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Linkage for platelet monoamine oxidase (MAO) activity: results from a replication sample
Nancy L Saccone1, John P Rice, Nan Rochberg
1Department of Psychiatry, Washington University School of Medicine, St. Louis, Missouri 63110, USA. nlims@vodka.wustl.edu
Alcoholism, Clinical and Experimental Research
|June 5, 2002
Summary
Genetic linkage analysis identified a potential locus on chromosome 9 associated with monoamine oxidase B (MAO-B) activity. This finding, consistent across independent family samples, suggests a specific gene influences MAO-B levels.
Area of Science:
- Genetics
- Biochemistry
- Neuroscience
Background:
- Monoamine oxidase B (MAO-B) is crucial for catecholamine degradation in nerve endings and platelets.
- Evidence suggests a distinct genetic locus, separate from the X chromosome, influences platelet MAO-B activity.
Purpose of the Study:
- To perform linkage analyses for platelet MAO-B activity using initial and replication family samples.
- To investigate potential genetic loci controlling MAO-B activity in families from the Collaborative Study on the Genetics of Alcoholism (COGA).
Main Methods:
- Utilized 105 extended families (initial sample) and 157 extended families (replication sample).
- Employed Haseman-Elston regression on sib pairs and variance component analysis on pedigrees.
- Accounted for covariates including cigarette smoking and gender.
Main Results:
- Consistent evidence for linkage was observed on chromosomes 2, 9, and 12 across both datasets.
- Variance component analysis strongly supported linkage on chromosome 9 (lod > 3) near D9S261.
- Sib-pair analysis showed suggestive linkage on chromosomes 2 and 12, with weaker support from variance component analysis.
Conclusions:
- Findings are consistent across independent family samples, strengthening the evidence for genetic linkage.
- Variance component analysis provides robust support for a MAO-B activity linkage on chromosome 9.
- Suggestive linkages on chromosomes 2 and 12 require further investigation.