Linkage analysis of pure depressive disease
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Cited by (22)
Reduced expression of glyoxalase-1 mRNA in mood disorder patients
2008, Neuroscience LettersCandidate genes of anxiety-related behavior in HAB/LAB rats and mice: Focus on vasopressin and glyoxalase-I
2007, Neuroscience and Biobehavioral ReviewsCitation Excerpt :Although the enzyme is certainly not one of the usual suspects in signal transduction of emotionality, a possible connection between glyoxalase-I and depression was found in a linkage study of families with depressive disease. Subgroups with unipolar affective disease showed evidence for an association with the glyoxalase-I locus; unfortunately, the level of anxiety was not scored in this study (Tanna et al., 1989). In both brain tissue and blood, HAB-Ms were recently reported to underexpress and LAB-Ms to overexpress the enzyme relative to unselected NAB-M and cross-mated animals.
Protein biomarkers in a mouse model extremes in trait anxiety
2006, Molecular and Cellular ProteomicsCitation Excerpt :A possible connection between GLX1 and depression has been found in a linkage study of families with depressive disease. Subgroups of families with unipolar affective disease showed evidence for a linkage or association with the GLX1 locus (20). In a recent study using different inbred strains of mice Hovatta et al. (21) found that GLX1 and glutathione reductase 1 play a causal role in anxiety.
Chapter 13 Implications for the practice of psychiatry
2006, Progress in Brain ResearchCitation Excerpt :This increase in protein expression was accompanied by an increase in mRNA expression. Interestingly, the glyoxalase I locus shows possible linkage or association with unipolar depression (Tanna et al., 1989). Two groups have used proteomics methods to investigate CSF in psychiatric disorders so far and both have focused on schizophrenia.
Predisposition Locus for Major Depression at Chromosome 12q22-12q23.2
2003, American Journal of Human GeneticsCitation Excerpt :The results of segregation analyses are usually inconsistent with a Mendelian mode of inheritance (Cox et al. 1989), although other studies have indicated the possibility of a relatively straightforward inheritance pattern (Marazita et al. 1997). Even though genetic predisposition to MDD is well established, and despite the importance of the disease, few linkage results for MDD have been reported (Tanna et al. 1976, 1989; Craddock et al. 1994; Balciuniene et al. 1998; Jones et al. 2002; Zubenko et al. 2002b). This may be due to the multifactorial etiology of MDD, with vulnerability being influenced in a complex way by both environmental and genetic factors.