-regulation was greater in queens than in workers, resulting in significantly queen-biased expression in 2-month-old individuals in both legs and brains. Overall, these differences are consistent with the hypothesis that higher longevity is associated with increased investment into somatic repair.
                ER  -

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PPARβ/δ selectively regulates phenotypic features of age-related macular degeneration

Mayur Choudhary, Jin-dong Ding, Xiaoping Qi, Michael E. Boulton, Pei-Li Yao, Jeffrey M. Peters, Goldis Malek,

https://doi.org/10.18632/aging.101031 pp 1952—1978

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Choudhary M, Ding J, Qi X, Boulton ME, Yao P, Peters JM, Malek G, . PPARβ/δ selectively regulates phenotypic features of age-related macular degeneration. . 8:1952-1978. https://doi.org/10.18632/aging.101031

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                TY  - JOUR
                AU  - Choudhary, Mayur 
                AU  - Ding, Jin-dong 
                AU  - Qi, Xiaoping 
                AU  - Boulton, Michael E.
                AU  - Yao, Pei-Li 
                AU  - Peters, Jeffrey M.
                AU  - Malek, Goldis 
                TI  - PPARβ/δ selectively regulates phenotypic features of age-related macular degeneration
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101031
                DO  - 10.18632/aging.101031
                SP  - 1952
                EP  - 1978
                PY  - 
                AB  - Peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) is a nuclear receptor that regulates differentiation, inflammation, lipid metabolism, extracellular matrix remodeling, and angiogenesis in multiple tissues. These pathways are also central to the pathogenesis of age-related macular degeneration (AMD), the leading cause of vision loss globally. With the goal of identifying signaling pathways that may be important in the development of AMD, we investigated the impact of PPARβ/δ activation on ocular tissues affected in the disease. PPARβ/δ is expressed and can be activated in AMD vulnerable cells, including retinal pigment epithelial (RPE) and choroidal endothelial cells. Further, PPARβ/δ knockdown modulates AMD-related pathways selectively. Specifically, genetic ablation of Pparβ/δ in aged mice resulted in exacerbation of several phenotypic features of early dry AMD, but attenuation of experimentally induced choroidal neovascular (CNV) lesions. Antagonizing PPARβ/δ in both in vitro angiogenesis assays and in the in vivo experimentally induced CNV model, inhibited angiogenesis and angiogenic pathways, while ligand activation of PPARβ/δ, in vitro, decreased RPE lipid accumulation, characteristic of dry AMD. This study demonstrates for the first time, selective regulation of a nuclear receptor in the eye and establishes that selective targeting of PPARβ/δ may be a suitable strategy for treatment of different clinical sub-types of AMD.
                ER  -

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An intestinal microRNA modulates the homeostatic adaptation to chronic oxidative stress in C. elegans

Masaomi Kato, Mohammed Abul Kashem, Chao Cheng,

https://doi.org/10.18632/aging.101029 pp 1979—2005

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Kato M, Kashem MA, Cheng C, . An intestinal microRNA modulates the homeostatic adaptation to chronic oxidative stress in C. elegans. . 8:1979-2005. https://doi.org/10.18632/aging.101029

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Provider: 
 TY - JOUR
 AU - Kato, Masaomi 
 AU - Kashem, Mohammed Abul 
 AU - Cheng, Chao 
 TI - An intestinal microRNA modulates the homeostatic adaptation to chronic oxidative stress in C. elegans
 JO - 
 JA - 
 VL - 8
 IS - 9
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101029
 DO - 10.18632/aging.101029
 SP - 1979
 EP - 2005
 PY - 
 AB - Adaptation to an environmental or metabolic perturbation is a feature of the evolutionary process. Recent insights into microRNA function suggest that microRNAs serve as key players in a robust adaptive response against stress in animals through their capacity to fine-tune gene expression. However, it remains largely unclear how a microRNA-modulated downstream mechanism contributes to the process of homeostatic adaptation. Here we show that loss of an intestinally expressed microRNA gene, mir-60, in the nematode C. elegans promotes an adaptive response to chronic – a mild and long-term – oxidative stress exposure. The pathway involved appears to be unique since the canonical stress-responsive factors, such as DAF-16/FOXO, are dispensable for mir-60 loss to enhance oxidative stress resistance. Gene expression profiles revealed that genes encoding lysosomal proteases and those involved in xenobiotic metabolism and pathogen defense responses are up-regulated by the loss of mir-60. Detailed genetic studies and computational microRNA target prediction suggest that endocytosis components and a bZip transcription factor gene zip-10, which functions in innate immune response, are directly modulated by miR-60 in the intestine. Our findings suggest that the mir-60 loss facilitates adaptive response against chronic oxidative stress by ensuring the maintenance of cellular homeostasis.
 ER -

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SATB2-Nanog axis links age-related intrinsic changes of mesenchymal stem cells from craniofacial bone

Peipei Zhou, Geng Wu, Ping Zhang, Rongyao Xu, Jie Ge, Yu Fu, Yuchao Zhang, Yifei Du, Jinhai Ye, Jie Cheng, Hongbing Jiang,

https://doi.org/10.18632/aging.101041 pp 2006—2022

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Zhou P, Wu G, Zhang P, Xu R, Ge J, Fu Y, Zhang Y, Du Y, Ye J, Cheng J, Jiang H, . SATB2-Nanog axis links age-related intrinsic changes of mesenchymal stem cells from craniofacial bone. . 8:2006-2022. https://doi.org/10.18632/aging.101041

