Previous studies using a candidate gene approach, family linkage studies, and gene expression profiling uncovered a number of type 2 genes, but the genetic basis of common type 2 diabetes remained unknown.
Given the comorbidity of facial neuralgia and somnambulism in this family, linkage between responsible gene loci could be postulated.
Human twin and family linkage studies as well as animal model studies have confirmed the importance of genetic factors in the individual variance in peak bone mass acquisition, BMD, bone geometry, and metabolism and thus the predisposition to osteoporosis and related fragility fractures.
Within a few years scientists supplanted these largely inferential family linkage techniques with more sophisticated and precise mitochondrial DNA analysis; over time incorporating reliable techniques of autosomal marker analysis.
These BMD determinants are known to be polygenic, and objective evidence for this is provided by candidate gene SNPs (single nucleotide polymorphisms), quantitative trait locus and family linkage studies [7] [20].
In humans, family linkage studies have low statistical power and can usually only identify Mendelian traits; in mice, QTL studies using F2 or recombinant inbred (RI) crosses have poor genetic resolution, with an average locus size greater than 20 Mb [70].
