A meta-analysis of the risk of major affective disorder in relatives of individuals affected by major depressive disorder or bipolar disorder

Wilde, Alex; Chan, Herng Nieng; Rahman, Bayzidur; Meiser, Bettina; Mitchell, Philip B.; Schofield, Peter R.; Green, Melissa

doi:10.1016/j.jad.2014.01.014

Cited by 47 publications

(31 citation statements)

References 90 publications

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“…Although the heritability of depression is relatively low (Sullivan et al, 2012) and no single nucleotide polymorphism has yet been significantly associated with MDD in genomewide studies (Levinson et al, 2014), there is robust evidence of increased familial load (Sullivan et al, 2000). First-degree kinship with an MDD patient is one of the strongest predictors of early onset (Klein et al, 2013) and multiplies risk to develop the disorder by the factor 2 to 3 in offspring (Wilde et al, 2014), siblings (Li et al, 2008), and first-degree relatives in general (Sullivan et al, 2000). It has been shown that, similar to patients with MDD or anxiety disorders (Mathews and MacLeod, 2005), individuals at familial risk for depression exhibit a negative bias when processing emotional information (Foland-Ross et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Influence of Familial Risk for Depression on Cortico-Limbic Connectivity During Implicit Emotional Processing

Wackerhagen

Wüstenberg

Mohnke

et al. 2017

Neuropsychopharmacol

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Imbalances in cortico-limbic activity and functional connectivity (FC) supposedly underlie biased emotional processing and present putative intermediate phenotypes (IPs) for major depressive disorder (MDD). To prove the validity of these IPs, we assessed them in familial risk. In 70 healthy first-degree relatives of MDD patients and 70 controls, brain activity and seed-based amygdala FC were assessed during an implicit emotional processing task for fMRI containing angry and fearful faces. Using the generalized psychophysiological interaction approach, amygdala FC was assessed (a) across conditions to provide comparable data to previous studies and (b) compared between conditions to elucidate its implications for emotional processing. Associations of amygdala FC with self-reported negative affect were explored post hoc. Groups did not differ in brain activation. In relatives, amygdala FC across conditions was decreased with superior and medial frontal gyrus (SFG, MFG) and increased with subgenual and perigenual anterior cingulate cortex (sgACC, pgACC). NA was inversely correlated with amygdala FC with MFG, pgACC and their interaction in relatives. Relatives showed aberrant condition-dependent modulations of amygdala FC with visual cortex, thalamus and orbitofrontal cortex. Our results do not support imbalanced cortico-limbic activity as IP for MDD. Diminished amygdala-dorsomedial prefrontal FC in relatives might indicate insufficient regulatory capacity, which appears to be compensated by ventromedial prefrontal regions. Differential task-dependent modulations of amygdala FC are discussed as a stronger involvement of automatic instead of voluntary emotional processing pathways. Reliability and etiological implications of these results should be investigated in future studies including longitudinal designs and patient-risk-control comparisons.

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Section: Introductionmentioning

confidence: 99%

Influence of Familial Risk for Depression on Cortico-Limbic Connectivity During Implicit Emotional Processing

Wackerhagen

Wüstenberg

Mohnke

et al. 2017

Neuropsychopharmacol

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“…Studies focusing on the offspring of affected parents, frequently referred to as the high-risk study design [1], utilize the well-established familial aggregation of mood disorders [2][3][4] as a powerful tool for the identification of risk factors, early clinical manifestations and prodromes of mood disorders in these offspring [5]. Given the elevated risk of offspring of affected parents to also develop the parental disorder, studying these offspring maximizes the potential case yield by reducing the sample size of offspring needed to observe a given number of incident cases [6].…”

Section: Introductionmentioning

confidence: 99%

The Lausanne–Geneva cohort study of offspring of parents with mood disorders: methodology, findings, current sample characteristics, and perspectives

Vandeleur

Strippoli

Castelao

et al. 2017

Soc Psychiatry Psychiatr Epidemiol

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“…Twin studies have indicated high degrees of heritability for schizophrenia (approximately 80%)4, major depressive disorder (45%)56 and bipolar disorder (85%)78. Psychiatric family history is a major risk factor for these disorders910. Patients who present with major psychiatric disorder often have a history of familial loading11.…”

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confidence: 99%

“…Patients who present with major psychiatric disorder often have a history of familial loading11. People with first- or second-degree relatives who have a family history of schizophrenia, major depressive disorder or bipolar disorder have 10-, 2- and 8-fold higher risks of developing schizophrenia, major depressive disorder or bipolar disorder, respectively, compared with the general population10121314. Premorbid neuropsychological deficits are found in a substantial proportion of children who later develop schizophrenia, especially in the subgroup of schizophrenia patients with a family history15.…”

mentioning

confidence: 99%

Impact of Familial Loading on Prefrontal Activation in Major Psychiatric Disorders: A Near-Infrared Spectroscopy (NIRS) Study

Ohi

Shimada

Kihara

et al. 2017

Sci Rep

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Family history (FH) is predictive of the development of major psychiatric disorders (PSY). Familial psychiatric disorders are largely a consequence of genetic factors and typically exhibit more severe impairments. Decreased prefrontal activity during verbal fluency testing (VFT) may constitute an intermediate phenotype for PSY. We investigated whether familial PSY were associated with a greater severity of prefrontal dysfunction in accordance with genetic loading. We measured prefrontal activity during VFT using near-infrared spectroscopy (NIRS) in patients with schizophrenia (SCZ, n = 45), major depressive disorder (MDD, n = 26) or bipolar disorder (BIP, n = 22) and healthy controls (HC, n = 51). We compared prefrontal activity among patients with or without FH and HC. Patients in the SCZ, MDD and BIP patient groups had lower prefrontal activity than HC subjects. Patients with and without FH in all diagnostic groups had lower prefrontal activity than HC subjects. Moreover, SCZ patients with FH had lower prefrontal activity than SCZ patients without FH. When we included patients with SCZ, MDD or BIP in the group of patients with PSY, the effects of psychiatric FH on prefrontal activity were enhanced. These findings demonstrate the association of substantially more severe prefrontal dysfunction with higher genetic loading in major psychiatric disorders.

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A meta-analysis of the risk of major affective disorder in relatives of individuals affected by major depressive disorder or bipolar disorder

Cited by 47 publications

References 90 publications

Influence of Familial Risk for Depression on Cortico-Limbic Connectivity During Implicit Emotional Processing

Influence of Familial Risk for Depression on Cortico-Limbic Connectivity During Implicit Emotional Processing

The Lausanne–Geneva cohort study of offspring of parents with mood disorders: methodology, findings, current sample characteristics, and perspectives

Impact of Familial Loading on Prefrontal Activation in Major Psychiatric Disorders: A Near-Infrared Spectroscopy (NIRS) Study

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