Emotional cognition subgroups in unaffected first-degree relatives of patients with mood disorders

2021 ◽  
pp. 1-11
Author(s):  
Hanne Lie Kjærstad ◽  
Cristina Varo ◽  
Iselin Meluken ◽  
Eduard Vieta ◽  
Maj Vinberg ◽  
...  

Abstract Background Patients with major depressive disorder (MDD) or bipolar disorder (BD) exhibit difficulties with emotional cognition even during remission. There is evidence for aberrant emotional cognition in unaffected relatives of patients with these mood disorders, but studies are conflicting. We aimed to investigate whether emotional cognition in unaffected first-degree relatives of patients with mood disorders is characterised by heterogeneity using a data-driven approach. Methods Data from 94 unaffected relatives (33 of MDD patients; 61 of BD patients) and 203 healthy controls were pooled from two cohort studies. Emotional cognition was assessed with the Social Scenarios Test, Facial Expression Recognition Test and Faces Dot-Probe Test. Hierarchical cluster analysis was conducted using emotional cognition data from the 94 unaffected relatives. The resulting emotional cognition clusters and controls were compared for emotional and non-emotional cognition, demographic characteristics and functioning. Results Two distinct clusters of unaffected relatives were identified: a relatively ‘emotionally preserved’ cluster (55%; 40% relatives of MDD probands) and an ‘emotionally blunted’ cluster (45%; 29% relatives of MDD probands). ‘Emotionally blunted’ relatives presented with poorer neurocognitive performance (global cognition p = 0.010), heightened subsyndromal mania symptoms (p = 0.004), lower years of education (p = 0.004) and difficulties with interpersonal functioning (p = 0.005) than controls, whereas ‘emotionally preserved’ relatives were comparable to controls on these measures. Conclusions Our findings show discrete emotional cognition profiles that occur across healthy first-degree relatives of patients with MDD and BD. These emotional cognition clusters may provide insight into emotional cognitive markers of genetically distinct subgroups of individuals at familial risk of mood disorders.

2021 ◽  
Vol 51 ◽  
pp. 71-83
Author(s):  
Cristina Varo ◽  
Hanne Lie Kjærstad ◽  
Emilie Poulsen ◽  
Iselin Meluken ◽  
Eduard Vieta ◽  
...  

2015 ◽  
Vol 45 (15) ◽  
pp. 3317-3327 ◽  
Author(s):  
M. Papmeyer ◽  
J. E. Sussmann ◽  
J. Hall ◽  
J. McKirdy ◽  
A. Peel ◽  
...  

BackgroundNeurocognitive performance deficits have been observed in mood disorder patients and their unaffected relatives and may therefore qualify as endophenotypes. However, the precise time course of neurocognitive deficits has not been studied so that it is unknown whether neurocognitive abnormalities reflect the early effects of familial vulnerability to mood disorders or if they emerge at illness onset.MethodA neuropsychological test battery was administered at baseline and after a 2-year follow-up interval in 111 initially unaffected young adults at high familial risk of mood disorders and 93 healthy controls (HC). During the follow-up period, 20 high-risk subjects developed major depressive disorder (HR-MDD), with the remainder remaining well (HR-well). Linear mixed-effects models were used to investigate differences and longitudinal changes in the domains of attentional processing, working memory, verbal learning and memory, and cognitive flexibility.ResultsReduced long delay verbal memory and extradimensional set-shifting performance across both time points were found in the HR-well group relative to controls. The HR-MDD group displayed decreased extradimensional set-shifting abilities across both time points as compared with the HC group only. There were no significant performance differences between the two high-risk groups.ConclusionsReduced verbal memory and cognitive flexibility are familial trait markers for vulnerability to mood disorders in individuals with a close family history of bipolar disorder. Both neurocognitive performance deficits appear to be relatively stable over a 2-year time period and do not appear to be linked to the onset of MDD. These findings support their use as stable quantitative endophenotypes for mood disorders.


1993 ◽  
Vol 38 (9) ◽  
pp. 590-594 ◽  
Author(s):  
Ronald A. Remick ◽  
Adele D. Sadovnick ◽  
Boris Gimbarzevsky ◽  
Raymond W. Lam ◽  
Athanasios P. Zis ◽  
...  

