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1. Meeting Report: Aging Research and Drug Discovery.

Author

Meron, Esther, Meron, Esther, Thaysen, Maria, Angeli, Suzanne, Antebi, Adam, Barzilai, Nir, Baur, Joseph A, Bekker-Jensen, Simon, Birkisdottir, Maria, Bischof, Evelyne, Bruening, Jens, Brunet, Anne, Buchwalter, Abigail, Cabreiro, Filipe, Cai, Shiqing, Chen, Brian H, Ermolaeva, Maria, Ewald, Collin Y, Ferrucci, Luigi, Florian, Maria Carolina, Fortney, Kristen, Freund, Adam, Georgievskaya, Anastasia, Gladyshev, Vadim N, Glass, David, Golato, Tyler, Gorbunova, Vera, Hoejimakers, Jan, Houtkooper, Riekelt H, Jager, Sibylle, Jaksch, Frank, Janssens, Georges, Jensen, Martin Borch, Kaeberlein, Matt, Karsenty, Gerard, de Keizer, Peter, Kennedy, Brian, Kirkland, James L, Kjaer, Michael, Kroemer, Guido, Lee, Kai-Fu, Lemaitre, Jean-Marc, Liaskos, David, Longo, Valter D, Lu, Yu-Xuan, MacArthur, Michael R, Maier, Andrea B, Manakanatas, Christina, Mitchell, Sarah J, Moskalev, Alexey, Niedernhofer, Laura, Ozerov, Ivan, Partridge, Linda, Passegué, Emmanuelle, Petr, Michael A, Peyer, James, Radenkovic, Dina, Rando, Thomas A, Rattan, Suresh, Riedel, Christian G, Rudolph, Lenhard, Ai, Ruixue, Serrano, Manuel, Schumacher, Björn, Sinclair, David A, Smith, Ryan, Suh, Yousin, Taub, Pam, Trapp, Alexandre, Trendelenburg, Anne-Ulrike, Valenzano, Dario Riccardo, Verburgh, Kris, Verdin, Eric, Vijg, Jan, Westendorp, Rudi GJ, Zonari, Alessandra, Bakula, Daniela, Zhavoronkov, Alex, Scheibye-Knudsen, Morten, Meron, Esther, Meron, Esther, Thaysen, Maria, Angeli, Suzanne, Antebi, Adam, Barzilai, Nir, Baur, Joseph A, Bekker-Jensen, Simon, Birkisdottir, Maria, Bischof, Evelyne, Bruening, Jens, Brunet, Anne, Buchwalter, Abigail, Cabreiro, Filipe, Cai, Shiqing, Chen, Brian H, Ermolaeva, Maria, Ewald, Collin Y, Ferrucci, Luigi, Florian, Maria Carolina, Fortney, Kristen, Freund, Adam, Georgievskaya, Anastasia, Gladyshev, Vadim N, Glass, David, Golato, Tyler, Gorbunova, Vera, Hoejimakers, Jan, Houtkooper, Riekelt H, Jager, Sibylle, Jaksch, Frank, Janssens, Georges, Jensen, Martin Borch, Kaeberlein, Matt, Karsenty, Gerard, de Keizer, Peter, Kennedy, Brian, Kirkland, James L, Kjaer, Michael, Kroemer, Guido, Lee, Kai-Fu, Lemaitre, Jean-Marc, Liaskos, David, Longo, Valter D, Lu, Yu-Xuan, MacArthur, Michael R, Maier, Andrea B, Manakanatas, Christina, Mitchell, Sarah J, Moskalev, Alexey, Niedernhofer, Laura, Ozerov, Ivan, Partridge, Linda, Passegué, Emmanuelle, Petr, Michael A, Peyer, James, Radenkovic, Dina, Rando, Thomas A, Rattan, Suresh, Riedel, Christian G, Rudolph, Lenhard, Ai, Ruixue, Serrano, Manuel, Schumacher, Björn, Sinclair, David A, Smith, Ryan, Suh, Yousin, Taub, Pam, Trapp, Alexandre, Trendelenburg, Anne-Ulrike, Valenzano, Dario Riccardo, Verburgh, Kris, Verdin, Eric, Vijg, Jan, Westendorp, Rudi GJ, Zonari, Alessandra, Bakula, Daniela, Zhavoronkov, Alex, and Scheibye-Knudsen, Morten

Abstract

Aging is the single largest risk factor for most chronic diseases, and thus possesses large socioeconomic interest to continuously aging societies. Consequently, the field of aging research is expanding alongside a growing focus from the industry and investors in aging research. This year's 8th Annual Aging Research and Drug Discovery (ARDD) meeting was organized as a hybrid meeting from August 30th to September 3rd 2021 with more than 130 attendees participating on-site at the Ceremonial Hall at University of Copenhagen, Denmark, and 1800 engaging online. The conference comprised of presentations from 75 speakers focusing on new research in topics including mechanisms of aging and how these can be modulated as well as the use of AI and new standards of practices within aging research. This year, a longevity workshop was included to build stronger connections with the clinical community.

Published
2022

2. Meeting Report:Aging Research and Drug Discovery

Author

Meron, Esther, Thaysen, Maria, Angeli, Suzanne, Antebi, Adam, Barzilai, Nir, Baur, Joseph A., Bekker-Jensen, Simon, Birkisdottir, Maria, Bischof, Evelyne, Bruening, Jens, Brunet, Anne, Buchwalter, Abigail, Cabreiro, Filipe, Cai, Shiqing, Chen, Brian H., Ermolaeva, Maria, Ewald, Collin Y., Ferrucci, Luigi, Florian, Maria Carolina, Fortney, Kristen, Freund, Adam, Georgievskaya, Anastasia, Gladyshev, Vadim N., Glass, David, Golato, Tyler, Gorbunova, Vera, Hoejimakers, Jan, Houtkooper, Riekelt H., Jager, Sibylle, Jaksch, Frank, Janssens, Georges, Jensen, Martin Borch, Kaeberlein, Matt, Karsenty, Gerard, de Keizer, Peter, Kennedy, Brian, Kirkland, James L., Kjaer, Michael, Kroemer, Guido, Lee, Kai Fu, Lemaitre, Jean Marc, Liaskos, David, Longo, Valter D., Lu, Yu Xuan, MacArthur, Michael R., Maier, Andrea B., Manakanatas, Christina, Mitchell, Sarah J., Moskalev, Alexey, Niedernhofer, Laura, Ozerov, Ivan, Partridge, Linda, Passegué, Emmanuelle, Petr, Michael A., Peyer, James, Radenkovic, Dina, Rando, Thomas A., Rattan, Suresh, Riedel, Christian G., Rudolph, Lenhard, Ai, Ruixue, Serrano, Manuel, Schumacher, Björn, Sinclair, David A., Smith, Ryan, Suh, Yousin, Taub, Pam, Trapp, Alexandre, Trendelenburg, Anne Ulrike, Valenzano, Dario Riccardo, Verburgh, Kris, Verdin, Eric, Vijg, Jan, Westendorp, Rudi G.J., Zonari, Alessandra, Bakula, Daniela, Zhavoronkov, Alex, Scheibye-Knudsen, Morten, Meron, Esther, Thaysen, Maria, Angeli, Suzanne, Antebi, Adam, Barzilai, Nir, Baur, Joseph A., Bekker-Jensen, Simon, Birkisdottir, Maria, Bischof, Evelyne, Bruening, Jens, Brunet, Anne, Buchwalter, Abigail, Cabreiro, Filipe, Cai, Shiqing, Chen, Brian H., Ermolaeva, Maria, Ewald, Collin Y., Ferrucci, Luigi, Florian, Maria Carolina, Fortney, Kristen, Freund, Adam, Georgievskaya, Anastasia, Gladyshev, Vadim N., Glass, David, Golato, Tyler, Gorbunova, Vera, Hoejimakers, Jan, Houtkooper, Riekelt H., Jager, Sibylle, Jaksch, Frank, Janssens, Georges, Jensen, Martin Borch, Kaeberlein, Matt, Karsenty, Gerard, de Keizer, Peter, Kennedy, Brian, Kirkland, James L., Kjaer, Michael, Kroemer, Guido, Lee, Kai Fu, Lemaitre, Jean Marc, Liaskos, David, Longo, Valter D., Lu, Yu Xuan, MacArthur, Michael R., Maier, Andrea B., Manakanatas, Christina, Mitchell, Sarah J., Moskalev, Alexey, Niedernhofer, Laura, Ozerov, Ivan, Partridge, Linda, Passegué, Emmanuelle, Petr, Michael A., Peyer, James, Radenkovic, Dina, Rando, Thomas A., Rattan, Suresh, Riedel, Christian G., Rudolph, Lenhard, Ai, Ruixue, Serrano, Manuel, Schumacher, Björn, Sinclair, David A., Smith, Ryan, Suh, Yousin, Taub, Pam, Trapp, Alexandre, Trendelenburg, Anne Ulrike, Valenzano, Dario Riccardo, Verburgh, Kris, Verdin, Eric, Vijg, Jan, Westendorp, Rudi G.J., Zonari, Alessandra, Bakula, Daniela, Zhavoronkov, Alex, and Scheibye-Knudsen, Morten

Abstract

Aging is the single largest risk factor for most chronic diseases, and thus possesses large socioeconomic interest to continuously aging societies. Consequently, the field of aging research is expanding alongside a growing focus from the industry and investors in aging research. This year's 8th Annual Aging Research and Drug Discovery (ARDD) meeting was organized as a hybrid meeting from August 30th to September 3rd 2021 with more than 130 attendees participating on-site at the Ceremonial Hall at University of Copenhagen, Denmark, and 1800 engaging online. The conference comprised of presentations from 75 speakers focusing on new research in topics including mechanisms of aging and how these can be modulated as well as the use of AI and new standards of practices within aging research. This year, a longevity workshop was included to build stronger connections with the clinical community.