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                TY  - JOUR
                AU  - Zhou, Peipei 
                AU  - Wu, Geng 
                AU  - Zhang, Ping 
                AU  - Xu, Rongyao 
                AU  - Ge, Jie 
                AU  - Fu, Yu 
                AU  - Zhang, Yuchao 
                AU  - Du, Yifei 
                AU  - Ye, Jinhai 
                AU  - Cheng, Jie 
                AU  - Jiang, Hongbing 
                TI  - SATB2-Nanog axis links age-related intrinsic changes of mesenchymal stem cells from craniofacial bone
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101041
                DO  - 10.18632/aging.101041
                SP  - 2006
                EP  - 2022
                PY  - 
                AB  - Bone mesenchymal stem cells (BMSCs) senescence contributes to age-related bone loss. The alveolar bone in jaws originates from neural crest cells and possesses significant site- and age-related properties. However, such intrinsic characteristics of BMSCs from alveolar bone (AB-BMSCs) and the underlying regulatory mechanisms still remain unknown. Here, we found that the expression of special AT-rich binding protein 2 (SATB2) in human AB-BMSCs significantly decreased with aging. SATB2 knockdown on AB-BMSCs from young donors displayed these aging-related phenotypes in vitro. Meanwhile, enforced SATB2 overexpression could rejuvenate AB-BMSCs from older donors. Importantly, satb2 gene- modified BMSCs therapy could prevent the alveolar bone loss during the aging of rats. Mechanistically, the stemness regulator Nanog was identified as the direct transcriptional target of SATB2 in BMSCs and functioned as a downstream mediator of SATB2. Collectively, our data reveal that SATB2 in AB-BMSCs associates with their age-related properties, and prevents AB-BMSCs senescence via maintaining Nanog expression. These findings highlight the translational potential of transcriptional factor-based cellular reprogramming for anti-aging therapy.
                ER  -

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Increased expression of long-noncoding RNA ZFAS1 is associated with epithelial-mesenchymal transition of gastric cancer

Hu Zhou, Fubing Wang, Hao Chen, Qian Tan, Shili Qiu, Shanshan Chen, Wei Jing, Mingxia Yu, Chunzi Liang, Shengwei Ye, Jiancheng Tu,

https://doi.org/10.18632/aging.101048 pp 2023—2038

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Zhou H, Wang F, Chen H, Tan Q, Qiu S, Chen S, Jing W, Yu M, Liang C, Ye S, Tu J, . Increased expression of long-noncoding RNA ZFAS1 is associated with epithelial-mesenchymal transition of gastric cancer. . 8:2023-2038. https://doi.org/10.18632/aging.101048

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                TY  - JOUR
                AU  - Zhou, Hu 
                AU  - Wang, Fubing 
                AU  - Chen, Hao 
                AU  - Tan, Qian 
                AU  - Qiu, Shili 
                AU  - Chen, Shanshan 
                AU  - Jing, Wei 
                AU  - Yu, Mingxia 
                AU  - Liang, Chunzi 
                AU  - Ye, Shengwei 
                AU  - Tu, Jiancheng 
                TI  - Increased expression of long-noncoding RNA ZFAS1 is associated with epithelial-mesenchymal transition of gastric cancer
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101048
                DO  - 10.18632/aging.101048
                SP  - 2023
                EP  - 2038
                PY  - 
                AB  - LncRNAs play critical roles in gastric cancer (GC). In this study, the expression of fourteen cancer related lncRNAs were investigated in paired tissues of 66 patients with GC, real-time RT-PCR revealed that ZFAS1 was significantly upregulated. We then examined the expression of ZFAS1 in plasmas derived from 77 GC patients before- and post-operations and 60 healthy individuals, and found that circulating ZFAS1 was also upregulated in GC patients and operation can reduce its presence in plasma. To investigate the potential mechanisms, we compared the expression of ZFAS1 in multiple gastric cell lines and one normal cell line and found that ZFAS1 was up-regulated in GC cell lines. Furthermore, circulating tumor cells (CTC) were simulated by mixing GC cells with peripheral blood. After EpCAM antibody-based cell sorting, we found that the expression of ZFAS1 was positively correlated with EMT property of CTCs. In GC patient tissue samples, we found that Twist was positively correlated with ZFAS1 by immunohistochemical staining. Taken together, our results suggested that ZFAS1 was up-regulated in both tissues and plasmas of GC patients, and may be involved in regulation of EMT in GC progression. Thus, ZFAS1 might serve as a potential diagnostic marker and/or therapeutic target for GC.
                ER  -

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Early life characteristics and late life burden of cerebral small vessel disease in the Lothian Birth Cohort 1936

Thalia S. Field, Fergus N. Doubal, Wendy Johnson, Ellen Backhouse, Caroline McHutchison, Simon Cox, Janie Corley, Alison Pattie, Alan J. Gow, Susan Shenkin, Vera Cvoro, Zoe Morris, Julie Staals, Mark Bastin, Ian J. Deary, Joanna M. Wardlaw,

https://doi.org/10.18632/aging.101043 pp 2039—2061

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Field TS, Doubal FN, Johnson W, Backhouse E, McHutchison C, Cox S, Corley J, Pattie A, Gow AJ, Shenkin S, Cvoro V, Morris Z, Staals J, et al, . Early life characteristics and late life burden of cerebral small vessel disease in the Lothian Birth Cohort 1936. . 8:2039-2061. https://doi.org/10.18632/aging.101043

