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Analysis of human genetic linkage

Over the past several decades, research has focused increasingly on developmental precursors to psychological disorders that were previously assumed to emerge only in adulthood. This change in focus follows from the recognition that complex transactions between biological vulnerabilities and psychosocial risk factors shape emotional and behavioral development beginning at conception. To date, however, empirical research on the development of borderline personality is extremely limited. Indeed, in the decade since M. M. Linehan initially proposed a biosocial model of the development of borderline personality disorder, there have been few attempts to test the model among at-risk youth. In this review, diverse literatures are reviewed that can inform understanding of the ontogenesis of borderline pathology, and testable hypotheses are proposed to guide future research with at-risk children and adolescents. One probable pathway is identified that leads to borderline personality disorder; it begins with early vulnerability, expressed initially as impulsivity and followed by heightened emotional sensitivity. These vulnerabilities are potentiated across development by environmental risk factors that give rise to more extreme emotional, behavioral, and cognitive dysregulation.

A biosocial developmental model of borderline personality: Elaborating and extending Linehan's theory.

Importance The neuroinflammatory hypothesis of major depressive disorder is supported by several main findings. First, in humans and animals, activation of the immune system causes sickness behaviors that present during a major depressive episode (MDE), such as low mood, anhedonia, anorexia, and weight loss. Second, peripheral markers of inflammation are frequently reported in major depressive disorder. Third, neuroinflammatory illnesses are associated with high rates of MDEs. However, a fundamental limitation of the neuroinflammatory hypothesis is a paucity of evidence of brain inflammation during MDE. Translocator protein density measured by distribution volume (TSPO V T ) is increased in activated microglia, an important aspect of neuroinflammation. Objective To determine whether TSPO V T is elevated in the prefrontal cortex, anterior cingulate cortex (ACC), and insula in patients with MDE secondary to major depressive disorder. Design, Setting, and Participants Case-control study in a tertiary care psychiatric hospital from May 1, 2010, through February 1, 2014. Twenty patients with MDE secondary to major depressive disorder and 20 healthy control participants underwent positron emission tomography with fluorine F 18–labeled N -(2-(2-fluoroethoxy)benzyl)- N -(4-phenoxypyridin-3-yl)acetamide ([ 18 F]FEPPA). Patients with MDE were medication free for at least 6 weeks. All participants were otherwise healthy and nonsmokers. Main Outcomes and Measures Values of TSPO V T in the prefrontal cortex, ACC, and insula. Results In MDE, TSPO V T was significantly elevated in all brain regions examined (multivariate analysis of variance, F 15,23  = 4.5 [ P  = .001]). The magnitude of TSPO V T elevation was 26% in the prefrontal cortex (mean [SD] TSPO V T , 12.5 [3.6] in patients with MDE and 10.0 [2.4] in controls), 32% in the ACC (mean [SD] TSPO V T , 12.3 [3.5] in patients with MDE and 9.3 [2.2] in controls), and 33% in the insula (mean [SD] TSPO V T , 12.9 [3.7] in patients with MDE and 9.7 [2.3] in controls). In MDE, greater TSPO V T in the ACC correlated with greater depression severity ( r  = 0.63 [ P  = .005]). Conclusions and Relevance This finding provides the most compelling evidence to date of brain inflammation, and more specifically microglial activation, in MDE. This finding is important for improving treatment because it implies that therapeutics that reduce microglial activation should be promising for MDE. The correlation between higher ACC TSPO V T and the severity of MDE is consistent with the concept that neuroinflammation in specific regions may contribute to sickness behaviors that overlap with the symptoms of MDE.

https://jamanetwork.com/journals/jamapsychiatry/articlepdf/2091919/yoi140100.pdf

Role of translocator protein density, a marker of neuroinflammation, in the brain during major depressive episodes.

We report analyses from a study of gene-environment interaction in adolescent depression. The sample was selected from 1990 adolescents aged 10-20 years: those with depression symptoms in the top or bottom 15% were identified and divided into high or low environmental risk groups. DNA was obtained from 377 adolescents, representing the four quadrants of high or low depression and high or low environmental risk. Markers within, or close to, each of the serotonergic genes 5HTT, HTR2A, HTR2C, MAOA (monoamine oxidase type A) and tryptophan hydroxylase (TPH) were genotyped. Environmental risk group was a nonsignificant predictor and sex was a significant predictor of the depression group. HTR2A and TPH significantly predicted the depression group, independent of the effects of sex, environmental risk group and their interaction. In addition, there was a trend for an effect of 5HTTLPR, which was significant in female subjects. Furthermore, there was a significant genotype-environmental risk interaction for 5HTTLPR in female subjects only, with the effect being in the same direction as another recent study, reaffirming that an important source of genetic heterogeneity is exposure to environmental risk.