The purpose of this study was to determine whether, for first-degree relatives of patients presenting to a mood disorders clinic, family history information on psychiatric conditions collected by a psychiatrist and incorporated into the patient's medical records is as informative as that gathered during an interview specifically designed to collect family history data. The study group consisted of 472 first-degree relatives of 78 randomly selected index cases from a large mood disorders genetic database. Family history of psychiatric disorders recorded in regular psychiatric medical records (“clinician history”), and data obtained by a genetic counsellor administering specific family psychiatric history questionnaires to patients and multiple family informants (“family history”) were compared using a kappa statistic. Good agreement between the two methods on the presence or absence of a psychiatric disorder was found among first-degree relatives of index cases, but poor agreement was found with respect to the presence or absence of a specific mood disorder diagnosis(es) in a relative. The results suggest that a clinician-generated family psychiatric history is sensitive to the presence or absence of a psychiatric disorder when compared to a more structured detailed genetic interview. However, for research purposes, a clinician-generated family psychiatric history of a specific mood disorder diagnosis, without supporting collateral information, may not be reliable for use in supporting a mood disorder diagnosis in a patient and/or his relatives.


2021 ◽  
pp. 1-10
Author(s):  
Amanda V. Bakian ◽  
Danli Chen ◽  
Chong Zhang ◽  
Heidi A. Hanson ◽  
Anna R. Docherty ◽  
...  

Abstract Background The degree to which suicide risk aggregates in US families is unknown. The authors aimed to determine the familial risk of suicide in Utah, and tested whether familial risk varies based on the characteristics of the suicides and their relatives. Methods A population-based sample of 12 160 suicides from 1904 to 2014 were identified from the Utah Population Database and matched 1:5 to controls based on sex and age using at-risk sampling. All first through third- and fifth-degree relatives of suicide probands and controls were identified (N = 13 480 122). The familial risk of suicide was estimated based on hazard ratios (HR) from an unsupervised Cox regression model in a unified framework. Moderation by sex of the proband or relative and age of the proband at time of suicide (<25 v. ⩾25 years) was examined. Results Significantly elevated HRs were observed in first- (HR 3.45; 95% CI 3.12–3.82) through fifth-degree relatives (HR 1.07; 95% CI 1.02–1.12) of suicide probands. Among first-degree relatives of female suicide probands, the HR of suicide was 6.99 (95% CI 3.99–12.25) in mothers, 6.39 in sisters (95% CI 3.78–10.82), and 5.65 (95% CI 3.38–9.44) in daughters. The HR in first-degree relatives of suicide probands under 25 years at death was 4.29 (95% CI 3.49–5.26). Conclusions Elevated familial suicide risk in relatives of female and younger suicide probands suggests that there are unique risk groups to which prevention efforts should be directed – namely suicidal young adults and women with a strong family history of suicide.


2019 ◽  
Vol 85 (10) ◽  
pp. S262-S263
Author(s):  
Akua Nimarko ◽  
Sarthak Angal ◽  
Corrina Fonseca ◽  
Esther Rah ◽  
Whitney Tang ◽  
...  

2010 ◽  
Vol 40 (12) ◽  
pp. 2001-2011 ◽  
Author(s):  
C. Segalàs ◽  
P. Alonso ◽  
E. Real ◽  
A. Garcia ◽  
A. Miñambres ◽  
...  

BackgroundThe same executive dysfunctions and alterations in neuroimaging tests (both functional and structural) have been found in obsessive-compulsive patients and their first-degree relatives. These neurobiological findings are considered to be intermediate markers of the disease. The aim of our study was to assess verbal and non-verbal memory in unaffected first-degree relatives, in order to determine whether these neuropsychological functions constitute a new cognitive marker for obsessive-compulsive disorder (OCD).MethodRecall and use of organizational strategies in verbal and non-verbal memory tasks were measured in 25 obsessive-compulsive patients, 25 unaffected first-degree relatives and 25 healthy volunteers.ResultsFirst-degree relatives and healthy volunteers did not show differences on most measures of verbal memory. However, during the recall and processing of non-verbal information, deficits were found in first-degree relatives and patients compared with healthy volunteers.ConclusionsThe presence of the same deficits in the execution of non-verbal memory tasks in OCD patients and unaffected first-degree relatives suggests the influence of certain genetic and/or familial factors on this cognitive function in OCD and supports the hypothesis that deficits in non-verbal memory tasks could be considered as cognitive markers of the disorder.


2015 ◽  
Vol 78 (1) ◽  
pp. 58-66 ◽  
Author(s):  
Martina Papmeyer ◽  
Stephen Giles ◽  
Jessica E. Sussmann ◽  
Shauna Kielty ◽  
Tiffany Stewart ◽  
...  