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                TY  - JOUR
                AU  - Field, Thalia S.
                AU  - Doubal, Fergus N.
                AU  - Johnson, Wendy 
                AU  - Backhouse, Ellen 
                AU  - McHutchison, Caroline 
                AU  - Cox, Simon 
                AU  - Corley, Janie 
                AU  - Pattie, Alison 
                AU  - Gow, Alan J.
                AU  - Shenkin, Susan 
                AU  - Cvoro, Vera 
                AU  - Morris, Zoe 
                AU  - Staals, Julie 
                AU  - Bastin, Mark 
                AU  - Deary, Ian J.
                AU  - Wardlaw, Joanna M.
                TI  - Early life characteristics and late life burden of cerebral small vessel disease in the Lothian Birth Cohort 1936
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101043
                DO  - 10.18632/aging.101043
                SP  - 2039
                EP  - 2061
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Field, Thalia S.
                AU  - Doubal, Fergus N.
                AU  - Johnson, Wendy 
                AU  - Backhouse, Ellen 
                AU  - McHutchison, Caroline 
                AU  - Cox, Simon 
                AU  - Corley, Janie 
                AU  - Pattie, Alison 
                AU  - Gow, Alan J.
                AU  - Shenkin, Susan 
                AU  - Cvoro, Vera 
                AU  - Morris, Zoe 
                AU  - Staals, Julie 
                AU  - Bastin, Mark 
                AU  - Deary, Ian J.
                AU  - Wardlaw, Joanna M.
                TI  - Early life characteristics and late life burden of cerebral small vessel disease in the Lothian Birth Cohort 1936
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101043
                DO  - 10.18632/aging.101043
                SP  - 2039
                EP  - 2061
                PY  - 
                AB  - It is unknown whether relations between early-life factors and overall health in later life apply to burden of cerebral small vessel disease (cSVD), a major cause of stroke and dementia. We explored relations between early-life factors and cSVD in the Lothian Birth Cohort, a healthy aging cohort. Participants were recruited at age 70 (N = 1091); most had completed a test of cognitive ability at age 11 as part of the Scottish Mental Survey of 1947. Of those, 700 participants had brain MRI that could be rated for cSVD conducted at age 73. Presence of lacunes, white matter hyperintensities, microbleeds, and perivascular spaces were summed in a score of 0-4 representing all MRI cSVD features. We tested associations with early-life factors using multivariate logistic regression. Greater SVD score was significantly associated with lower age-11 IQ (OR higher SVD score per SD age-11 IQ = .78, 95%CI 0.65-.95, p=.01). The associations between SVD score and own job class (OR higher job class, .64 95%CI .43-.95, p=.03), age-11 deprivation index (OR per point deprivation score, 1.08, 95%CI 1.00-1.17, p=.04), and education (OR some qualifying education, .60 95%CI .37-.98, p=.04) trended towards significance (p&lt;.05 for all) but did not meet thresholds for multiple testing. No early-life factor was significantly associated with any one individual score component. Early-life factors may contribute to age-73 burden of cSVD. These relations, and the potential for early social interventions to improve brain health, deserve further study.
                ER  -

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Age-associated repression of type 1 inositol 1, 4, 5-triphosphate receptor impairs muscle regeneration

Jeong Yi Choi, Chae Young Hwang, Bora Lee, Seung-Min Lee, Young Jae Bahn, Kwang-Pyo Lee, Moonkyung Kang, Yeon-Soo Kim, Sun-Hee Woo, Jae-Young Lim, Eunhee Kim, Ki-Sun Kwon,

https://doi.org/10.18632/aging.101039 pp 2062—2080

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Choi JY, Hwang CY, Lee B, Lee S, Bahn YJ, Lee K, Kang M, Kim Y, Woo S, Lim J, Kim E, Kwon K, . Age-associated repression of type 1 inositol 1, 4, 5-triphosphate receptor impairs muscle regeneration. . 8:2062-2080. https://doi.org/10.18632/aging.101039

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                TY  - JOUR
                AU  - Choi, Jeong Yi
                AU  - Hwang, Chae Young
                AU  - Lee, Bora 
                AU  - Lee, Seung-Min 
                AU  - Bahn, Young Jae
                AU  - Lee, Kwang-Pyo 
                AU  - Kang, Moonkyung 
                AU  - Kim, Yeon-Soo 
                AU  - Woo, Sun-Hee 
                AU  - Lim, Jae-Young 
                AU  - Kim, Eunhee 
                AU  - Kwon, Ki-Sun 
                TI  - Age-associated repression of type 1 inositol 1, 4, 5-triphosphate receptor impairs muscle regeneration
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101039
                DO  - 10.18632/aging.101039
                SP  - 2062
                EP  - 2080
                PY  - 
                AB  - Skeletal muscle mass and power decrease with age, leading to impairment of mobility and metabolism in the elderly. Ca2+ signaling is crucial for myoblast differentiation as well as muscle contraction through activation of transcription factors and Ca2+-dependent kinases and phosphatases. Ca2+ channels, such as dihydropyridine receptor (DHPR), two-pore channel (TPC) and inositol 1,4,5-triphosphate receptor (ITPR), function to maintain Ca2+ homeostasis in myoblasts. Here, we observed a significant decrease in expression of type 1 IP3 receptor (ITPR1), but not types 2 and 3, in aged mice skeletal muscle and isolated myoblasts, compared with those of young mice. ITPR1 knockdown using shRNA-expressing viruses in C2C12 myoblasts and tibialis anterior muscle of mice inhibited myotube formation and muscle regeneration after injury, respectively, a typical phenotype of aged muscle. This aging phenotype was associated with repression of muscle-specific genes and activation of the epidermal growth factor receptor (EGFR)-Ras-extracellular signal-regulated kinase (ERK) pathway. ERK inhibition by U0126 not only induced recovery of myotube formation in old myoblasts but also facilitated muscle regeneration after injury in aged muscle. The conserved decline in ITPR1 expression in aged human skeletal muscle suggests utility as a potential therapeutic target for sarcopenia, which can be treated using ERK inhibition strategies.
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Age-related hearing loss: prevention of threshold declines, cell loss and apoptosis in spiral ganglion neurons