Published
2022

3. Meeting Report:Aging Research and Drug Discovery

Author

Meron, Esther, Thaysen, Maria, Angeli, Suzanne, Antebi, Adam, Barzilai, Nir, Baur, Joseph A., Bekker-Jensen, Simon, Birkisdottir, Maria, Bischof, Evelyne, Bruening, Jens, Brunet, Anne, Buchwalter, Abigail, Cabreiro, Filipe, Cai, Shiqing, Chen, Brian H., Ermolaeva, Maria, Ewald, Collin Y., Ferrucci, Luigi, Florian, Maria Carolina, Fortney, Kristen, Freund, Adam, Georgievskaya, Anastasia, Gladyshev, Vadim N., Glass, David, Golato, Tyler, Gorbunova, Vera, Hoejimakers, Jan, Houtkooper, Riekelt H., Jager, Sibylle, Jaksch, Frank, Janssens, Georges, Jensen, Martin Borch, Kaeberlein, Matt, Karsenty, Gerard, de Keizer, Peter, Kennedy, Brian, Kirkland, James L., Kjaer, Michael, Kroemer, Guido, Lee, Kai Fu, Lemaitre, Jean Marc, Liaskos, David, Longo, Valter D., Lu, Yu Xuan, MacArthur, Michael R., Maier, Andrea B., Manakanatas, Christina, Mitchell, Sarah J., Moskalev, Alexey, Niedernhofer, Laura, Ozerov, Ivan, Partridge, Linda, Passegué, Emmanuelle, Petr, Michael A., Peyer, James, Radenkovic, Dina, Rando, Thomas A., Rattan, Suresh, Riedel, Christian G., Rudolph, Lenhard, Ai, Ruixue, Serrano, Manuel, Schumacher, Björn, Sinclair, David A., Smith, Ryan, Suh, Yousin, Taub, Pam, Trapp, Alexandre, Trendelenburg, Anne Ulrike, Valenzano, Dario Riccardo, Verburgh, Kris, Verdin, Eric, Vijg, Jan, Westendorp, Rudi G.J., Zonari, Alessandra, Bakula, Daniela, Zhavoronkov, Alex, Scheibye-Knudsen, Morten, Meron, Esther, Thaysen, Maria, Angeli, Suzanne, Antebi, Adam, Barzilai, Nir, Baur, Joseph A., Bekker-Jensen, Simon, Birkisdottir, Maria, Bischof, Evelyne, Bruening, Jens, Brunet, Anne, Buchwalter, Abigail, Cabreiro, Filipe, Cai, Shiqing, Chen, Brian H., Ermolaeva, Maria, Ewald, Collin Y., Ferrucci, Luigi, Florian, Maria Carolina, Fortney, Kristen, Freund, Adam, Georgievskaya, Anastasia, Gladyshev, Vadim N., Glass, David, Golato, Tyler, Gorbunova, Vera, Hoejimakers, Jan, Houtkooper, Riekelt H., Jager, Sibylle, Jaksch, Frank, Janssens, Georges, Jensen, Martin Borch, Kaeberlein, Matt, Karsenty, Gerard, de Keizer, Peter, Kennedy, Brian, Kirkland, James L., Kjaer, Michael, Kroemer, Guido, Lee, Kai Fu, Lemaitre, Jean Marc, Liaskos, David, Longo, Valter D., Lu, Yu Xuan, MacArthur, Michael R., Maier, Andrea B., Manakanatas, Christina, Mitchell, Sarah J., Moskalev, Alexey, Niedernhofer, Laura, Ozerov, Ivan, Partridge, Linda, Passegué, Emmanuelle, Petr, Michael A., Peyer, James, Radenkovic, Dina, Rando, Thomas A., Rattan, Suresh, Riedel, Christian G., Rudolph, Lenhard, Ai, Ruixue, Serrano, Manuel, Schumacher, Björn, Sinclair, David A., Smith, Ryan, Suh, Yousin, Taub, Pam, Trapp, Alexandre, Trendelenburg, Anne Ulrike, Valenzano, Dario Riccardo, Verburgh, Kris, Verdin, Eric, Vijg, Jan, Westendorp, Rudi G.J., Zonari, Alessandra, Bakula, Daniela, Zhavoronkov, Alex, and Scheibye-Knudsen, Morten

Abstract

Aging is the single largest risk factor for most chronic diseases, and thus possesses large socioeconomic interest to continuously aging societies. Consequently, the field of aging research is expanding alongside a growing focus from the industry and investors in aging research. This year's 8th Annual Aging Research and Drug Discovery (ARDD) meeting was organized as a hybrid meeting from August 30th to September 3rd 2021 with more than 130 attendees participating on-site at the Ceremonial Hall at University of Copenhagen, Denmark, and 1800 engaging online. The conference comprised of presentations from 75 speakers focusing on new research in topics including mechanisms of aging and how these can be modulated as well as the use of AI and new standards of practices within aging research. This year, a longevity workshop was included to build stronger connections with the clinical community.

Published
2022

4. Meeting Report:Aging Research and Drug Discovery

Author

Meron, Esther, Thaysen, Maria, Angeli, Suzanne, Antebi, Adam, Barzilai, Nir, Baur, Joseph A., Bekker-Jensen, Simon, Birkisdottir, Maria, Bischof, Evelyne, Bruening, Jens, Brunet, Anne, Buchwalter, Abigail, Cabreiro, Filipe, Cai, Shiqing, Chen, Brian H., Ermolaeva, Maria, Ewald, Collin Y., Ferrucci, Luigi, Florian, Maria Carolina, Fortney, Kristen, Freund, Adam, Georgievskaya, Anastasia, Gladyshev, Vadim N., Glass, David, Golato, Tyler, Gorbunova, Vera, Hoejimakers, Jan, Houtkooper, Riekelt H., Jager, Sibylle, Jaksch, Frank, Janssens, Georges, Jensen, Martin Borch, Kaeberlein, Matt, Karsenty, Gerard, de Keizer, Peter, Kennedy, Brian, Kirkland, James L., Kjaer, Michael, Kroemer, Guido, Lee, Kai Fu, Lemaitre, Jean Marc, Liaskos, David, Longo, Valter D., Lu, Yu Xuan, MacArthur, Michael R., Maier, Andrea B., Manakanatas, Christina, Mitchell, Sarah J., Moskalev, Alexey, Niedernhofer, Laura, Ozerov, Ivan, Partridge, Linda, Passegué, Emmanuelle, Petr, Michael A., Peyer, James, Radenkovic, Dina, Rando, Thomas A., Rattan, Suresh, Riedel, Christian G., Rudolph, Lenhard, Ai, Ruixue, Serrano, Manuel, Schumacher, Björn, Sinclair, David A., Smith, Ryan, Suh, Yousin, Taub, Pam, Trapp, Alexandre, Trendelenburg, Anne Ulrike, Valenzano, Dario Riccardo, Verburgh, Kris, Verdin, Eric, Vijg, Jan, Westendorp, Rudi G.J., Zonari, Alessandra, Bakula, Daniela, Zhavoronkov, Alex, Scheibye-Knudsen, Morten, Meron, Esther, Thaysen, Maria, Angeli, Suzanne, Antebi, Adam, Barzilai, Nir, Baur, Joseph A., Bekker-Jensen, Simon, Birkisdottir, Maria, Bischof, Evelyne, Bruening, Jens, Brunet, Anne, Buchwalter, Abigail, Cabreiro, Filipe, Cai, Shiqing, Chen, Brian H., Ermolaeva, Maria, Ewald, Collin Y., Ferrucci, Luigi, Florian, Maria Carolina, Fortney, Kristen, Freund, Adam, Georgievskaya, Anastasia, Gladyshev, Vadim N., Glass, David, Golato, Tyler, Gorbunova, Vera, Hoejimakers, Jan, Houtkooper, Riekelt H., Jager, Sibylle, Jaksch, Frank, Janssens, Georges, Jensen, Martin Borch, Kaeberlein, Matt, Karsenty, Gerard, de Keizer, Peter, Kennedy, Brian, Kirkland, James L., Kjaer, Michael, Kroemer, Guido, Lee, Kai Fu, Lemaitre, Jean Marc, Liaskos, David, Longo, Valter D., Lu, Yu Xuan, MacArthur, Michael R., Maier, Andrea B., Manakanatas, Christina, Mitchell, Sarah J., Moskalev, Alexey, Niedernhofer, Laura, Ozerov, Ivan, Partridge, Linda, Passegué, Emmanuelle, Petr, Michael A., Peyer, James, Radenkovic, Dina, Rando, Thomas A., Rattan, Suresh, Riedel, Christian G., Rudolph, Lenhard, Ai, Ruixue, Serrano, Manuel, Schumacher, Björn, Sinclair, David A., Smith, Ryan, Suh, Yousin, Taub, Pam, Trapp, Alexandre, Trendelenburg, Anne Ulrike, Valenzano, Dario Riccardo, Verburgh, Kris, Verdin, Eric, Vijg, Jan, Westendorp, Rudi G.J., Zonari, Alessandra, Bakula, Daniela, Zhavoronkov, Alex, and Scheibye-Knudsen, Morten