Gene-environment interaction analysis of serotonin system markers with adolescent depression.

In the past 10 years, restless legs syndrome (RLS) has gained recognition as a common sleep disorder. There are several therapeutic options in treating patients with RLS. RLS causes significant sleep disturbance and negatively impacts on patient quality of life. Pharmacologic treatment can result in improved sleep and quality of life issues. RLS patients should be evaluated for iron deficiency anemia; iron replacement in deficient patients may lead to a resolution of symptoms or may reduce the severity of their symptoms. For patients with daily symptoms, the initial therapy is dopamine agonists. Low doses given in the evening or 2 hours before bed provide adequate relief of symptoms for many RLS patients. Augmentation can be seen with all dopamine agents, but is most prevalent with levodopa. Levodopa therapy is best used for milder intermittent symptoms or in aggravating situations, such as long car rides. Opiates and antiepileptics remain a beneficial therapy for RLS and are useful in patients who experience pain as part of their RLS. Newer anticonvulsants may provide additional treatment options, but they have yet to undergo clinical trials. Intravenous iron also may provide relief of RLS symptoms; however, dosing and safety issues have not been fully evaluated in a RLS population.

Restless legs syndrome

Context: A large body of evidence suggests that predisposition to suicide, an important public health problem, is mediated to a certain extent by neurobiological factors. Objective: To investigate patterns of expression in suicide with and without major depression and to identify new molecular targets that may play a role in the neurobiology of these conditions. Design: Brain gene expression analysis was performed using the Affymetrix HG-U133 chipset in the orbital cortex (Brodmann area [BA]11), the dorsolateral prefrontal cortex (BA8/9), and motor cortex (BA4). Subsequent studies were carried out in independent samples from adjacent areas to validate positive findings, confirm their relevance at the protein level, and investigate possible effects of genetic variation.

https://jamanetwork.com/journals/jamapsychiatry/articlepdf/209200/YOA40521.pdf

Implication of SSAT by Gene Expression and Genetic Variation in Suicide and Major Depression

Background Genes are involved in the etiology of restless legs syndrome, a common sensorimotor disorder. Objectives To replicate and to further characterize our previously reported chromosome 12q linkage results. Design Family linkage study. Setting and Participants A total of 276 individuals from 19 families have been examined using a selection of markers spanning the identified candidate interval on chromosome 12q. Results Two-point analyses of individual pedigrees indicated that 5 kindreds were consistent with linkage to chromosome 12q. When considering these 5 pedigrees along with the family in which linkage was originally reported, we observed a maximum 2-point logarithm-of-odds score of 5.67 (at θ = 0.10; for marker D12S1636 ; autosomal recessive) and a maximum multipoint logarithm-of-odds score of 8.84 between the interval defined by markers D12S326 and D12S304 . Furthermore, our results also suggest the presence of heterogeneity in restless legs syndrome as linkage was formally excluded across the region in 6 pedigrees. Interestingly, significantly higher periodic leg movements during sleep indices were observed for all probands with restless legs syndrome from linked families. Conclusions These results support the presence of a major restless legs syndrome–susceptibility locus on chromosome 12q, which has been designated as RLS1 , and also suggest that at least one additional locus may be involved in the origin of this prevalent condition.

https://jamanetwork.com/journals/jamaneurology/articlepdf/788245/noc40124.pdf

Restless Legs Syndrome Confirmation of Linkage to Chromosome 12q, Genetic Heterogeneity, and Evidence of Complexity

Suicide is an important public health problem, accounting for a significant proportion of total mortality among young people, particularly males. There is growing and consistent evidence suggesting that genetic factors play an important role in the predisposition to suicide. Based on several lines of evidence supporting a reduced serotonergic neurotransmission in subjects who committed suicide, we investigated variation at genes that code for serotonin receptor 1B (5-HTR1B), 1Dα (5-HTR1Dα), 1E (5-HTR1E), 1F (5-HTR1F), 2C (5-HTR2C), 5A (5-HTR5A), and 6 (5-HTR6) in a total sample of 106 suicide completers and 120 normal controls. No differences were observed in allelic or genotypic distributions between groups for any of the loci investigated. Moreover, further analysis according to suicide method or psychopathology also failed to reveal differences between groups. Our results do not support a substantial role of these serotonergic receptors in suicide completion. © 2003 Wiley-Liss, Inc.

Yves Gingras

Papers

Implication of SSAT by Gene Expression and Genetic Variation in Suicide and Major Depression

Restless Legs Syndrome Confirmation of Linkage to Chromosome 12q, Genetic Heterogeneity, and Evidence of Complexity

Suicide and serotonin: study of variation at seven serotonin receptor genes in suicide completers.