Robert D. Frisina, Bo Ding, Xiaoxia Zhu, Joseph P. Walton,

https://doi.org/10.18632/aging.101045 pp 2081—2099

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Frisina RD, Ding B, Zhu X, Walton JP, . Age-related hearing loss: prevention of threshold declines, cell loss and apoptosis in spiral ganglion neurons. . 8:2081-2099. https://doi.org/10.18632/aging.101045

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                TY  - JOUR
                AU  - Frisina, Robert D.
                AU  - Ding, Bo 
                AU  - Zhu, Xiaoxia 
                AU  - Walton, Joseph P.
                TI  - Age-related hearing loss: prevention of threshold declines, cell loss and apoptosis in spiral ganglion neurons
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101045
                DO  - 10.18632/aging.101045
                SP  - 2081
                EP  - 2099
                PY  - 
                AB  - Age-related hearing loss (ARHL) -presbycusis - is the most prevalent neurodegenerative disease and number one communication disorder of our aged population; and affects hundreds of millions of people worldwide. Its prevalence is close to that of cardiovascular disease and arthritis, and can be a precursor to dementia. The auditory perceptual dysfunction is well understood, but knowledge of the biological bases of ARHL is still somewhat lacking. Surprisingly, there are no FDA-approved drugs for treatment. Based on our previous studies of human subjects, where we discovered relations between serum aldosterone levels and the severity of ARHL, we treated middle age mice with aldosterone, which normally declines with age in all mammals. We found that hearing thresholds and suprathreshold responses significantly improved in the aldosterone-treated mice compared to the non-treatment group. In terms of cellular and molecular mechanisms underlying this therapeutic effect, additional experiments revealed that spiral ganglion cell survival was significantly improved, mineralocorticoid receptors were upregulated via post-translational protein modifications, and age-related intrinsic and extrinsic apoptotic pathways were blocked by the aldosterone therapy. Taken together, these novel findings pave the way for translational drug development towards the first medication to prevent the progression of ARHL.
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Cell cycle controls stress response and longevity in C. elegans

Matthias Dottermusch, Theresa Lakner, Tobias Peyman, Marinella Klein, Gerd Walz, Elke Neumann-Haefelin,

https://doi.org/10.18632/aging.101052 pp 2100—2126

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Dottermusch M, Lakner T, Peyman T, Klein M, Walz G, Neumann-Haefelin E, . Cell cycle controls stress response and longevity in C. elegans. . 8:2100-2126. https://doi.org/10.18632/aging.101052

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Provider: 
 TY - JOUR
 AU - Dottermusch, Matthias 
 AU - Lakner, Theresa 
 AU - Peyman, Tobias 
 AU - Klein, Marinella 
 AU - Walz, Gerd 
 AU - Neumann-Haefelin, Elke 
 TI - Cell cycle controls stress response and longevity in C. elegans
 JO - 
 JA - 
 VL - 8
 IS - 9
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101052
 DO - 10.18632/aging.101052
 SP - 2100
 EP - 2126
 PY - 
 AB - Recent studies have revealed a variety of genes and mechanisms that influence the rate of aging progression. In this study, we identified cell cycle factors as potent regulators of health and longevity in C. elegans. Focusing on the cyclin-dependent kinase 2 (cdk-2) and cyclin E (cye-1), we show that inhibition of cell cycle genes leads to tolerance towards environmental stress and longevity. The reproductive system is known as a key regulator of longevity in C. elegans. We uncovered the gonad as the central organ mediating the effects of cell cycle inhibition on lifespan. In particular, the proliferating germ cells were essential for conferring longevity. Steroid hormone signaling and the FOXO transcription factor DAF-16 were required for longevity associated with cell cycle inhibition. Furthermore, we discovered that SKN-1 (ortholog of mammalian Nrf proteins) activates protective gene expression and induces longevity when cell cycle genes are inactivated. We conclude that both, germline absence and inhibition through impairment of cell cycle machinery results in longevity through similar pathways. In addition, our studies suggest further roles of cell cycle genes beyond cell cycle progression and support the recently described connection of SKN-1/Nrf to signals deriving from the germline.
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In search for geroprotectors: in silico screening and in vitro validation of signalome-level mimetics of young healthy state