Abstract

Aging is the single largest risk factor for most chronic diseases, and thus possesses large socioeconomic interest to continuously aging societies. Consequently, the field of aging research is expanding alongside a growing focus from the industry and investors in aging research. This year’s 8th Annual Aging Research and Drug Discovery (ARDD) meeting was organized as a hybrid meeting from August 30th to September 3rd 2021 with more than 130 attendees participating on-site at the Ceremonial Hall at University of Copenhagen, Denmark, and 1800 engaging online. The conference comprised of presentations from 75 speakers focusing on new research in topics including mechanisms of aging and how these can be modulated as well as the use of AI and new standards of practices within aging research. This year, a longevity workshop was included to build stronger connections with the clinical community.

Published
2022

5. Age-related telomere attrition causes aberrant gene expression in sub-telomeric regions.

Author

Dong, Xiao, Dong, Xiao, Sun, Shixiang, Zhang, Lei, Kim, Seungsoo, Tu, Zhidong, Montagna, Cristina, Maslov, Alexander Y, Suh, Yousin, Wang, Tao, Campisi, Judith, Vijg, Jan, Dong, Xiao, Dong, Xiao, Sun, Shixiang, Zhang, Lei, Kim, Seungsoo, Tu, Zhidong, Montagna, Cristina, Maslov, Alexander Y, Suh, Yousin, Wang, Tao, Campisi, Judith, and Vijg, Jan

Abstract

Telomere attrition has been proposed as a biomarker and causal factor in aging. In addition to causing cellular senescence and apoptosis, telomere shortening has been found to affect gene expression in subtelomeric regions. Here, we analyzed the distribution of age-related differentially expressed genes from the GTEx RNA sequencing database of 54 tissue types from 979 human subjects and found significantly more upregulated than downregulated genes in subtelomeric regions as compared to the genome-wide average. Our data demonstrate spatial relationships between telomeres and gene expression in aging.

Published
2021

6. The central role of DNA damage in the ageing process

Author

Schumacher, Bjoern, Pothof, Joris, Vijg, Jan, Hoeijmakers, Jan H. J., Schumacher, Bjoern, Pothof, Joris, Vijg, Jan, and Hoeijmakers, Jan H. J.

Abstract

Ageing is a complex, multifaceted process leading to widespread functional decline that affects every organ and tissue, but it remains unknown whether ageing has a unifying causal mechanism or is grounded in multiple sources. Phenotypically, the ageing process is associated with a wide variety of features at the molecular, cellular and physiological level-for example, genomic and epigenomic alterations, loss of proteostasis, declining overall cellular and subcellular function and deregulation of signalling systems. However, the relative importance, mechanistic interrelationships and hierarchical order of these features of ageing have not been clarified. Here we synthesize accumulating evidence that DNA damage affects most, if not all, aspects of the ageing phenotype, making it a potentially unifying cause of ageing. Targeting DNA damage and its mechanistic links with the ageing phenotype will provide a logical rationale for developing unified interventions to counteract age-related dysfunction and disease. This Review examines the evidence showing that DNA damage is associated with ageing phenotypes, suggesting that it may have a central role as the cause of ageing.

Published
2021

7. Age-related telomere attrition causes aberrant gene expression in sub-telomeric regions.

Author

Dong, Xiao, Dong, Xiao, Sun, Shixiang, Zhang, Lei, Kim, Seungsoo, Tu, Zhidong, Montagna, Cristina, Maslov, Alexander Y, Suh, Yousin, Wang, Tao, Campisi, Judith, Vijg, Jan, Dong, Xiao, Dong, Xiao, Sun, Shixiang, Zhang, Lei, Kim, Seungsoo, Tu, Zhidong, Montagna, Cristina, Maslov, Alexander Y, Suh, Yousin, Wang, Tao, Campisi, Judith, and Vijg, Jan

Abstract

Telomere attrition has been proposed as a biomarker and causal factor in aging. In addition to causing cellular senescence and apoptosis, telomere shortening has been found to affect gene expression in subtelomeric regions. Here, we analyzed the distribution of age-related differentially expressed genes from the GTEx RNA sequencing database of 54 tissue types from 979 human subjects and found significantly more upregulated than downregulated genes in subtelomeric regions as compared to the genome-wide average. Our data demonstrate spatial relationships between telomeres and gene expression in aging.

Published
2021

8. The central role of DNA damage in the ageing process

Author

Schumacher, Bjoern, Pothof, Joris, Vijg, Jan, Hoeijmakers, Jan H. J., Schumacher, Bjoern, Pothof, Joris, Vijg, Jan, and Hoeijmakers, Jan H. J.

Abstract

Ageing is a complex, multifaceted process leading to widespread functional decline that affects every organ and tissue, but it remains unknown whether ageing has a unifying causal mechanism or is grounded in multiple sources. Phenotypically, the ageing process is associated with a wide variety of features at the molecular, cellular and physiological level-for example, genomic and epigenomic alterations, loss of proteostasis, declining overall cellular and subcellular function and deregulation of signalling systems. However, the relative importance, mechanistic interrelationships and hierarchical order of these features of ageing have not been clarified. Here we synthesize accumulating evidence that DNA damage affects most, if not all, aspects of the ageing phenotype, making it a potentially unifying cause of ageing. Targeting DNA damage and its mechanistic links with the ageing phenotype will provide a logical rationale for developing unified interventions to counteract age-related dysfunction and disease. This Review examines the evidence showing that DNA damage is associated with ageing phenotypes, suggesting that it may have a central role as the cause of ageing.

