Finding the missing heritability of complex diseases Export

@article{citeulike:5907455, abstract = {Genome-wide association studies have identified hundreds of genetic variants associated with complex human diseases and traits, and have provided valuable insights into their genetic architecture. Most variants identified so far confer relatively small increments in risk, and explain only a small proportion of familial clustering, leading many to question how the remaining, 'missing' heritability can be explained. Here we examine potential sources of missing heritability and propose research strategies, including and extending beyond current genome-wide association approaches, to illuminate the genetics of complex diseases and enhance its potential to enable effective disease prevention or treatment.}, author = {Manolio, Teri A. and Collins, Francis S. and Cox, Nancy J. and Goldstein, David B. and Hindorff, Lucia A. and Hunter, David J. and McCarthy, Mark I. and Ramos, Erin M. and Cardon, Lon R. and Chakravarti, Aravinda and Cho, Judy H. and Guttmacher, Alan E. and Kong, Augustine and Kruglyak, Leonid and Mardis, Elaine and Rotimi, Charles N. and Slatkin, Montgomery and Valle, David and Whittemore, Alice S. and Boehnke, Michael and Clark, Andrew G. and Eichler, Evan E. and Gibson, Greg and Haines, Jonathan L. and Mackay, Trudy F. C. and McCarroll, Steven A. and Visscher, Peter M.}, booktitle = {Nature}, citeulike-article-id = {5907455}, citeulike-linkout-0 = {http://dx.doi.org/10.1038/nature08494}, citeulike-linkout-1 = {http://dx.doi.org/10.1038/nature08494}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/19812666}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=19812666}, day = {08}, doi = {10.1038/nature08494}, issn = {0028-0836}, journal = {Nature}, keywords = {association, disease, popgen, review}, month = {October}, number = {7265}, pages = {747--753}, posted-at = {2009-10-07 21:25:36}, priority = {2}, publisher = {Nature Publishing Group}, title = {Finding the missing heritability of complex diseases}, url = {http://dx.doi.org/10.1038/nature08494}, volume = {461}, year = {2009} }

TY - JOUR ID - citeulike:5907455 L3 - citeulike-article-id:5907455 N2 - Genome-wide association studies have identified hundreds of genetic variants associated with complex human diseases and traits, and have provided valuable insights into their genetic architecture. Most variants identified so far confer relatively small increments in risk, and explain only a small proportion of familial clustering, leading many to question how the remaining, 'missing' heritability can be explained. Here we examine potential sources of missing heritability and propose research strategies, including and extending beyond current genome-wide association approaches, to illuminate the genetics of complex diseases and enhance its potential to enable effective disease prevention or treatment. IS - 7265 JF - Nature SN - 0028-0836 EP - 753 TI - Finding the missing heritability of complex diseases PB - Nature Publishing Group VL - 461 T2 - Nature SP - 747 KW - association KW - disease KW - popgen KW - review AU - Manolio, Teri AU - Collins, Francis AU - Cox, Nancy AU - Goldstein, David AU - Hindorff, Lucia AU - Hunter, David AU - McCarthy, Mark AU - Ramos, Erin AU - Cardon, Lon AU - Chakravarti, Aravinda AU - Cho, Judy AU - Guttmacher, Alan AU - Kong, Augustine AU - Kruglyak, Leonid AU - Mardis, Elaine AU - Rotimi, Charles AU - Slatkin, Montgomery AU - Valle, David AU - Whittemore, Alice AU - Boehnke, Michael AU - Clark, Andrew AU - Eichler, Evan AU - Gibson, Greg AU - Haines, Jonathan AU - Mackay, Trudy AU - McCarroll, Steven AU - Visscher, Peter PY - 2009/10/08/ UR - http://dx.doi.org/10.1038/nature08494 ER -