Alexander Aliper, Aleksey V. Belikov, Andrew Garazha, Leslie Jellen, Artem Artemov, Maria Suntsova, Alena Ivanova, Larisa Venkova, Nicolas Borisov, Anton Buzdin, Polina Mamoshina, Evgeny Putin, Andrew G. Swick, Alexey Moskalev, Alex Zhavoronkov,

https://doi.org/10.18632/aging.101047 pp 2127—2152

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Aliper A, Belikov AV, Garazha A, Jellen L, Artemov A, Suntsova M, Ivanova A, Venkova L, Borisov N, Buzdin A, Mamoshina P, Putin E, Swick AG, et al, . In search for geroprotectors: in silico screening and in vitro validation of signalome-level mimetics of young healthy state. . 8:2127-2152. https://doi.org/10.18632/aging.101047

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                TY  - JOUR
                AU  - Aliper, Alexander 
                AU  - Belikov, Aleksey V. 
                AU  - Garazha, Andrew 
                AU  - Jellen, Leslie 
                AU  - Artemov, Artem 
                AU  - Suntsova, Maria 
                AU  - Ivanova, Alena 
                AU  - Venkova, Larisa 
                AU  - Borisov, Nicolas 
                AU  - Buzdin, Anton 
                AU  - Mamoshina, Polina 
                AU  - Putin, Evgeny 
                AU  - Swick, Andrew G. 
                AU  - Moskalev, Alexey 
                AU  - Zhavoronkov, Alex 
                TI  - In search for geroprotectors: in silico screening and in vitro validation of signalome-level mimetics of young healthy state
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101047
                DO  - 10.18632/aging.101047
                SP  - 2127
                EP  - 2152
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Aliper, Alexander 
                AU  - Belikov, Aleksey V. 
                AU  - Garazha, Andrew 
                AU  - Jellen, Leslie 
                AU  - Artemov, Artem 
                AU  - Suntsova, Maria 
                AU  - Ivanova, Alena 
                AU  - Venkova, Larisa 
                AU  - Borisov, Nicolas 
                AU  - Buzdin, Anton 
                AU  - Mamoshina, Polina 
                AU  - Putin, Evgeny 
                AU  - Swick, Andrew G. 
                AU  - Moskalev, Alexey 
                AU  - Zhavoronkov, Alex 
                TI  - In search for geroprotectors: in silico screening and in vitro validation of signalome-level mimetics of young healthy state
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101047
                DO  - 10.18632/aging.101047
                SP  - 2127
                EP  - 2152
                PY  - 
                AB  - Populations in developed nations throughout the world are rapidly aging, and the search for geroprotectors, or anti-aging interventions, has never been more important. Yet while hundreds of geroprotectors have extended lifespan in animal models, none have yet been approved for widespread use in humans. GeroScope is a computational tool that can aid prediction of novel geroprotectors from existing human gene expression data. GeroScope maps expression differences between samples from young and old subjects to aging-related signaling pathways, then profiles pathway activation strength (PAS) for each condition. Known substances are then screened and ranked for those most likely to target differential pathways and mimic the young signalome. Here we used GeroScope and shortlisted ten substances, all of which have lifespan-extending effects in animal models, and tested 6 of them for geroprotective effects in senescent human fibroblast cultures. PD-98059, a highly selective MEK1 inhibitor, showed both life-prolonging and rejuvenating effects. Natural compounds like N-acetyl-L-cysteine, Myricetin and Epigallocatechin gallate also improved several senescence-associated properties and were further investigated with pathway analysis. This work not only highlights several potential geroprotectors for further study, but also serves as a proof-of-concept for GeroScope, Oncofinder and other PAS-based methods in streamlining drug prediction, repurposing and personalized medicine.
                ER  -

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Age-related changes in cerebellar and hypothalamic function accompany non-microglial immune gene expression, altered synapse organization, and excitatory amino acid neurotransmission deficits

Stephen J. Bonasera, Jyothi Arikkath, Michael D. Boska, Tammy R. Chaudoin, Nicholas W. DeKorver, Evan H. Goulding, Traci A. Hoke, Vahid Mojtahedzedah, Crystal D. Reyelts, Balasrinivasa Sajja, A. Katrin Schenk, Laurence H. Tecott, Tiffany A. Volden,

https://doi.org/10.18632/aging.101040 pp 2153—2181

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Bonasera SJ, Arikkath J, Boska MD, Chaudoin TR, DeKorver NW, Goulding EH, Hoke TA, Mojtahedzedah V, Reyelts CD, Sajja B, Schenk AK, Tecott LH, Volden TA, . Age-related changes in cerebellar and hypothalamic function accompany non-microglial immune gene expression, altered synapse organization, and excitatory amino acid neurotransmission deficits. . 8:2153-2181. https://doi.org/10.18632/aging.101040