Published
2021

9. ARDD 2020: from aging mechanisms to interventions.

Author

Mkrtchyan, Garik V, Mkrtchyan, Garik V, Abdelmohsen, Kotb, Andreux, Pénélope, Bagdonaite, Ieva, Barzilai, Nir, Brunak, Søren, Cabreiro, Filipe, de Cabo, Rafael, Campisi, Judith, Cuervo, Ana Maria, Demaria, Marco, Ewald, Collin Y, Fang, Evandro Fei, Faragher, Richard, Ferrucci, Luigi, Freund, Adam, Silva-García, Carlos G, Georgievskaya, Anastasia, Gladyshev, Vadim N, Glass, David J, Gorbunova, Vera, de Grey, Aubrey, He, Wei-Wu, Hoeijmakers, Jan, Hoffmann, Eva, Horvath, Steve, Houtkooper, Riekelt H, Jensen, Majken K, Jensen, Martin Borch, Kane, Alice, Kassem, Moustapha, de Keizer, Peter, Kennedy, Brian, Karsenty, Gerard, Lamming, Dudley W, Lee, Kai-Fu, MacAulay, Nanna, Mamoshina, Polina, Mellon, Jim, Molenaars, Marte, Moskalev, Alexey, Mund, Andreas, Niedernhofer, Laura, Osborne, Brenna, Pak, Heidi H, Parkhitko, Andrey, Raimundo, Nuno, Rando, Thomas A, Rasmussen, Lene Juel, Reis, Carolina, Riedel, Christian G, Franco-Romero, Anais, Schumacher, Björn, Sinclair, David A, Suh, Yousin, Taub, Pam R, Toiber, Debra, Treebak, Jonas T, Valenzano, Dario Riccardo, Verdin, Eric, Vijg, Jan, Young, Sergey, Zhang, Lei, Bakula, Daniela, Zhavoronkov, Alex, Scheibye-Knudsen, Morten, Mkrtchyan, Garik V, Mkrtchyan, Garik V, Abdelmohsen, Kotb, Andreux, Pénélope, Bagdonaite, Ieva, Barzilai, Nir, Brunak, Søren, Cabreiro, Filipe, de Cabo, Rafael, Campisi, Judith, Cuervo, Ana Maria, Demaria, Marco, Ewald, Collin Y, Fang, Evandro Fei, Faragher, Richard, Ferrucci, Luigi, Freund, Adam, Silva-García, Carlos G, Georgievskaya, Anastasia, Gladyshev, Vadim N, Glass, David J, Gorbunova, Vera, de Grey, Aubrey, He, Wei-Wu, Hoeijmakers, Jan, Hoffmann, Eva, Horvath, Steve, Houtkooper, Riekelt H, Jensen, Majken K, Jensen, Martin Borch, Kane, Alice, Kassem, Moustapha, de Keizer, Peter, Kennedy, Brian, Karsenty, Gerard, Lamming, Dudley W, Lee, Kai-Fu, MacAulay, Nanna, Mamoshina, Polina, Mellon, Jim, Molenaars, Marte, Moskalev, Alexey, Mund, Andreas, Niedernhofer, Laura, Osborne, Brenna, Pak, Heidi H, Parkhitko, Andrey, Raimundo, Nuno, Rando, Thomas A, Rasmussen, Lene Juel, Reis, Carolina, Riedel, Christian G, Franco-Romero, Anais, Schumacher, Björn, Sinclair, David A, Suh, Yousin, Taub, Pam R, Toiber, Debra, Treebak, Jonas T, Valenzano, Dario Riccardo, Verdin, Eric, Vijg, Jan, Young, Sergey, Zhang, Lei, Bakula, Daniela, Zhavoronkov, Alex, and Scheibye-Knudsen, Morten

Abstract

Aging is emerging as a druggable target with growing interest from academia, industry and investors. New technologies such as artificial intelligence and advanced screening techniques, as well as a strong influence from the industry sector may lead to novel discoveries to treat age-related diseases. The present review summarizes presentations from the 7th Annual Aging Research and Drug Discovery (ARDD) meeting, held online on the 1st to 4th of September 2020. The meeting covered topics related to new methodologies to study aging, knowledge about basic mechanisms of longevity, latest interventional strategies to target the aging process as well as discussions about the impact of aging research on society and economy. More than 2000 participants and 65 speakers joined the meeting and we already look forward to an even larger meeting next year. Please mark your calendars for the 8th ARDD meeting that is scheduled for the 31st of August to 3rd of September, 2021, at Columbia University, USA.

Published
2020

10. ARDD 2020: from aging mechanisms to interventions.

Author

Mkrtchyan, Garik V, Mkrtchyan, Garik V, Abdelmohsen, Kotb, Andreux, Pénélope, Bagdonaite, Ieva, Barzilai, Nir, Brunak, Søren, Cabreiro, Filipe, de Cabo, Rafael, Campisi, Judith, Cuervo, Ana Maria, Demaria, Marco, Ewald, Collin Y, Fang, Evandro Fei, Faragher, Richard, Ferrucci, Luigi, Freund, Adam, Silva-García, Carlos G, Georgievskaya, Anastasia, Gladyshev, Vadim N, Glass, David J, Gorbunova, Vera, de Grey, Aubrey, He, Wei-Wu, Hoeijmakers, Jan, Hoffmann, Eva, Horvath, Steve, Houtkooper, Riekelt H, Jensen, Majken K, Jensen, Martin Borch, Kane, Alice, Kassem, Moustapha, de Keizer, Peter, Kennedy, Brian, Karsenty, Gerard, Lamming, Dudley W, Lee, Kai-Fu, MacAulay, Nanna, Mamoshina, Polina, Mellon, Jim, Molenaars, Marte, Moskalev, Alexey, Mund, Andreas, Niedernhofer, Laura, Osborne, Brenna, Pak, Heidi H, Parkhitko, Andrey, Raimundo, Nuno, Rando, Thomas A, Rasmussen, Lene Juel, Reis, Carolina, Riedel, Christian G, Franco-Romero, Anais, Schumacher, Björn, Sinclair, David A, Suh, Yousin, Taub, Pam R, Toiber, Debra, Treebak, Jonas T, Valenzano, Dario Riccardo, Verdin, Eric, Vijg, Jan, Young, Sergey, Zhang, Lei, Bakula, Daniela, Zhavoronkov, Alex, Scheibye-Knudsen, Morten, Mkrtchyan, Garik V, Mkrtchyan, Garik V, Abdelmohsen, Kotb, Andreux, Pénélope, Bagdonaite, Ieva, Barzilai, Nir, Brunak, Søren, Cabreiro, Filipe, de Cabo, Rafael, Campisi, Judith, Cuervo, Ana Maria, Demaria, Marco, Ewald, Collin Y, Fang, Evandro Fei, Faragher, Richard, Ferrucci, Luigi, Freund, Adam, Silva-García, Carlos G, Georgievskaya, Anastasia, Gladyshev, Vadim N, Glass, David J, Gorbunova, Vera, de Grey, Aubrey, He, Wei-Wu, Hoeijmakers, Jan, Hoffmann, Eva, Horvath, Steve, Houtkooper, Riekelt H, Jensen, Majken K, Jensen, Martin Borch, Kane, Alice, Kassem, Moustapha, de Keizer, Peter, Kennedy, Brian, Karsenty, Gerard, Lamming, Dudley W, Lee, Kai-Fu, MacAulay, Nanna, Mamoshina, Polina, Mellon, Jim, Molenaars, Marte, Moskalev, Alexey, Mund, Andreas, Niedernhofer, Laura, Osborne, Brenna, Pak, Heidi H, Parkhitko, Andrey, Raimundo, Nuno, Rando, Thomas A, Rasmussen, Lene Juel, Reis, Carolina, Riedel, Christian G, Franco-Romero, Anais, Schumacher, Björn, Sinclair, David A, Suh, Yousin, Taub, Pam R, Toiber, Debra, Treebak, Jonas T, Valenzano, Dario Riccardo, Verdin, Eric, Vijg, Jan, Young, Sergey, Zhang, Lei, Bakula, Daniela, Zhavoronkov, Alex, and Scheibye-Knudsen, Morten

Abstract

Aging is emerging as a druggable target with growing interest from academia, industry and investors. New technologies such as artificial intelligence and advanced screening techniques, as well as a strong influence from the industry sector may lead to novel discoveries to treat age-related diseases. The present review summarizes presentations from the 7th Annual Aging Research and Drug Discovery (ARDD) meeting, held online on the 1st to 4th of September 2020. The meeting covered topics related to new methodologies to study aging, knowledge about basic mechanisms of longevity, latest interventional strategies to target the aging process as well as discussions about the impact of aging research on society and economy. More than 2000 participants and 65 speakers joined the meeting and we already look forward to an even larger meeting next year. Please mark your calendars for the 8th ARDD meeting that is scheduled for the 31st of August to 3rd of September, 2021, at Columbia University, USA.

Published
2020

11. A direct comparison of interphase FISH versus low-coverage single cell sequencing to detect aneuploidy reveals respective strengths and weaknesses.

Author

Andriani, Grasiella A, Andriani, Grasiella A, Maggi, Elaine, Piqué, Daniel, Zimmerman, Samuel E, Lee, Moonsook, Quispe-Tintaya, Wilber, Maslov, Alexander, Campisi, Judith, Vijg, Jan, Mar, Jessica C, Montagna, Cristina, Andriani, Grasiella A, Andriani, Grasiella A, Maggi, Elaine, Piqué, Daniel, Zimmerman, Samuel E, Lee, Moonsook, Quispe-Tintaya, Wilber, Maslov, Alexander, Campisi, Judith, Vijg, Jan, Mar, Jessica C, and Montagna, Cristina

Abstract

Aneuploidy has been reported to occur at remarkably high levels in normal somatic tissues using Fluorescence In Situ Hybridization (FISH). Recently, these reports were contradicted by single-cell low-coverage whole genome sequencing (scL-WGS) analyses, which showed aneuploidy frequencies at least an order of magnitude lower. To explain these seemingly contradictory findings, we used both techniques to analyze artificially generated mock aneuploid cells and cells with natural random aneuploidy. Our data indicate that while FISH tended to over-report aneuploidies, a modified 2-probe approach can accurately detect low levels of aneuploidy. Further, scL-WGS tends to underestimate aneuploidy levels, especially in a polyploid background.

Published
2019

12. A direct comparison of interphase FISH versus low-coverage single cell sequencing to detect aneuploidy reveals respective strengths and weaknesses.

