This article talks about pedigrees! Apparently, researchers have found evidence to connect bipolar disorder to chromosome 6 and 17. They found this evidence through a pedigree series.
First, bipolar disorder is a condition in which people go back and forth between periods of a very good or irritable mood and depression.
Prior to the actual study, researchers had reported results of a linkage analysis of bipolar disorder in what started as a set of twenty pedigrees newly discovered by the synergy of three various sites. They now report the results. They had a genome-wide linkage analysis in an independent sample of thirty-four pedigrees that separated, or sought out bipolar disorder.
Here's how: Researchers used families that were known to have a bipolar I or II disorder; individuals affected with this disorder were the first subjects in a study for the presence of bipolar I disorder, bipolar II disorder, or returning and constant major depression in a few other family members. "A total of 440 markers at an average spacing of 8 cM were genotyped in 229 family members using fluorescent methods" say researchers when
asked about their methods.
In conclusion, first nonparametric analyses of chromosomes 6 and 17 proved for a simple replication of linkage to these chromosomes that had been pointed at before and speculated in previous studies. Using multipoint parametric methods, other analyses, showed further evidence to support the 6q25 region ( a region where specific genes are encoded on chromosome 6) with a heterogeneity logarithm of odds score of 3.28. From the two-point parametric analyses we also found further evidence that again showed a simple replication of the researchers previous findings of linkage to the 23 cM region of chromosome 22q13, thus proving their theory right, further. Their results pretty much stated that there is replication of certain proven linkage peaks, like that of 6q25 and 17p12 (chromosomes 6 and 17). Other peaks from previous studies had to have not been replicated or were only modestly replicated in these analyses.
First, bipolar disorder is a condition in which people go back and forth between periods of a very good or irritable mood and depression.
Prior to the actual study, researchers had reported results of a linkage analysis of bipolar disorder in what started as a set of twenty pedigrees newly discovered by the synergy of three various sites. They now report the results. They had a genome-wide linkage analysis in an independent sample of thirty-four pedigrees that separated, or sought out bipolar disorder.
Here's how: Researchers used families that were known to have a bipolar I or II disorder; individuals affected with this disorder were the first subjects in a study for the presence of bipolar I disorder, bipolar II disorder, or returning and constant major depression in a few other family members. "A total of 440 markers at an average spacing of 8 cM were genotyped in 229 family members using fluorescent methods" say researchers when
asked about their methods.
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| This is a picture of chromosome 6. You can see that certain parts of this chromosome have stripes representing the different gene locations. These gene locations have names like the 6q25 region- referenced below. |
In conclusion, first nonparametric analyses of chromosomes 6 and 17 proved for a simple replication of linkage to these chromosomes that had been pointed at before and speculated in previous studies. Using multipoint parametric methods, other analyses, showed further evidence to support the 6q25 region ( a region where specific genes are encoded on chromosome 6) with a heterogeneity logarithm of odds score of 3.28. From the two-point parametric analyses we also found further evidence that again showed a simple replication of the researchers previous findings of linkage to the 23 cM region of chromosome 22q13, thus proving their theory right, further. Their results pretty much stated that there is replication of certain proven linkage peaks, like that of 6q25 and 17p12 (chromosomes 6 and 17). Other peaks from previous studies had to have not been replicated or were only modestly replicated in these analyses.
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