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                TY  - JOUR
                AU  - Bonasera, Stephen J. 
                AU  - Arikkath, Jyothi 
                AU  - Boska, Michael D. 
                AU  - Chaudoin, Tammy R. 
                AU  - DeKorver, Nicholas W. 
                AU  - Goulding, Evan H. 
                AU  - Hoke, Traci A. 
                AU  - Mojtahedzedah, Vahid 
                AU  - Reyelts, Crystal D. 
                AU  - Sajja, Balasrinivasa 
                AU  - Schenk, A. Katrin 
                AU  - Tecott, Laurence H. 
                AU  - Volden, Tiffany A. 
                TI  - Age-related changes in cerebellar and hypothalamic function accompany non-microglial immune gene expression, altered synapse organization, and excitatory amino acid neurotransmission deficits
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101040
                DO  - 10.18632/aging.101040
                SP  - 2153
                EP  - 2181
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Bonasera, Stephen J. 
                AU  - Arikkath, Jyothi 
                AU  - Boska, Michael D. 
                AU  - Chaudoin, Tammy R. 
                AU  - DeKorver, Nicholas W. 
                AU  - Goulding, Evan H. 
                AU  - Hoke, Traci A. 
                AU  - Mojtahedzedah, Vahid 
                AU  - Reyelts, Crystal D. 
                AU  - Sajja, Balasrinivasa 
                AU  - Schenk, A. Katrin 
                AU  - Tecott, Laurence H. 
                AU  - Volden, Tiffany A. 
                TI  - Age-related changes in cerebellar and hypothalamic function accompany non-microglial immune gene expression, altered synapse organization, and excitatory amino acid neurotransmission deficits
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101040
                DO  - 10.18632/aging.101040
                SP  - 2153
                EP  - 2181
                PY  - 
                AB  - We describe age-related molecular and neuronal changes that disrupt mobility or energy balance based on brain region and genetic background. Compared to young mice, aged C57BL/6 mice exhibit marked locomotor (but not energy balance) impairments. In contrast, aged BALB mice exhibit marked energy balance (but not locomotor) impairments. Age-related changes in cerebellar or hypothalamic gene expression accompany these phenotypes. Aging evokes upregulation of immune pattern recognition receptors and cell adhesion molecules. However, these changes do not localize to microglia, the major CNS immunocyte. Consistent with a neuronal role, there is a marked age-related increase in excitatory synapses over the cerebellum and hypothalamus. Functional imaging of these regions is consistent with age-related synaptic impairments. These studies suggest that aging reactivates a developmental program employed during embryogenesis where immune molecules guide synapse formation and pruning. Renewed activity in this program may disrupt excitatory neurotransmission, causing significant behavioral deficits.
                ER  -

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LncRNA mediated regulation of aging pathways in Drosophila melanogaster during dietary restriction

Deying Yang, Ting Lian, Jianbo Tu, Uma Gaur, Xueping Mao, Xiaolan Fan, Diyan Li, Ying Li, Mingyao Yang,

https://doi.org/10.18632/aging.101062 pp 2182—2203

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Yang D, Lian T, Tu J, Gaur U, Mao X, Fan X, Li D, Li Y, Yang M, . LncRNA mediated regulation of aging pathways in Drosophila melanogaster during dietary restriction. . 8:2182-2203. https://doi.org/10.18632/aging.101062

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Provider: 
 TY - JOUR
 AU - Yang, Deying 
 AU - Lian, Ting 
 AU - Tu, Jianbo 
 AU - Gaur, Uma 
 AU - Mao, Xueping 
 AU - Fan, Xiaolan 
 AU - Li, Diyan 
 AU - Li, Ying 
 AU - Yang, Mingyao 
 TI - LncRNA mediated regulation of aging pathways in Drosophila melanogaster during dietary restriction
 JO - 
 JA - 
 VL - 8
 IS - 9
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101062
 DO - 10.18632/aging.101062
 SP - 2182
 EP - 2203
 PY - 
 AB - Dietary restriction (DR) extends lifespan in many species which is a well-known phenomenon. Long non-coding RNAs (lncRNAs) play an important role in regulation of cell senescence and important age-related signaling pathways. Here, we profiled the lncRNA and mRNA transcriptome of fruit flies at 7 day and 42 day during DR and fully-fed conditions, respectively. In general, 102 differentially expressed lncRNAs and 1406 differentially expressed coding genes were identified. Most informatively we found a large number of differentially expressed lncRNAs and their targets enriched in GO and KEGG analysis. We discovered some new aging related signaling pathways during DR, such as hippo signaling pathway-fly, phototransduction-fly and protein processing in endoplasmic reticulum etc. Novel lncRNAs XLOC_092363 and XLOC_166557 are found to be located in 10 kb upstream sequences of hairy and ems promoters, respectively. Furthermore, tissue specificity of some novel lncRNAs had been analyzed at 7 day of DR in fly head, gut and fat body. Also the silencing of lncRNA XLOC_076307 resulted in altered expression level of its targets including Gadd45 (involved in FoxO signaling pathway). Together, the results implicated many lncRNAs closely associated with dietary restriction, which could provide a resource for lncRNA in aging and age-related disease field.
 ER -

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Clinical significance and prognostic value of TRIM24 expression in esophageal squamous cell carcinoma

Jun Chi, Qing Yang, Xiao-Feng Xie, Xian-Zi Yang, Mei-Yin Zhang, Hui-Yun Wang, Guo-Liang Xu,

https://doi.org/10.18632/aging.101037 pp 2204—2221

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Chi J, Yang Q, Xie X, Yang X, Zhang M, Wang H, Xu G, . Clinical significance and prognostic value of TRIM24 expression in esophageal squamous cell carcinoma. . 8:2204-2221. https://doi.org/10.18632/aging.101037