Author

Andriani, Grasiella A, Andriani, Grasiella A, Maggi, Elaine, Piqué, Daniel, Zimmerman, Samuel E, Lee, Moonsook, Quispe-Tintaya, Wilber, Maslov, Alexander, Campisi, Judith, Vijg, Jan, Mar, Jessica C, Montagna, Cristina, Andriani, Grasiella A, Andriani, Grasiella A, Maggi, Elaine, Piqué, Daniel, Zimmerman, Samuel E, Lee, Moonsook, Quispe-Tintaya, Wilber, Maslov, Alexander, Campisi, Judith, Vijg, Jan, Mar, Jessica C, and Montagna, Cristina

Abstract

Aneuploidy has been reported to occur at remarkably high levels in normal somatic tissues using Fluorescence In Situ Hybridization (FISH). Recently, these reports were contradicted by single-cell low-coverage whole genome sequencing (scL-WGS) analyses, which showed aneuploidy frequencies at least an order of magnitude lower. To explain these seemingly contradictory findings, we used both techniques to analyze artificially generated mock aneuploid cells and cells with natural random aneuploidy. Our data indicate that while FISH tended to over-report aneuploidies, a modified 2-probe approach can accurately detect low levels of aneuploidy. Further, scL-WGS tends to underestimate aneuploidy levels, especially in a polyploid background.

Published
2019

13. Analysis of individual cells identifies cell-to-cell variability following induction of cellular senescence.

Author

Wiley, Christopher D, Wiley, Christopher D, Flynn, James M, Morrissey, Christapher, Lebofsky, Ronald, Shuga, Joe, Dong, Xiao, Unger, Marc A, Vijg, Jan, Melov, Simon, Campisi, Judith, Wiley, Christopher D, Wiley, Christopher D, Flynn, James M, Morrissey, Christapher, Lebofsky, Ronald, Shuga, Joe, Dong, Xiao, Unger, Marc A, Vijg, Jan, Melov, Simon, and Campisi, Judith

Abstract

Senescent cells play important roles in both physiological and pathological processes, including cancer and aging. In all cases, however, senescent cells comprise only a small fraction of tissues. Senescent phenotypes have been studied largely in relatively homogeneous populations of cultured cells. In vivo, senescent cells are generally identified by a small number of markers, but whether and how these markers vary among individual cells is unknown. We therefore utilized a combination of single-cell isolation and a nanofluidic PCR platform to determine the contributions of individual cells to the overall gene expression profile of senescent human fibroblast populations. Individual senescent cells were surprisingly heterogeneous in their gene expression signatures. This cell-to-cell variability resulted in a loss of correlation among the expression of several senescence-associated genes. Many genes encoding senescence-associated secretory phenotype (SASP) factors, a major contributor to the effects of senescent cells in vivo, showed marked variability with a subset of highly induced genes accounting for the increases observed at the population level. Inflammatory genes in clustered genomic loci showed a greater correlation with senescence compared to nonclustered loci, suggesting that these genes are coregulated by genomic location. Together, these data offer new insights into how genes are regulated in senescent cells and suggest that single markers are inadequate to identify senescent cells in vivo.

Published
2017

14. Analysis of individual cells identifies cell-to-cell variability following induction of cellular senescence.

Author

Wiley, Christopher D, Wiley, Christopher D, Flynn, James M, Morrissey, Christapher, Lebofsky, Ronald, Shuga, Joe, Dong, Xiao, Unger, Marc A, Vijg, Jan, Melov, Simon, Campisi, Judith, Wiley, Christopher D, Wiley, Christopher D, Flynn, James M, Morrissey, Christapher, Lebofsky, Ronald, Shuga, Joe, Dong, Xiao, Unger, Marc A, Vijg, Jan, Melov, Simon, and Campisi, Judith

Abstract

Senescent cells play important roles in both physiological and pathological processes, including cancer and aging. In all cases, however, senescent cells comprise only a small fraction of tissues. Senescent phenotypes have been studied largely in relatively homogeneous populations of cultured cells. In vivo, senescent cells are generally identified by a small number of markers, but whether and how these markers vary among individual cells is unknown. We therefore utilized a combination of single-cell isolation and a nanofluidic PCR platform to determine the contributions of individual cells to the overall gene expression profile of senescent human fibroblast populations. Individual senescent cells were surprisingly heterogeneous in their gene expression signatures. This cell-to-cell variability resulted in a loss of correlation among the expression of several senescence-associated genes. Many genes encoding senescence-associated secretory phenotype (SASP) factors, a major contributor to the effects of senescent cells in vivo, showed marked variability with a subset of highly induced genes accounting for the increases observed at the population level. Inflammatory genes in clustered genomic loci showed a greater correlation with senescence compared to nonclustered loci, suggesting that these genes are coregulated by genomic location. Together, these data offer new insights into how genes are regulated in senescent cells and suggest that single markers are inadequate to identify senescent cells in vivo.

Published
2017

15. Whole Chromosome Instability induces senescence and promotes SASP.

Author

Andriani, Grasiella Angelina, Andriani, Grasiella Angelina, Almeida, Vinnycius Pereira, Faggioli, Francesca, Mauro, Maurizio, Tsai, Wanxia Li, Santambrogio, Laura, Maslov, Alexander, Gadina, Massimo, Campisi, Judith, Vijg, Jan, Montagna, Cristina, Andriani, Grasiella Angelina, Andriani, Grasiella Angelina, Almeida, Vinnycius Pereira, Faggioli, Francesca, Mauro, Maurizio, Tsai, Wanxia Li, Santambrogio, Laura, Maslov, Alexander, Gadina, Massimo, Campisi, Judith, Vijg, Jan, and Montagna, Cristina

Abstract

Age-related accumulation of ploidy changes is associated with decreased expression of genes controlling chromosome segregation and cohesin functions. To determine the consequences of whole chromosome instability (W-CIN) we down-regulated the spindle assembly checkpoint component BUB1 and the mitotic cohesin SMC1A, and used four-color-interphase-FISH coupled with BrdU incorporation and analyses of senescence features to reveal the fate of W-CIN cells. We observed significant correlations between levels of not-diploid cells and senescence-associated features (SAFs). W-CIN induced DNA double strand breaks and elevated oxidative stress, but caused low apoptosis. SAFs of W-CIN cells were remarkably similar to those induced by replicative senescence but occurred in only 13 days versus 4 months. Cultures enriched with not-diploid cells acquired a senescence-associated secretory phenotype (SASP) characterized by IL1B, CXCL8, CCL2, TNF, CCL27 and other pro-inflammatory factors including a novel SASP component CLEC11A. These findings suggest that W-CIN triggers premature senescence, presumably to prevent the propagation of cells with an abnormal DNA content. Cells deviating from diploidy have the ability to communicate with their microenvironment by secretion of an array of signaling factors. Our results suggest that aneuploid cells that accumulate during aging in some mammalian tissues potentially contribute to age-related pathologies and inflammation through SASP secretion.

Published
2016

16. Whole Chromosome Instability induces senescence and promotes SASP.

Author

Andriani, Grasiella Angelina, Andriani, Grasiella Angelina, Almeida, Vinnycius Pereira, Faggioli, Francesca, Mauro, Maurizio, Tsai, Wanxia Li, Santambrogio, Laura, Maslov, Alexander, Gadina, Massimo, Campisi, Judith, Vijg, Jan, Montagna, Cristina, Andriani, Grasiella Angelina, Andriani, Grasiella Angelina, Almeida, Vinnycius Pereira, Faggioli, Francesca, Mauro, Maurizio, Tsai, Wanxia Li, Santambrogio, Laura, Maslov, Alexander, Gadina, Massimo, Campisi, Judith, Vijg, Jan, and Montagna, Cristina

Abstract

Age-related accumulation of ploidy changes is associated with decreased expression of genes controlling chromosome segregation and cohesin functions. To determine the consequences of whole chromosome instability (W-CIN) we down-regulated the spindle assembly checkpoint component BUB1 and the mitotic cohesin SMC1A, and used four-color-interphase-FISH coupled with BrdU incorporation and analyses of senescence features to reveal the fate of W-CIN cells. We observed significant correlations between levels of not-diploid cells and senescence-associated features (SAFs). W-CIN induced DNA double strand breaks and elevated oxidative stress, but caused low apoptosis. SAFs of W-CIN cells were remarkably similar to those induced by replicative senescence but occurred in only 13 days versus 4 months. Cultures enriched with not-diploid cells acquired a senescence-associated secretory phenotype (SASP) characterized by IL1B, CXCL8, CCL2, TNF, CCL27 and other pro-inflammatory factors including a novel SASP component CLEC11A. These findings suggest that W-CIN triggers premature senescence, presumably to prevent the propagation of cells with an abnormal DNA content. Cells deviating from diploidy have the ability to communicate with their microenvironment by secretion of an array of signaling factors. Our results suggest that aneuploid cells that accumulate during aging in some mammalian tissues potentially contribute to age-related pathologies and inflammation through SASP secretion.

