One early study using only 95 markers found linkage for low voltage alpha EEG on chromosome 20q and noted evidence for genetic heterogeneity [47].
These six electrodes were selected to focus on alpha power nevertheless we found linkage peaks for beta and theta power.
Moreover, we also found linkage disequilibrium for multiple paired comparisons in many populations, but it is difficult to make inferences about linkage disequilibrium given the deviations from HWE observed in these populations.
Interestingly, Bauer and colleagues previously identified a locus (Cia28) associated with anti-CII antibody production at 53 cM on chromosome 13 [ 19], which is approximately at the same position as where we find the linkage for this trait in the present study.
We studied a family from northern Pakistan with two microcephalic children using homozygosity mapping and found suggestive linkage for regions on chromosomes 2, 4, and 9.
The fact that we did not find any association between DTNBP1 SNPs and schizophrenia is consistent with our previous linkage studies which did not find evidence for linkage across the DTNBP1 region.
Evidence has been found for linkage with the non-HLA loci 2q33, 5q31-33 and 19p13 [ 6] and candidate gene association studies within these loci have concentrated on genes known to be immunologically relevant to disease pathogenesis.
Interestingly, in both our study and the one from Hougaard et al. [ 13], it was almost impossible to find synteny for linkage groups B05 and B10 due to few anchor markers in these regions suggesting that these linkage groups have lower number of conserved or transcribed sequences.
We found evidence of linkage for three pairs of loci (P < 0.00022, the adjusted critical value): BswD312w x BswD235w, BswA303w x BswD234w, and BswD123w x BswD223w.
In addition, we found evidence of linkage for comorbid ADHD phenotypes to loci at 8q24, 2p21 22.3, 5p13.1 p13.3, 12p11.23 13.3, 8q15, 11q22, and 14q21.1 22.2, suggesting that these patterns of cosegregation of ADHD with disruptive behavior and substance abuse comorbidities, and the linkage to similar regions, were indicative of a common major genetic cause (Jain et al. 2007).