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                TY  - JOUR
                AU  - Chi, Jun 
                AU  - Yang, Qing 
                AU  - Xie, Xiao-Feng 
                AU  - Yang, Xian-Zi 
                AU  - Zhang, Mei-Yin 
                AU  - Wang, Hui-Yun 
                AU  - Xu, Guo-Liang 
                TI  - Clinical significance and prognostic value of TRIM24 expression in esophageal squamous cell carcinoma
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101037
                DO  - 10.18632/aging.101037
                SP  - 2204
                EP  - 2221
                PY  - 
                AB  - Tripartite motif-containing 24 (TRIM24), a member of the transcription intermediary factor 1 family, is defined as a co-regulator with several nuclear receptors, such as RARα. TRIM24 has been reported to be involved in many cancers. In this study, we aimed to investigate the expression pattern and prognostic significance of TRIM24 and its relationship with RARα in esophageal squamous cell cancer (ESCC). Both mRNA and protein expression levels of TRIM24 were found to be significantly decreased in ESCC, as judged by qRT-PCR and western blot. Immunohistochemistry staining shows that the reduced TRIM24 protein is associated with lymph node metastasis (P=0.024), advance pathological TNM (pTNM) stage (P=0.046) and recurrence/metastasis (P=0.001). Upregulated TRIM24 protein predicts longer overall survival and disease-free survival (both P&lt;0.001) and is an independent predictor for good prognosis (HR, 0.519; 95%CI, 0.341-0.788; P=0.002). TRIM24 expression has been proven remarkably to improve prediction of survival of pTNM stage in ESCC patients, especially in stage I and II. However, no significant relationship was found between TRIM24 and RARα expression levels. In conclusion, reduced TRIM24 protein is associated with poor survival in ESCC patients, suggesting TRIM24 protein is a potential prognostic biomarker for ESCC.
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Specific premature epigenetic aging of cartilage in osteoarthritis

Laura Vidal-Bralo, Yolanda Lopez-Golan, Antonio Mera-Varela, Ignacio Rego-Perez, Steve Horvath, Yuhua Zhang, Álvaro del Real, Guangju Zhai, Francisco J. Blanco, Jose A. Riancho, Juan J. Gomez-Reino, Antonio Gonzalez,

https://doi.org/10.18632/aging.101053 pp 2222—2231

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Vidal-Bralo L, Lopez-Golan Y, Mera-Varela A, Rego-Perez I, Horvath S, Zhang Y, del Real Á, Zhai G, Blanco FJ, Riancho JA, Gomez-Reino JJ, Gonzalez A, . Specific premature epigenetic aging of cartilage in osteoarthritis. . 8:2222-2231. https://doi.org/10.18632/aging.101053

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                TY  - JOUR
                AU  - Vidal-Bralo, Laura 
                AU  - Lopez-Golan, Yolanda 
                AU  - Mera-Varela, Antonio 
                AU  - Rego-Perez, Ignacio 
                AU  - Horvath, Steve 
                AU  - Zhang, Yuhua 
                AU  - del Real, Álvaro 
                AU  - Zhai, Guangju 
                AU  - Blanco, Francisco J. 
                AU  - Riancho, Jose A. 
                AU  - Gomez-Reino, Juan J. 
                AU  - Gonzalez, Antonio 
                TI  - Specific premature epigenetic aging of cartilage in osteoarthritis
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101053
                DO  - 10.18632/aging.101053
                SP  - 2222
                EP  - 2231
                PY  - 
                AB  - Osteoarthritis (OA) is a disease affecting multiple tissues of the joints in the elderly, but most notably articular cartilage. Premature biological aging has been described in this tissue and in blood cells, suggesting a systemic component of premature aging in the pathogenesis of OA. Here, we have explored epigenetic aging in OA at the local (cartilage and bone) and systemic (blood) levels. Two DNA methylation age-measures (DmAM) were used: the multi-tissue age estimator for cartilage and bone; and a blood-specific biomarker for blood. Differences in DmAM between OA patients and controls showed an accelerated aging of 3.7 years in articular cartilage (95% CI = 1.1 to 6.3, P = 0.008) of OA patients. By contrast, no difference in epigenetic aging was observed in bone (0.04 years; 95% CI = -1.8 to 1.9, P = 0.3) and in blood (-0.6 years; 95% CI = -1.5 to 0.3, P = 0.2) between OA patients and controls. Therefore, premature epigenetic aging according to DNA methylation changes was specific of OA cartilage, adding further evidence and insight on premature aging of cartilage as a component of OA pathogenesis that reflects damage and vulnerability.
                ER  -

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Global gene profiling of aging lungs in Atp8b1 mutant mice

Ramani Soundararajan, Timothy M. Stearns, Alexander Czachor, Jutaro Fukumoto, Christina Turn, Emma Westermann-Clark, Mason Breitzig, Lee Tan, Richard F. Lockey, Benjamin L. King, Narasaiah Kolliputi,

https://doi.org/10.18632/aging.101056 pp 2232—2252

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Soundararajan R, Stearns TM, Czachor A, Fukumoto J, Turn C, Westermann-Clark E, Breitzig M, Tan L, Lockey RF, King BL, Kolliputi N, . Global gene profiling of aging lungs in Atp8b1 mutant mice. . 8:2232-2252. https://doi.org/10.18632/aging.101056