Published
2016

17. Controlled induction of DNA double-strand breaks in the mouse liver induces features of tissue ageing

Author

White, Ryan R, Milholland, Brandon, de Bruin, Alain, Curran, Samuel, Laberge, Remi-Martin, van Steeg, Harry, Campisi, Judith, Maslov, Alexander Y, Vijg, Jan, White, Ryan R, Milholland, Brandon, de Bruin, Alain, Curran, Samuel, Laberge, Remi-Martin, van Steeg, Harry, Campisi, Judith, Maslov, Alexander Y, and Vijg, Jan

Abstract

DNA damage has been implicated in ageing, but direct evidence for a causal relationship is lacking, owing to the difficulty of inducing defined DNA lesions in cells and tissues without simultaneously damaging other biomolecules and cellular structures. Here we directly test whether highly toxic DNA double-strand breaks (DSBs) alone can drive an ageing phenotype using an adenovirus-based system based on tetracycline-controlled expression of the SacI restriction enzyme. We deliver the adenovirus to mice and compare molecular and cellular end points in the liver with normally aged animals. Treated, 3-month-old mice display many, but not all signs of normal liver ageing as early as 1 month after treatment, including ageing pathologies, markers of senescence, fused mitochondria and alterations in gene expression profiles. These results, showing that DSBs alone can cause distinct ageing phenotypes in mouse liver, provide new insights in the role of DNA damage as a driver of tissue ageing.

Published
2015

18. Comparative analysis of genome maintenance genes in naked mole rat, mouse, and human

Author

MacRae, Sheila, Zhang, Quanwei, Lemetre, Christophe, Seim, Inge, Calder, Robert, Hoeijmakers, Jan, Suh, Yousin, Gladyshev, Vadim, Seluanov, Andrei, Gorbunova, Vera, Vijg, Jan, Zhang, Zhengdong, MacRae, Sheila, Zhang, Quanwei, Lemetre, Christophe, Seim, Inge, Calder, Robert, Hoeijmakers, Jan, Suh, Yousin, Gladyshev, Vadim, Seluanov, Andrei, Gorbunova, Vera, Vijg, Jan, and Zhang, Zhengdong

Abstract

Genome maintenance (GM) is an essential defense system against aging and cancer, as both are characterized by increased genome instability. Here, we compared the copy number variation and mutation rate of 518 GM-associated genes in the naked mole rat (NMR), mouse, and human genomes. GM genes appeared to be strongly conserved, with copy number variation in only four genes. Interestingly, we found NMR to have a higher copy number of CEBPG, a regulator of DNA repair, and TINF2, a protector of telomere integrity. NMR, as well as human, was also found to have a lower rate of germline nucleotide substitution than the mouse. Together, the data suggest that the long-lived NMR, as well as human, has more robust GM than mouse and identifies new targets for the analysis of the exceptional longevity of the NMR.

Published
2015

19. Controlled induction of DNA double-strand breaks in the mouse liver induces features of tissue ageing

Author

LS Pathobiologie, Tissue Repair, PB TR, Regenerative Medicine, Stem Cells & Cancer, White, Ryan R, Milholland, Brandon, de Bruin, Alain, Curran, Samuel, Laberge, Remi-Martin, van Steeg, Harry, Campisi, Judith, Maslov, Alexander Y, Vijg, Jan, LS Pathobiologie, Tissue Repair, PB TR, Regenerative Medicine, Stem Cells & Cancer, White, Ryan R, Milholland, Brandon, de Bruin, Alain, Curran, Samuel, Laberge, Remi-Martin, van Steeg, Harry, Campisi, Judith, Maslov, Alexander Y, and Vijg, Jan

Published
2015

20. Controlled induction of DNA double-strand breaks in the mouse liver induces features of tissue ageing

Author

LS Pathobiologie, Tissue Repair, PB TR, Regenerative Medicine, Stem Cells & Cancer, White, Ryan R, Milholland, Brandon, de Bruin, Alain, Curran, Samuel, Laberge, Remi-Martin, van Steeg, Harry, Campisi, Judith, Maslov, Alexander Y, Vijg, Jan, LS Pathobiologie, Tissue Repair, PB TR, Regenerative Medicine, Stem Cells & Cancer, White, Ryan R, Milholland, Brandon, de Bruin, Alain, Curran, Samuel, Laberge, Remi-Martin, van Steeg, Harry, Campisi, Judith, Maslov, Alexander Y, and Vijg, Jan

Published
2015

21. Controlled induction of DNA double-strand breaks in the mouse liver induces features of tissue ageing

Author

LS Pathobiologie, Tissue Repair, PB TR, Regenerative Medicine, Stem Cells & Cancer, White, Ryan R, Milholland, Brandon, de Bruin, Alain, Curran, Samuel, Laberge, Remi-Martin, van Steeg, Harry, Campisi, Judith, Maslov, Alexander Y, Vijg, Jan, LS Pathobiologie, Tissue Repair, PB TR, Regenerative Medicine, Stem Cells & Cancer, White, Ryan R, Milholland, Brandon, de Bruin, Alain, Curran, Samuel, Laberge, Remi-Martin, van Steeg, Harry, Campisi, Judith, Maslov, Alexander Y, and Vijg, Jan

Published
2015

22. The progeroid phenotype of Ku80 deficiency is dominant over DNA-PKCS deficiency

Author

Reiling, Erwin, Dollé, Martijn E T, Youssef, Sameh A, Lee, Moonsook, Nagarajah, Bhawani, Roodbergen, Marianne, de With, Piet, de Bruin, Alain, Hoeijmakers, Jan H, Vijg, Jan, van Steeg, Harry, Hasty, Paul, Reiling, Erwin, Dollé, Martijn E T, Youssef, Sameh A, Lee, Moonsook, Nagarajah, Bhawani, Roodbergen, Marianne, de With, Piet, de Bruin, Alain, Hoeijmakers, Jan H, Vijg, Jan, van Steeg, Harry, and Hasty, Paul

Abstract

Ku80 and DNA-PKCS are both involved in the repair of double strand DNA breaks via the nonhomologous end joining (NHEJ) pathway. While ku80-/- mice exhibit a severely reduced lifespan and size, this phenotype is less pronounced in dna-pkcs-/- mice. However, these observations are based on independent studies with varying genetic backgrounds. Here, we generated ku80-/-, dna-pkcs-/- and double knock out mice in a C57Bl6/J*FVB F1 hybrid background and compared their lifespan, end of life pathology and mutation frequency in liver and spleen using a lacZ reporter. Our data confirm that inactivation of Ku80 and DNA-PKCS causes reduced lifespan and bodyweights, which is most severe in ku80-/- mice. All mutant mice exhibited a strong increase in lymphoma incidence as well as other aging-related pathology (skin epidermal and adnexal atrophy, trabacular bone reduction, kidney tubular anisokaryosis, and cortical and medullar atrophy) and severe lymphoid depletion. LacZ mutation frequency analysis did not show strong differences in mutation frequencies between knock out and wild type mice. The ku80-/- mice had the most severe phenotype and the Ku80-mutation was dominant over the DNA-PKCS-mutation. Presumably, the more severe degenerative effect of Ku80 inactivation on lifespan compared to DNA-PKCS inactivation is caused by additional functions of Ku80 or activity of free Ku70 since both Ku80 and DNA-PKCS are essential for NHEJ.

Published
2014

23. An Essential Role for Senescent Cells in Optimal Wound Healing through Secretion of PDGF-AA

Author

PB TR, Tissue Repair, LS Pathobiologie, Demaria, Marco, Ohtani, Naoko, Youssef Hassan, Sameh, Rodier, Francis, Toussaint, Wendy, Mitchell, James R, Laberge, Remi-Martin, Vijg, Jan, Van Steeg, Harry, Dollé, Martijn E T, Hoeijmakers, Jan H J, de Bruin, Alain, Hara, Eiji, Campisi, Judith, PB TR, Tissue Repair, LS Pathobiologie, Demaria, Marco, Ohtani, Naoko, Youssef Hassan, Sameh, Rodier, Francis, Toussaint, Wendy, Mitchell, James R, Laberge, Remi-Martin, Vijg, Jan, Van Steeg, Harry, Dollé, Martijn E T, Hoeijmakers, Jan H J, de Bruin, Alain, Hara, Eiji, and Campisi, Judith

