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Depression How It Affect You

In: Philosophy and Psychology

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sychologyHow depression affects people

Kim Branim
Psychology 326 Sonja Bethune
October 16, 2012

This study was design to find loci major depression via linkage analysis of a large sibling pair sample. Depressions in twins and families have been shown moderate high.
“However the gene that caused depression had not been detected says” Lewis Cathryn but Gerome Breen “says that Chromosome3 it a link to severe depression. Breen study took 417 families with 479 concordant sibling pairs to perform genome-wide linkage analysis. Breen used the first wave of families, suggestive and modest suggestive and modest evidence for linkage was found on chromosomes 1p36, 12q, 13q, and 15q. The peaks on chromosomes 12q and 15q also showed evidence for linkage in other samples (8-10). In the present study, we report linkage analysis results using an expanded sample that includes 325 additional families contributing 474 sibling pairs, resulting in a total of 971 concordant sibling pairs with recurrent depression. The total sample also consisted of 118 discordant sibling pairs and 12 unaffected sibling pairs. Linkage can be detected when heterogeneity and error in phenotype are decreased. Also for depression, reliability is improved by focusing on severe cause ad indexed by symptom count or impairment. (Breen,2011)

. Literature review The article name is Genome-Wide Association Study of Major Recurrent Depression in the U.K. Population. The Studies of major depression in twins and families have shown moderate to high heritability, but extensive molecular studies have failed to identify susceptibility genes convincingly. To detect genetic variants contributing to major depression, the authors performed a genome-wide association study using 1,636 cases of depression ascertained in the U.K. and 1,594 comparison subjects screened negative for psychiatric disorders .depression is a common and disabling condition and is a leading cause of disability it also impairs the quality of life, poor quality of life, and death by suicide. Kindler also says” Stressful life events are associated with the onset of episodes of major depression. However, exposure to stressful life events is influenced by genetic factors, and these factors are correlated with those that predispose to major depression.”(kindler,1999) de Graaf also said “Minor depression is common in the general population and seriously affects quality of life, daily functioning, and health care use”(de Graaf010). And according to Mejia “family is one of the main factors, not only in the development of adolescent depression, but also in the treatment, being a double-edge sword that can affect in both good and bad ways”(Mejia,2011) so family has the greatest impact on our lives and our emotions. Anyone under the age of 18 was eliminated. Also Pairs were excluded if either sibling had ever fulfilled criteria for mania, hypomania, or schizophrenia or if either experienced psychotic symptoms that were mood incongruent or present when there was no evidence of a mood disturbance. Other exclusion criteria were intravenous drug dependency and depression occurring solely in relation to alcohol use. Individuals were excluded if their genotypic data showed a missing rate >1%, abnormal heterozygosity, or a sex assignment that conflicted with phenotypic data or that they were related (up to second-degree relatives) to other study participants or were of non-European ancestry. This had no effect on the rest of the study
Cases were collected form a controlled case study of recurrent depression. They were drawn from two studies of recurrent depression and a pharmacogenetic study of antidepressant response using similar methods of case and collected by the same clinical team. Single paired affected with recurrent unipolar depression were recruited from eight clinical sites those sites were (Aarhus, Denmark; Bonn, Germany; Dublin; Lausanne, Switzerland; St. Louis; London; Cardiff, United Kingdom; and Birmingham, United Kingdom). All the participants gave their consent for this study. The participants were all interview using the Schedules for Clinical Assessments in Neuropsychiatry. The items of psychopathology in the interview were rated for presence and severity according from worst to second worst. They were asked about a four –six week period when their symptoms were the worst. They were coded as 0= absence, 1= present but mild, 2= moderately severe and present for 50% of peal intensity,3= severe for 50% of the time. All the participants were also in a four day training course and took part in a joint interrater reliability exercise. There were blood samples taken in the amount of 25 ml of whole blood they were also drops of blood placed on Guthrie blood spot card. Genotyping was performed using standard methods by deCODE Genetics (Reykjavik, Iceland). Briefly, 1,130 microsatellite markers were typed in two waves of genotyping. A total of 350 individuals from wave 1 were regenotyped to ensure marker allele calling consistency. Seventy-five markers with Hardy-Weinberg equilibrium p values <0.001 were excluded. After exclusions, marker density was 3.3 cM, with a maximum gap of 10.2 cM. The average heterozygosity was 72.4%. Their relationship was examined using graphical representation of relationship application which detected half-sibling and coded them as full siblings. Duplicate samples or monozygotic twins and unexpected relatedness were used to detect mendelization errors. In which 201 families across 303 markers which all were genotypes for the specific markers within the families showing the error recoded as fails this was used to remove unlikely recombinants. The simulate procedure was used to empirically estimate the false positive rate. The study consisted of sibling paired without parents was 58% the average informative family size was 2.45 persons with the majority 82.1% having affected offspring. There three different phenotypes performed and analyzed in addition to affected status based on recurrent depression. Two more categories were added sever recurrent depression and very severe recurrent depression. Case patients and comparison subjects were drawn from two studies of recurrent depression. (The Depression Case Control study and the Depression Network Study) they used identical methods of case definition and the aforementioned phenotyping. This method was approved by the local ethnical committees. The means of age at onset was 22.9 years. Markers were selected for analysis if they were within the one-LOD interval of a genome-wide significant linkage. The main test was association between SNP’s and depression was logistic regression. It also included ancestry principal components, assuming a log-additive genetic model. It also had fitting dominance –deviance model to allow for recessive or dominant effects. .
TABLE 1. Demographic Characteristics and Genetic Phenotypes Among Affected Sibling Pairs With Recurrent Depression | Phenotype | Clinical Site | Number of Probands Ascertained | Age of Onset (Years) | Male (%) | Recurrent Depression | Severe Recurrent Depression | Very Severe Recurrent Depression | St. Louis | 732 | 19.1 | 24.9 | 575 | 262 | 95 | London | 233 | 21.1 | 24.5 | 222 | 170 | 84 | Dublin | 274 | 22.3 | 32.8 | 262 | 195 | 113 | Cardiff, United Kingdom | 248 | 24.9 | 25.8 | 232 | 162 | 96 | Birmingham, United Kingdom | 303 | 24.0 | 31.4 | 295 | 232 | 143 | Bonn, Germany | 276 | 29.8 | 25.4 | 260 | 249 | 238 | Lausanne, Switzerland | 208 | 24.6 | 27.9 | 194 | 126 | 46 | Aarhus, Denmark | 138 | 25.9 | 34.8 | 124 | 51 | 12 | Total | 2,412 | 2,164 | 1,447 | 827 | | |