2013 ◽  
Vol 31 (7) ◽  
pp. 938-943 ◽  
Author(s):  
Silva Saarinen ◽  
Eero Pukkala ◽  
Pia Vahteristo ◽  
Markus J. Mäkinen ◽  
Kaarle Franssila ◽  
...  

Purpose Nodular lymphocyte-predominant Hodgkin lymphoma (NLPHL) is one of the two established Hodgkin lymphoma (HL) subtypes. The risk factors of NLPHL are largely unknown. In general, genetic factors are known to have a modest effect on the risk of HL; however, familial risk in NLPHL has not been previously examined. We conducted a population-based study by using the Finnish registries and evaluated the familial risk in NLPHL. Patients and Methods We launched a population-based search to identify patients with NLPHL and their relatives by examining the records of the Finnish Cancer Registry, established in 1953, and the official Finnish population registries. We collected a data set of 692 patients with NLPHL, identified their 4,280 first-degree relatives, and calculated the registry-based standardized incidence ratios (SIRs) for different cancers in the first-degree relatives. In addition, the primary tumor biopsies of HL-affected relatives were collected when possible, the HL diagnoses were re-reviewed by a hematopathologist, and the SIR for NLPHL was calculated on the basis of confirmed NLPHL diagnoses. Results On the basis of confirmed NLPHL diagnoses, the SIR for NLPHL was 19 (95% CI, 8.8 to 36) in the first-degree relatives. The risk was most prominent in female relatives of young patients. The registry-based SIR for classical HL was 5.3 (95% CI, 3.0 to 8.8), and for non-Hodgkin lymphoma, it was 1.9 (95% CI, 1.3 to 2.6). Conclusion Our results implicate an unexpectedly high familial component in the development of NLPHL. Research is warranted to identify the putative genetic and environmental factors underlying this finding and to develop strategies for better management of patients with NLPHL and their relatives.


PLoS ONE ◽  
2013 ◽  
Vol 8 (3) ◽  
pp. e57357 ◽  
Author(s):  
Heather C. Whalley ◽  
Jessika E. Sussmann ◽  
Liana Romaniuk ◽  
Tiffany Stewart ◽  
Martina Papmeyer ◽  
...  

2021 ◽  
Author(s):  
Spiro Pantazatos ◽  
Nadine M. Melhem ◽  
David Brent ◽  
Francesca Zanderigo ◽  
Elizabeth Bartlett ◽  
...  

BACKGROUND: Mood disorders and suicidality have moderate heritability and are associated with altered corticolimbic serotonin 1A receptor (5-HT1A) binding potential. However, it is unclear whether these alterations reflect heritable risk or resilience markers, compensatory mechanisms, or illness-related changes as 5-HT1A binding has never been reported in unaffected high risk individuals (HR) who have passed through the age of greatest risk for psychopathology onset. METHODS: PET imaging quantified brain 5-HT1A binding potential BPND using [11C]CUMI-101 in healthy volunteers (HV) and three groups with one or more relatives with early-onset mood disorder and suicide attempt: 1. HR individuals; 2. HR individuals with a lifetime mood disorder (HR-MOOD); and 3. HR-MOOD individuals with lifetime history of suicide attempt (HR-MOOD/SA). Two additional studies included HV, individuals with low familial risk and current mood disorder (MOOD) and MOOD with lifetime suicide attempt (MOOD/SA) to identify differences persisting across independent cohorts (total N=185: 59 HV, 23 HR, 64 HR-MOOD or MOOD, and 39 HR-MOOD/SA or MOOD/SA). Univariate analysis tested for regional differences and multivoxel pattern analysis (MVPA) tested whether 5-HT1A BPND could distinguish HV, HR, HR-MOOD and HR-MOOD/SA. RESULTS: Low ventral prefrontal 5-HT1A BPND in lifetime MOOD/SA vs. HV and HR was consistently observed across study populations. MVPA distinguished HV from HR-MOOD/SA with informative regions in ventral prefrontal and temporal cortex (peak out-of-sample area under the ROC curve=0.74, p&lt;0.001 corrected). MOOD alone groups did not consistently differ from HV groups. CONCLUSIONS: Low ventral prefrontal 5-HT1A BPND may reflect suicide-related pathology. Further studies are needed to determine if higher ventral prefrontal 5-HT1A BPND may confer resilience for developing suicidal behavior in the context of mood disorders. If so, it could be a potential suicide prevention target.


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