Published
2014

24. The progeroid phenotype of Ku80 deficiency is dominant over DNA-PKCS deficiency

Author

LS Pathobiologie, PB TR, Tissue Repair, Reiling, Erwin, Dollé, Martijn E T, Youssef, Sameh A, Lee, Moonsook, Nagarajah, Bhawani, Roodbergen, Marianne, de With, Piet, de Bruin, Alain, Hoeijmakers, Jan H, Vijg, Jan, van Steeg, Harry, Hasty, Paul, LS Pathobiologie, PB TR, Tissue Repair, Reiling, Erwin, Dollé, Martijn E T, Youssef, Sameh A, Lee, Moonsook, Nagarajah, Bhawani, Roodbergen, Marianne, de With, Piet, de Bruin, Alain, Hoeijmakers, Jan H, Vijg, Jan, van Steeg, Harry, and Hasty, Paul

Published
2014

25. An Essential Role for Senescent Cells in Optimal Wound Healing through Secretion of PDGF-AA

Author

PB TR, Tissue Repair, LS Pathobiologie, Demaria, Marco, Ohtani, Naoko, Youssef Hassan, Sameh, Rodier, Francis, Toussaint, Wendy, Mitchell, James R, Laberge, Remi-Martin, Vijg, Jan, Van Steeg, Harry, Dollé, Martijn E T, Hoeijmakers, Jan H J, de Bruin, Alain, Hara, Eiji, Campisi, Judith, PB TR, Tissue Repair, LS Pathobiologie, Demaria, Marco, Ohtani, Naoko, Youssef Hassan, Sameh, Rodier, Francis, Toussaint, Wendy, Mitchell, James R, Laberge, Remi-Martin, Vijg, Jan, Van Steeg, Harry, Dollé, Martijn E T, Hoeijmakers, Jan H J, de Bruin, Alain, Hara, Eiji, and Campisi, Judith

Published
2014

26. The progeroid phenotype of Ku80 deficiency is dominant over DNA-PKCS deficiency

Author

LS Pathobiologie, PB TR, Tissue Repair, Reiling, Erwin, Dollé, Martijn E T, Youssef, Sameh A, Lee, Moonsook, Nagarajah, Bhawani, Roodbergen, Marianne, de With, Piet, de Bruin, Alain, Hoeijmakers, Jan H, Vijg, Jan, van Steeg, Harry, Hasty, Paul, LS Pathobiologie, PB TR, Tissue Repair, Reiling, Erwin, Dollé, Martijn E T, Youssef, Sameh A, Lee, Moonsook, Nagarajah, Bhawani, Roodbergen, Marianne, de With, Piet, de Bruin, Alain, Hoeijmakers, Jan H, Vijg, Jan, van Steeg, Harry, and Hasty, Paul

Published
2014

27. The progeroid phenotype of Ku80 deficiency is dominant over DNA-PKCS deficiency

Author

LS Pathobiologie, PB TR, Tissue Repair, Reiling, Erwin, Dollé, Martijn E T, Youssef, Sameh A, Lee, Moonsook, Nagarajah, Bhawani, Roodbergen, Marianne, de With, Piet, de Bruin, Alain, Hoeijmakers, Jan H, Vijg, Jan, van Steeg, Harry, Hasty, Paul, LS Pathobiologie, PB TR, Tissue Repair, Reiling, Erwin, Dollé, Martijn E T, Youssef, Sameh A, Lee, Moonsook, Nagarajah, Bhawani, Roodbergen, Marianne, de With, Piet, de Bruin, Alain, Hoeijmakers, Jan H, Vijg, Jan, van Steeg, Harry, and Hasty, Paul

Published
2014

28. An Essential Role for Senescent Cells in Optimal Wound Healing through Secretion of PDGF-AA

Author

PB TR, Tissue Repair, LS Pathobiologie, Demaria, Marco, Ohtani, Naoko, Youssef Hassan, Sameh, Rodier, Francis, Toussaint, Wendy, Mitchell, James R, Laberge, Remi-Martin, Vijg, Jan, Van Steeg, Harry, Dollé, Martijn E T, Hoeijmakers, Jan H J, de Bruin, Alain, Hara, Eiji, Campisi, Judith, PB TR, Tissue Repair, LS Pathobiologie, Demaria, Marco, Ohtani, Naoko, Youssef Hassan, Sameh, Rodier, Francis, Toussaint, Wendy, Mitchell, James R, Laberge, Remi-Martin, Vijg, Jan, Van Steeg, Harry, Dollé, Martijn E T, Hoeijmakers, Jan H J, de Bruin, Alain, Hara, Eiji, and Campisi, Judith

Published
2014

29. Impact papers on aging in 2009.

Author

Blagosklonny, Mikhail V, Blagosklonny, Mikhail V, Campisi, Judy, Sinclair, David A, Bartke, Andrzej, Blasco, Maria A, Bonner, William M, Bohr, Vilhelm A, Brosh, Robert M, Brunet, Anne, Depinho, Ronald A, Donehower, Lawrence A, Finch, Caleb E, Finkel, Toren, Gorospe, Myriam, Gudkov, Andrei V, Hall, Michael N, Hekimi, Siegfried, Helfand, Stephen L, Karlseder, Jan, Kenyon, Cynthia, Kroemer, Guido, Longo, Valter, Nussenzweig, Andre, Osiewacz, Heinz D, Peeper, Daniel S, Rando, Thomas A, Rudolph, K Lenhard, Sassone-Corsi, Paolo, Serrano, Manuel, Sharpless, Norman E, Skulachev, Vladimir P, Tilly, Jonathan L, Tower, John, Verdin, Eric, Vijg, Jan, Blagosklonny, Mikhail V, Blagosklonny, Mikhail V, Campisi, Judy, Sinclair, David A, Bartke, Andrzej, Blasco, Maria A, Bonner, William M, Bohr, Vilhelm A, Brosh, Robert M, Brunet, Anne, Depinho, Ronald A, Donehower, Lawrence A, Finch, Caleb E, Finkel, Toren, Gorospe, Myriam, Gudkov, Andrei V, Hall, Michael N, Hekimi, Siegfried, Helfand, Stephen L, Karlseder, Jan, Kenyon, Cynthia, Kroemer, Guido, Longo, Valter, Nussenzweig, Andre, Osiewacz, Heinz D, Peeper, Daniel S, Rando, Thomas A, Rudolph, K Lenhard, Sassone-Corsi, Paolo, Serrano, Manuel, Sharpless, Norman E, Skulachev, Vladimir P, Tilly, Jonathan L, Tower, John, Verdin, Eric, and Vijg, Jan

Abstract

The Editorial Board of Aging reviews research papers published in 2009, which they believe have or will have significant impact on aging research. Among many others, the topics include genes that accelerate aging or in contrast promote longevity in model organisms, DNA damage responses and telomeres, molecular mechanisms of life span extension by calorie restriction and pharmacological interventions into aging. The emerging message in 2009 is that aging is not random but determined by a genetically-regulated longevity network and can be decelerated both genetically and pharmacologically.

Published
2010

30. Impact papers on aging in 2009.

Author

Blagosklonny, Mikhail V, Blagosklonny, Mikhail V, Campisi, Judy, Sinclair, David A, Bartke, Andrzej, Blasco, Maria A, Bonner, William M, Bohr, Vilhelm A, Brosh, Robert M, Brunet, Anne, Depinho, Ronald A, Donehower, Lawrence A, Finch, Caleb E, Finkel, Toren, Gorospe, Myriam, Gudkov, Andrei V, Hall, Michael N, Hekimi, Siegfried, Helfand, Stephen L, Karlseder, Jan, Kenyon, Cynthia, Kroemer, Guido, Longo, Valter, Nussenzweig, Andre, Osiewacz, Heinz D, Peeper, Daniel S, Rando, Thomas A, Rudolph, K Lenhard, Sassone-Corsi, Paolo, Serrano, Manuel, Sharpless, Norman E, Skulachev, Vladimir P, Tilly, Jonathan L, Tower, John, Verdin, Eric, Vijg, Jan, Blagosklonny, Mikhail V, Blagosklonny, Mikhail V, Campisi, Judy, Sinclair, David A, Bartke, Andrzej, Blasco, Maria A, Bonner, William M, Bohr, Vilhelm A, Brosh, Robert M, Brunet, Anne, Depinho, Ronald A, Donehower, Lawrence A, Finch, Caleb E, Finkel, Toren, Gorospe, Myriam, Gudkov, Andrei V, Hall, Michael N, Hekimi, Siegfried, Helfand, Stephen L, Karlseder, Jan, Kenyon, Cynthia, Kroemer, Guido, Longo, Valter, Nussenzweig, Andre, Osiewacz, Heinz D, Peeper, Daniel S, Rando, Thomas A, Rudolph, K Lenhard, Sassone-Corsi, Paolo, Serrano, Manuel, Sharpless, Norman E, Skulachev, Vladimir P, Tilly, Jonathan L, Tower, John, Verdin, Eric, and Vijg, Jan

Abstract

The Editorial Board of Aging reviews research papers published in 2009, which they believe have or will have significant impact on aging research. Among many others, the topics include genes that accelerate aging or in contrast promote longevity in model organisms, DNA damage responses and telomeres, molecular mechanisms of life span extension by calorie restriction and pharmacological interventions into aging. The emerging message in 2009 is that aging is not random but determined by a genetically-regulated longevity network and can be decelerated both genetically and pharmacologically.