The results are for all three nested phenotypes are shown above and were generated using all available informative families. The most significant results were observed on chromosome 3 for the impairment restricted diagnostic categories. The maximum LOD was 4.01 for severe recurrent the highest LOD was for severe recurrent was on chromosome 11. For very severe recurrent depression the highest LOD was on chromosome 7. One peak was genome-wide significant after correction for multiple testing at both the phenotype and marker level, with two adjacent markers achieving an empirical p value <0.05 after simulations. From the simulations, the 5% significance threshold was a LOD score of 3.53, and the suggestive threshold was a LOD score of 2.23, after accounting for the three phenotypes and 1,065 markers examined. Most significant results were observed on chromosome 3(Breen,2011) with the use of combined analysis which had a LOD of 4.0. In this analysis was affected and defined as depression with a minimum total impairment severity. A LOD score of 4.0 corresponded with an empirical genome-wide p value of 0.015 after accounting for multiple testing at both markers and phenotypes via simulation of linkage (the proportion of times the observed LOD was exceeded by the maximum LOD scores from 1,000 simulations using MERLIN). Overall, the strongest marker was D3S1515 at 19.9 cM, with a LOD score of 4.0 and an empirical p value of 0.015, while its proximal flanking marker (D3S3591) at 23.9 cM had a LOD score of 3.567 and an empirical p value of 0.038. The distal flanking marker of D3S1515 was D3S2397, with a LOD score of 3.093 and an empirical p value of 0.254, which was the third most significant result (Breen, 2011). Another peak that was associated with depression was chromosome 7 it was the next significant results for very severe recurrent depression with a LOD score of 1.91 at 23.2 cM at marker D7S513 (11.6 Mb on hg18). This was the narrowest criteria used and the affected status was restricted to individual with a maximum severity score both their worst and second worst episode. There however was little support for linkage in the same region for other diagnostic definitions with an empirical p value of 1.0 for both phenotypes at this marker.

