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Genetic linkage
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=== Limitations === Linkage analysis has a number of methodological and theoretical limitations that can significantly increase the [[Type I and type II errors|type-1 error]] rate and reduce the power to map human quantitative trait loci (QTL).<ref>{{Cite journal |last=Ferreira |first=Manuel A. R. |date=2004-10-01 |title=Linkage Analysis: Principles and Methods for the Analysis of Human Quantitative Traits |journal=Twin Research and Human Genetics |language=en |volume=7 |issue=5 |pages=513β530 |doi=10.1375/twin.7.5.513 |issn=2053-6003 |pmid=15527667 |s2cid=199001341}}</ref> While linkage analysis was successfully used to identify genetic variants that contribute to rare disorders such as [[Huntington's disease|Huntington disease]], it did not perform that well when applied to more common disorders such as [[Cardiovascular disease|heart disease]] or different forms of [[cancer]].<ref>{{Cite journal |last1=Gusella |first1=James F. |last2=Frontali |first2=Marina |last3=Wasmuth |first3=John J. |last4=Collins |first4=Francis S. |last5=Lehrach |first5=Hans |last6=Myers |first6=Richard |last7=Altherr |first7=Michael |last8=Allitto |first8=Bernice |last9=Taylor |first9=Sherry |date=1992-05-01 |title=The Huntington's disease candidate region exhibits many different haplotypes |journal=Nature Genetics |language=en |volume=1 |issue=2 |pages=99β103 |doi=10.1038/ng0592-99 |issn=1546-1718 |pmid=1302016 |s2cid=25472459}}</ref> An explanation for this is that the genetic mechanisms affecting common disorders are different from those causing some rare disorders.<ref>{{Cite journal |last1=Mark J. Daly |last2=Hirschhorn |first2=Joel N. |date=2005-02-01 |title=Genome-wide association studies for common diseases and complex traits |journal=Nature Reviews Genetics |language=en |volume=6 |issue=2 |pages=95β108 |doi=10.1038/nrg1521 |issn=1471-0064 |pmid=15716906 |s2cid=2813666}}</ref>
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