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10.1111/acel.12362 http://scihub22266oqcxt.onion/10.1111/acel.12362 C4568968!4568968!26077337     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Aging+Cell 2015 ; 14 (5): 809-17 Nephropedia Template TP {{tp|p=26077337|t=2015. Genetic evidence for common pathways in human age-related diseases |pdf=|usr=}}{{26077337}} gab.com Text Genetic evidence for common pathways in human age-related diseases JO: Aging Cell http://www.kidney.de/pget.php?&tw=1&pmid=26077337 #FOAvip Aging is the single largest risk factor for chronic disease. Studies in model organisms have identified conserved pathways that modulate aging rate and the onset and progression of multiple age-related diseases, suggesting that common pathways of aging may influence age-related diseases in humans as well. To determine whether there is genetic evidence supporting the notion of common pathways underlying age-related diseases, we analyzed the genes and pathways found to be associated with five major categories of age-related disease using a total of 410 genomewide association studies (GWAS). While only a small number of genes are shared among all five disease categories, those found in at least three of the five major age-related disease categories are highly enriched for apoliprotein metabolism genes. We found that a more substantial number of gene ontology (GO) terms are shared among the 5 age-related disease categories and shared GO terms include canonical aging pathways identified in model organisms, such as nutrient-sensing signaling, translation, proteostasis, stress responses, and genome maintenance. Taking advantage of the vast amount of genetic data from the GWAS, our findings provide the first direct evidence that conserved pathways of aging simultaneously influence multiple age-related diseases in humans as has been demonstrated in model organisms. Twit Text FOAVip Genetic evidence for common pathways in human age-related diseases ????Aging Cell http://www.kidney.de/pget.php?&tw=1&pmid=26077337 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26077337 #FOAvip English Wikipedia <ref>{{Cite pmid|26077337}}</ref> Genetic evidence for common pathways in human age-related diseases #MMPMID26077337 Johnson SC; Dong X; Vijg J; Suh Y Aging Cell 2015[Oct]; 14 (5): 809-17 PMID26077337show ga Aging is the single largest risk factor for chronic disease. Studies in model organisms have identified conserved pathways that modulate aging rate and the onset and progression of multiple age-related diseases, suggesting that common pathways of aging may influence age-related diseases in humans as well. To determine whether there is genetic evidence supporting the notion of common pathways underlying age-related diseases, we analyzed the genes and pathways found to be associated with five major categories of age-related disease using a total of 410 genomewide association studies (GWAS). While only a small number of genes are shared among all five disease categories, those found in at least three of the five major age-related disease categories are highly enriched for apoliprotein metabolism genes. We found that a more substantial number of gene ontology (GO) terms are shared among the 5 age-related disease categories and shared GO terms include canonical aging pathways identified in model organisms, such as nutrient-sensing signaling, translation, proteostasis, stress responses, and genome maintenance. Taking advantage of the vast amount of genetic data from the GWAS, our findings provide the first direct evidence that conserved pathways of aging simultaneously influence multiple age-related diseases in humans as has been demonstrated in model organisms. äGenetic evidence for common pathways in human age-related diseases (epmc).pdf DeepDyve Pubget Overpricing