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The Max Planck Institute for Biology of Ageing, founded in 2008, is one of over 80 independent, non-profit-making institutes set up under the umbrella of the Max Planck Society. The overall research aim is to obtain fundamental insights into the aging process and thus to pave the way towards healthier aging in humans. An international research team drawn from almost 30 nations is working to uncover underlying molecular, physiological and evolutionary mechanisms.Located on the campus of Cologne University Hospital, this MPI forms a substantial part of a regional Life Science Cluster of closely interlinked research organizations focusing on research into ageing and ageing-associated diseases. Regional partners include the MPI for Neurological Research and the Cluster of Excellence CECAD as well as the DZNE and caesar Research Center .Together with their regional, national and international partners, such as ERIBA, researchers at the MPI for Biology of Ageing are exploring how cells age throughout the course of their life, which genes are involved and to what extent environmental factors play a role. Underlying processes are being studied in so-called model organisms: The genes of the mouse Mus musculus, the fruit fly Drosophila melanogaster and the roundworm Caenorhabditis elegans are known and the life expectancy of these organisms is relatively short. This makes them particularly suitable for research into the ageing process. Further model organisms in the form of the fish Nothobranchius furzeri and the yeast Saccharomyces cerevisiae are in use.Since the beginning of the research work in 2008 Adam Antebi , Nils-Göran Larsson and Linda Partridge are jointly directing the institute.The foundation stone for the new research premises was laid in 2010 and the building was inaugurated in 2013.As one of the youngest institutes of the Max Planck Society, the MPI for Biology of Ageing is expanding further and should eventually have a staff of about 350. At least ten research groups are planned as well as a fourth department under the leadership of a further director. Wikipedia.


Gems D.,University College London | Partridge L.,Max Planck Institute for Biology of Ageing
Annual Review of Physiology | Year: 2013

Discovering the biological basis of aging is one of the greatest remaining challenges for science. Work on the biology of aging has discovered a range of interventions and pathways that control aging rate. A picture is emerging of a signaling network that is sensitive to nutritional status and that controls growth, stress resistance, and aging. This network includes the insulin/IGF-1 and target of rapamycin (TOR) pathways and likely mediates the effects of dietary restriction on aging. Yet the biological processes upon which these pathways act to control life span remain unclear. A long-standing guiding assumption about aging is that it is caused by wear and tear, particularly damage at the molecular level. One view is that reactive oxygen species (ROS), including free radicals, generated as by-products of cellular metabolism, are a major contributor to this damage. Yet many recent tests of the oxidative damage theory have come up negative. Such tests have opened an exciting new phase in biogerontology in which fundamental assumptions about aging are being reexamined and revolutionary concepts are emerging. Among these concepts is the hyperfunction theory, which postulates that processes contributing to growth and reproduction run on in later life, leading to hypertrophic and hyperplastic pathologies. Here we reexamine central concepts about the nature of aging. Copyright © 2013 by Annual Reviews. All rights reserved. Source


Lopez-Otin C.,University of Oviedo | Blasco M.A.,Telomeres and Telomerase Group | Partridge L.,Max Planck Institute for Biology of Ageing | Partridge L.,University College London | And 4 more authors.
Cell | Year: 2013

Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. This deterioration is the primary risk factor for major human pathologies, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. Aging research has experienced an unprecedented advance over recent years, particularly with the discovery that the rate of aging is controlled, at least to some extent, by genetic pathways and biochemical processes conserved in evolution. This Review enumerates nine tentative hallmarks that represent common denominators of aging in different organisms, with special emphasis on mammalian aging. These hallmarks are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. A major challenge is to dissect the interconnectedness between the candidate hallmarks and their relative contributions to aging, with the final goal of identifying pharmaceutical targets to improve human health during aging, with minimal side effects. © 2013 Elsevier Inc. Source


Le H.Q.,Max Planck Institute for Biology of Ageing
Nature Cell Biology | Year: 2016

Tissue mechanics drive morphogenesis, but how forces are sensed and transmitted to control stem cell fate and self-organization remains unclear. We show that a mechanosensory complex of emerin (Emd), non-muscle myosin IIA (NMIIA) and actin controls gene silencing and chromatin compaction, thereby regulating lineage commitment. Force-driven enrichment of Emd at the outer nuclear membrane of epidermal stem cells leads to defective heterochromatin anchoring to the nuclear lamina and a switch from H3K9me2,3 to H3K27me3 occupancy at constitutive heterochromatin. Emd enrichment is accompanied by the recruitment of NMIIA to promote local actin polymerization that reduces nuclear actin levels, resulting in attenuation of transcription and subsequent accumulation of H3K27me3 at facultative heterochromatin. Perturbing this mechanosensory pathway by deleting NMIIA in mouse epidermis leads to attenuated H3K27me3-mediated silencing and precocious lineage commitment, abrogating morphogenesis. Our results reveal how mechanics integrate nuclear architecture and chromatin organization to control lineage commitment and tissue morphogenesis. © 2016 Nature Publishing Group Source


Larsson N.-G.,Max Planck Institute for Biology of Ageing
Annual Review of Biochemistry | Year: 2010

Mitochondrial dysfunction is heavily implicated in the multifactorial aging process. Aging humans have increased levels of somatic mtDNA mutations that tend to undergo clonal expansion to cause mosaic respiratory chain deficiency in various tissues, such as heart, brain, skeletal muscle, and gut. Genetic mouse models have shown that somatic mtDNA mutations and cell type-specific respiratory chain dysfunction can cause a variety of phenotypes associated with aging and age-related disease. There is thus strong observational and experimental evidence to implicate somatic mtDNA mutations and mosaic respiratory chain dysfunction in the mammalian aging process. The hypothesis that somatic mtDNA mutations are generated by oxidative damage has not been conclusively proven. Emerging data instead suggest that the inherent error rate of mitochondrial DNA (mtDNA) polymerase γ (Pol γ) may be responsible for the majority of somatic mtDNA mutations. The roles for mtDNA damage and replication errors in aging need to be further experimentally addressed. © 2010 by Annual Reviews. All rights reserved. Source


Tessarz P.,Gurdon Institute | Tessarz P.,Max Planck Institute for Biology of Ageing | Kouzarides T.,Gurdon Institute
Nature Reviews Molecular Cell Biology | Year: 2014

Post-translational modifications of histones regulate all DNA-templated processes, including replication, transcription and repair. These modifications function as platforms for the recruitment of specific effector proteins, such as transcriptional regulators or chromatin remodellers. Recent data suggest that histone modifications also have a direct effect on nucleosomal architecture. Acetylation, methylation, phosphorylation and citrullination of the histone core may influence chromatin structure by affecting histone-histone and histone-DNA interactions, as well as the binding of histones to chaperones. © 2014 Macmillan Publishers Limited. All rights reserved. Source

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