The finding was a genome-wide significant linkage of chromosome 3p25-26 and verified by simulations with a Lod score of 4.0 and an empirical p value of 0.015 at D35S1515 for severe recurrent depression. There is also some strong supporting evidence that D3S1515’s proximal flanking marker (D3S3591) also achieved genome-wide significance there was also another flanking marker on (D3S2397) which also had an empirical p value of 0.254and was the third most significant results in the genome across the phenotypes tested. There was multiple genes within the LOD region, including GRM7, which also encodes metabotropic glutamate receptor mGluR7. It is similar to it paralogues (mGluR4 and mGluR6) it inhibits forskolin-stimulated cAMP accumulation in response to agonist interaction but is widely expressed in many neuronal cells on the Central Nervous System . it also plays an important role in modulation of glutatmate transmission in the central nervous system, However GRM7 is one of many strong candidate genes in this region. To determine what gene of gene was important the attempted to mapping of the region in a large case-control cohort with identical phenotyping including the Depression Network Study probands. The extraction of genotypes within the one-LOD interval from illumine 610-quad genotyping there was nearly 1,600 case patients with the same severe depression phenotype and just fewer than 1,600 screened comparison subjects with lifetime and family absence of depression and other mental illness. According to vanderhasselt” suggest that individuals in remission from depression have difficulty disengaging from sad information to generate the oppositely valenced response. (Vanderhasselt,2012)
There were not robust associations with either recurrent depression or the severity – restricted diagnoses were found in the region. These findings suggest that the linkage may be a result of multiple rare variants or th at there was not sufficient power to detect multiple common variants of mild effect. There is a current study under way that will have considerably greater power to detect effect in regions. Overall the association of linkage was not encouraging. In the review the finding was that there was little replication of depression linkage found. The was a similar problem with the candidate depression genes and GWASs there was large suggest hits but no finding that had reached replicated genome-wide significances. According to Cervilla “Our results show a somewhat better model fit after adjustment for potential confounders, such as gender and family history. Age had little impact. The relationship between gender and this particular gene–environment interaction is puzzling as some studies have reported it as valid for both sexes, whereas others suggest an effect only in women.”(Cervilla,2007) there were some false positive results found which could mean that the finding on genetic in depression represents a false positive and requires replication or identification of the causal variant in the region. However the findings was observed by Pergadia et al (13) who reported a genome-wide significant multipoint LOD score of 4.14 on chromosome 3 at 2.49cM. This study appears to be one of the strongest replicated genetic finding in the studies for depression. The study was conducted at the Medical Research Council Social Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King’s College, London.


Breen, G., Webb, B. T., Butler, A. W., van den Oord, E.,J.C.G., Tozzi, F., Craddock, N., . . . McGuffin, P. (2011). A genome-wide significant linkage for severe depression on chromosome 3: The depression network study. The American Journal of Psychiatry, 168(8), 840-7. Retrieved from countid=32521
Cervilla, J. A., Molina, E., Rivera, M., Torres-González, F., Bellón, ,J.A., Moreno, B., . . . Nazareth, I. (2007). The risk for depression conferred by stressful life events is modified by variation at the serotonin transporter 5HTTLPR genotype: Evidence from the spanish PREDICT-gene cohort. Molecular Psychiatry, 12(8), 748-55. doi: de Graaf, L. E., Huibers, M. J. H., Cuijpers, P., & Arntz, A. (2010). Minor and major depression in the general population: Does dysfunctional thinking play a role? Comprehensive Psychiatry, 51(3), 266-274. doi:
Lewis, C. M., Ng, M. Y., Butler, A. W., Cohen-Woods, S., Uher, R., Pirlo, K., . . . McGuffin, P. (2010). Genome-wide association study of major recurrent depression in the U.K. population. The American Journal of Psychiatry, 167(8), 949-57. Retrieved from
Marie-Anne Vanderhasselt, Raedt, R. D., Daniel, G. D., Sunny, J. D., Brooks, N., & Diego, A. P. (2012). Decreased cognitive control in response to negative information in patients with remitted depression: An event-related potential study.Journal of Psychiatry & Neuroscience : JPN, 37(4), 250-8. Retrieved from
OD Mejia, M. (2011). What drives a teenager to depression? an insider's sociological look into its causes. Human Architecture, 9(2), 19-25. Retrieved from

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