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                TY  - JOUR
                AU  - Soundararajan, Ramani 
                AU  - Stearns, Timothy M.
                AU  - Czachor, Alexander 
                AU  - Fukumoto, Jutaro 
                AU  - Turn, Christina 
                AU  - Westermann-Clark, Emma 
                AU  - Breitzig, Mason 
                AU  - Tan, Lee 
                AU  - Lockey, Richard F.
                AU  - King, Benjamin L.
                AU  - Kolliputi, Narasaiah 
                TI  - Global gene profiling of aging lungs in Atp8b1 mutant mice
                JO  - 
                JA  - 
                VL  - 8
                IS  - 9
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101056
                DO  - 10.18632/aging.101056
                SP  - 2232
                EP  - 2252
                PY  - 
                AB  - Objective:Recent studies implicate cardiolipin oxidation in several age-related diseases. Atp8b1 encoding Type 4 P-type ATPases is a cardiolipin transporter. Mutation in Atp8b1 gene or inflammation of the lungs impairs the capacity of Atp8b1 to clear cardiolipin from lung fluid. However, the link between Atp8b1 mutation and age-related gene alteration is unknown. Therefore, we investigated how Atp8b1 mutation alters age-related genes. Methods: We performed Affymetrix gene profiling of lungs isolated from young (7-9 wks, n=6) and aged (14 months, 14 M, n=6) C57BL/6 and Atp8b1 mutant mice. In addition, Ingenuity Pathway Analysis (IPA) was performed. Differentially expressed genes were validated by quantitative real-time PCR (qRT-PCR). Results: Global transcriptome analysis revealed 532 differentially expressed genes in Atp8b1 lungs, 157 differentially expressed genes in C57BL/6 lungs, and 37 overlapping genes. IPA of age-related genes in Atp8b1 lungs showed enrichment of Xenobiotic metabolism and Nrf2-mediated signaling pathways. The increase in Adamts2 and Mmp13 transcripts in aged Atp8b1 lungs was validated by qRT-PCR. Similarly, the decrease in Col1a1 and increase in Cxcr6 transcripts was confirmed in both Atp8b1 mutant and C57BL/6 lungs. Conclusion: Based on transcriptome profiling, our study indicates that Atp8b1 mutant mice may be susceptible to age-related lung diseases.
                ER  -

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Deep biomarkers of aging are population-dependent

Alan A. Cohen, Vincent Morissette-Thomas, Luigi Ferrucci, Linda P. Fried,

https://doi.org/10.18632/aging.101034 pp 2253—2255

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Cohen AA, Morissette-Thomas V, Ferrucci L, Fried LP, . Deep biomarkers of aging are population-dependent. . 8:2253-2255. https://doi.org/10.18632/aging.101034

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Volume 8, Issue 9

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Editorials

Georg Karpel-Massler, Markus D. Siegelin,

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James C. Neil, Gillian Borland, Anna Kilbey,

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Yulin Li, Anja Deutzmann, Dean W. Felsher,

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Anusha Sriraman, Yizhu Li, Matthias Dobbelstein,

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Research Perspective

Tohru Hasegawa, Wataru Ukai,

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Research Papers

Vladimir N. Anisimov, Irina G. Popovich, Mark A. Zabezhinski, Maria N. Yurova, Margarita L. Tyndyk, Ivan V. Anikin, Peter A. Egormin, Irina A. Baldueva, Elena I. Fedoros, Sergey E. Pigarev, Andrey V. Panchenko,

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Faiza Kalfalah, Linda Janke, Alfonso Schiavi, Julia Tigges, Alexander Ix, Natascia Ventura, Fritz Boege, Hans Reinke,

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Wen-Jian Jiang, Wei-Hong Ren, Xu-Jie Liu, Yan Liu, Fu-Jian Wu, Li-Zhong Sun, Feng Lan, Jie Du, Hong-Jia Zhang,

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Eric R. Lucas, Eyal Privman, Laurent Keller,

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Mayur Choudhary, Jin-dong Ding, Xiaoping Qi, Michael E. Boulton, Pei-Li Yao, Jeffrey M. Peters, Goldis Malek,

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Masaomi Kato, Mohammed Abul Kashem, Chao Cheng,

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Peipei Zhou, Geng Wu, Ping Zhang, Rongyao Xu, Jie Ge, Yu Fu, Yuchao Zhang, Yifei Du, Jinhai Ye, Jie Cheng, Hongbing Jiang,

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Hu Zhou, Fubing Wang, Hao Chen, Qian Tan, Shili Qiu, Shanshan Chen, Wei Jing, Mingxia Yu, Chunzi Liang, Shengwei Ye, Jiancheng Tu,

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Thalia S. Field, Fergus N. Doubal, Wendy Johnson, Ellen Backhouse, Caroline McHutchison, Simon Cox, Janie Corley, Alison Pattie, Alan J. Gow, Susan Shenkin, Vera Cvoro, Zoe Morris, Julie Staals, Mark Bastin, Ian J. Deary, Joanna M. Wardlaw,

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Jeong Yi Choi, Chae Young Hwang, Bora Lee, Seung-Min Lee, Young Jae Bahn, Kwang-Pyo Lee, Moonkyung Kang, Yeon-Soo Kim, Sun-Hee Woo, Jae-Young Lim, Eunhee Kim, Ki-Sun Kwon,

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Robert D. Frisina, Bo Ding, Xiaoxia Zhu, Joseph P. Walton,

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Matthias Dottermusch, Theresa Lakner, Tobias Peyman, Marinella Klein, Gerd Walz, Elke Neumann-Haefelin,

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