Published
2010

31. Impact papers on aging in 2009

Author

Blagosklonny, Mikhail V., Campisi, Judy, Sinclair, David A., Bartke, Andrzej, Blasco, Maria A., Bonner, William M., Bohr, Vilhelm A., Brosh, Robert M., Brunet, Anne, DePinho, Ronald A., Donehower, Lawrence A., Finch, Caleb E., Finkel, Toren, Gorospe, Myriam, Gudkov, Andrei V., Hall, Michael N., Hekimi, Siegfried, Helfand, Stephen L., Karlseder, Jan, Kenyon, Cynthia, Kroemer, Guido, Longo, Valter, Nussenzweig, Andre, Osiewacz, Heinz D., Peeper, Daniel S., Rando, Thomas A., Rudolph, K. Lenhard, Sassone-Corsi, Paolo, Serrano, Manuel, Sharpless, Norman E., Skulachev, Vladimir P., Tilly, Jonathan L., Tower, John, Verdin, Eric, Vijg, Jan, Blagosklonny, Mikhail V., Campisi, Judy, Sinclair, David A., Bartke, Andrzej, Blasco, Maria A., Bonner, William M., Bohr, Vilhelm A., Brosh, Robert M., Brunet, Anne, DePinho, Ronald A., Donehower, Lawrence A., Finch, Caleb E., Finkel, Toren, Gorospe, Myriam, Gudkov, Andrei V., Hall, Michael N., Hekimi, Siegfried, Helfand, Stephen L., Karlseder, Jan, Kenyon, Cynthia, Kroemer, Guido, Longo, Valter, Nussenzweig, Andre, Osiewacz, Heinz D., Peeper, Daniel S., Rando, Thomas A., Rudolph, K. Lenhard, Sassone-Corsi, Paolo, Serrano, Manuel, Sharpless, Norman E., Skulachev, Vladimir P., Tilly, Jonathan L., Tower, John, Verdin, Eric, and Vijg, Jan

Abstract

The editorial board of Aging reviews research papers published in 2009,which they believe have or will have a significant impact on aging research.Among many others, the topics include genes that accelerate aging or incontrast promote longevity in model organisms, DNA damage responsesand telomeres, molecular mechanisms of life span extension by calorierestriction and pharmacologic interventions into aging. The emergingmessage in 2009 is that aging is not random but determined by agenetically-regulated longevity network and can be decelerated bothgenetically and pharmacologically.

Published
2010

32. Impact papers on aging in 2009

Author

Blagosklonny, Mikhail V, Campisi, Judy, Sinclair, David A, Bartke, Andrzej, Blasco, Maria A, Bonner, William M, Bohr, Vilhelm A, Brosh, Robert M, Brunet, Anne, Depinho, Ronald A, Donehower, Lawrence A, Finch, Caleb E, Finkel, Toren, Gorospe, Myriam, Gudkov, Andrei V, Hall, Michael N, Hekimi, Siegfried, Helfand, Stephen L, Karlseder, Jan, Kenyon, Cynthia, Kroemer, Guido, Longo, Valter, Nussenzweig, Andre, Osiewacz, Heinz D, Peeper, Daniel S, Rando, Thomas A, Rudolph, K Lenhard, Sassone-Corsi, Paolo, Serrano, Manuel, Sharpless, Norman E, Skulachev, Vladimir P, Tilly, Jonathan L, Tower, John, Verdin, Eric, Vijg, Jan, Blagosklonny, Mikhail V, Campisi, Judy, Sinclair, David A, Bartke, Andrzej, Blasco, Maria A, Bonner, William M, Bohr, Vilhelm A, Brosh, Robert M, Brunet, Anne, Depinho, Ronald A, Donehower, Lawrence A, Finch, Caleb E, Finkel, Toren, Gorospe, Myriam, Gudkov, Andrei V, Hall, Michael N, Hekimi, Siegfried, Helfand, Stephen L, Karlseder, Jan, Kenyon, Cynthia, Kroemer, Guido, Longo, Valter, Nussenzweig, Andre, Osiewacz, Heinz D, Peeper, Daniel S, Rando, Thomas A, Rudolph, K Lenhard, Sassone-Corsi, Paolo, Serrano, Manuel, Sharpless, Norman E, Skulachev, Vladimir P, Tilly, Jonathan L, Tower, John, Verdin, Eric, and Vijg, Jan

Abstract

The Editorial Board of Aging reviews research papers published in 2009, which they believe have or will have significant impact on aging research. Among many others, the topics include genes that accelerate aging or in contrast promote longevity in model organisms, DNA damage responses and telomeres, molecular mechanisms of life span extension by calorie restriction and pharmacological interventions into aging. The emerging message in 2009 is that aging is not random but determined by a genetically-regulated longevity network and can be decelerated both genetically and pharmacologically.

Published
2010

33. Impact papers on aging in 2009

Author

Blagosklonny, Mikhail V, Campisi, Judy, Sinclair, David A, Bartke, Andrzej, Blasco, Maria A, Bonner, William M, Bohr, Vilhelm A, Brosh, Robert M, Brunet, Anne, Depinho, Ronald A, Donehower, Lawrence A, Finch, Caleb E, Finkel, Toren, Gorospe, Myriam, Gudkov, Andrei V, Hall, Michael N, Hekimi, Siegfried, Helfand, Stephen L, Karlseder, Jan, Kenyon, Cynthia, Kroemer, Guido, Longo, Valter, Nussenzweig, Andre, Osiewacz, Heinz D, Peeper, Daniel S, Rando, Thomas A, Rudolph, K Lenhard, Sassone-Corsi, Paolo, Serrano, Manuel, Sharpless, Norman E, Skulachev, Vladimir P, Tilly, Jonathan L, Tower, John, Verdin, Eric, Vijg, Jan, Blagosklonny, Mikhail V, Campisi, Judy, Sinclair, David A, Bartke, Andrzej, Blasco, Maria A, Bonner, William M, Bohr, Vilhelm A, Brosh, Robert M, Brunet, Anne, Depinho, Ronald A, Donehower, Lawrence A, Finch, Caleb E, Finkel, Toren, Gorospe, Myriam, Gudkov, Andrei V, Hall, Michael N, Hekimi, Siegfried, Helfand, Stephen L, Karlseder, Jan, Kenyon, Cynthia, Kroemer, Guido, Longo, Valter, Nussenzweig, Andre, Osiewacz, Heinz D, Peeper, Daniel S, Rando, Thomas A, Rudolph, K Lenhard, Sassone-Corsi, Paolo, Serrano, Manuel, Sharpless, Norman E, Skulachev, Vladimir P, Tilly, Jonathan L, Tower, John, Verdin, Eric, and Vijg, Jan

Abstract

The Editorial Board of Aging reviews research papers published in 2009, which they believe have or will have significant impact on aging research. Among many others, the topics include genes that accelerate aging or in contrast promote longevity in model organisms, DNA damage responses and telomeres, molecular mechanisms of life span extension by calorie restriction and pharmacological interventions into aging. The emerging message in 2009 is that aging is not random but determined by a genetically-regulated longevity network and can be decelerated both genetically and pharmacologically.

Published
2010

34. Identity and Paternity Testing of Cattle:Application of a Deoxyribonucleic Acid Profiling Protocol

Author

Trommelen, Gerjan J.M., Den Daas, Nanke H.G., Vijg, Jan, Uitterlinden, André G., Trommelen, Gerjan J.M., Den Daas, Nanke H.G., Vijg, Jan, and Uitterlinden, André G.

Abstract

We have applied DNA profiling for identity and parentage studies of cattle using a standardized procedure based on synthetic micro- and minisatellite multilocus core probes in Southern blot hybridization assays. This protocol is useful for paternity analysis of cattle and for real case work (e.g., identity and paternity disputes).

Published
1993

35. The Caenorhabditis eleguns genome contains monomorphic minisatellites and simple sequences

Author

Uitterlinden, André G., Slagboom, P. Eline, Johnson, Thomas E., Vijg, Jan, Uitterlinden, André G., Slagboom, P. Eline, Johnson, Thomas E., and Vijg, Jan

Abstract

Many species have been shown to contain tandemly repeated short sequence DNA kinown as minisatellites and simple sequence motifs. Due to allelic variation in the copy number of the repeat unit these loci are usually highly polymorphic. Here we demonstrate the presence of sequences in the genome of the nematode Caenorhabditis elegans which are homologous to two sets of short sequence DNA. However, when two independent strains were compared no polymorphism for these sequences could be detected.

Published
1989

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