Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alpha 2 adrenergic receptors play an important role in regulating the neuronal release of norepinephrine through presynaptic feedback inhibition in the locus ceruleus. Therefore, alpha 2 adrenergic autoreceptors may underlie some aspects of the pathogenesis and symptomatic expression of depressive illness. We studied two brain-expressed alpha 2 adrenergic receptor genes as genetic markers in linkage analyses in 17 multiplex pedigrees of unipolar depression. Neither of the genes was supportive of linkage to depression. Lod scores of less than -2 were found in both familial pure depressive disease pedigrees and in depression spectrum disease pedigrees. Therefore, we conclude that depression in our pedigrees is not related to mutations in the two alpha 2 adrenergic receptor genes tested.
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PMID:Alpha 2 adrenergic receptor subtypes in depression: a candidate gene study. 132 69

Association and linkage relationships between alcoholism and 30 polymorphic marker loci were studied in a total of 42 families: 27 families originally collected as part of a study on depression spectrum disease, 14 previously reported families with depression spectrum disease, and 1 family with familial alcoholism. Since heterogeneity within a sample can confound genetic linkage analysis, obscuring linkage relationships, alcoholism was studied in these families as a disorder unrelated to depression or antisocial personality. No allelic associations were found to be significant after allowing for the multiple tests. In a sib-pair linkage analysis, significant differences between the mean proportion of genes identical by descent in concordant and discordant sib pairs were found for the esterase-D (ESD) marker locus (p less than or equal to .01). This suggested that a linkage may exist between a gene for alcoholism and the ESD locus on chromosome 13q. Lod score linkage analysis yielded odds in favor of linkage to ESD of 44 to 1, most of the information relevant to linkage residing in a single family in which three offspring were classified as alcoholic and five were not.
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PMID:Possible linkage between alcoholism and esterase-D. 321 52

This paper reports a Swiss family affected by a cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) linked to chromosome 19q12. In three generations several members of this family had recurrent stroke-like episodes and, some developed subcortical dementia, migraine-like headaches, and depression. The clinically affected family members had multiple subcortical infarcts and diffuse leukoencephalopathy on MRI. Necropsy of one patient showed a distinctive non-amyloid and non-atherosclerotic angiopathy of small cerebral and leptomeningeal arteries with concentric depositions of a basophilic granular material replacing the smooth muscle cells of the media. Linkage analysis with five chromosome 19 markers spanning the estimated CADASIL interval showed the absence of any recombinant and positive Lod scores, highly suggestive of linkage of this condition to the CADASIL locus. CADASIL might be an underestimated cause of familial stroke and should be considered in the differential diagnosis of hereditary stroke.
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PMID:Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy: a clinicopathological and genetic study of a Swiss family. 762 27

Antipsychotics can induce in schizophrenic (SZ) and bipolar disorder (BP) patients serious body weight changes that increase risk for noncompliance to medication, and risk for cardiovascular diseases and diabetes. A genetic origin for this susceptibility to weight changes has been hypothesized because only a proportion of treated patients are affected, the degree of affection differing also in rates and magnitudes. In a first genome scan on obesity under antipsychotics in SZ and BP, we analyzed 21 multigenerational kindreds (508 family members) including several patients treated for a minimum of 3 years mainly with haloperidol or chlopromazine. Obesity was defined from medical files and was shown to be 2.5 times more frequent in patients treated with antipsychotics than in untreated family members (30 vs 12%). The nine pedigrees that showed at least two occurrences of obesity under antipsychotics were submitted to model-based linkage analyses. We observed a suggestive linkage with a multipoint Lod score (MLS) of 2.74 at 12q24. This linkage finding vanished when we used as phenotypes, obesity unrelated to antipsychotics, and when we used SZ or BP. This suggests that this positive linkage result with obesity is specific to the use of antipsychotics. A potential candidate gene for this linkage is the pro-melanin-concentrating hormone (PMCH) gene located at less then 1 cM of the linkage. PMCH encodes a neuropeptide involved in the control of food intake, energy expenditure, and in anxiety/depression. This first genome scan targeting the obesity side effect of antipsychotics identified 12q24 as a susceptibility region.
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PMID:A genome wide linkage study of obesity as secondary effect of antipsychotics in multigenerational families of eastern Quebec affected by psychoses. 1522 1