784. Structural Dysconnectivity of Key Cognitive and Emotional Hubs in Young People at High Genetic Risk for Bipolar Disorder

BackgroundWhite matter (WM) impairments have been reported in patients with bipolar disorder (BD) and those at high familial risk of developing BD. However, the distribution of these impairments has not been well characterized. Few studies have examined WM integrity in young people early in the course of illness and in individuals at familial risk who have not yet passed the peak age of onset.MethodWM integrity was examined in 63 BD subjects, 150 high-risk (HR) individuals and 111 participants with no family history of mental illness (CON). All subjects were aged 12 to 30 years.ResultsThis young BD group had significantly lower fractional anisotropy within the genu of the corpus callosum (CC) compared with the CON and HR groups. Moreover, the abnormality in the genu of the CC was also present in HR participants with recurrent major depressive disorder (MDD) (n = 16) compared with CON participants.ConclusionsOur findings provide important validation of interhemispheric abnormalities in BD patients. The novel finding in HR subjects with recurrent MDD – a group at particular risk of future hypo/manic episodes – suggests that this may potentially represent a trait marker for BD, though this will need to be confirmed in longitudinal follow-up studies.

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Glycogen Synthase Kinase-3 Overexpression Replicates Electroretinogram Anomalies of Offspring at High Genetic Risk for Schizophrenia and Bipolar Disorder

Biological Psychiatry ◽

10.1016/j.biopsych.2013.08.035 ◽

2014 ◽

Vol 76 (2) ◽

pp. 93-100 ◽

Cited By ~ 17

Author(s):

Joëlle Lavoie ◽

Marc Hébert ◽

Jean-Martin Beaulieu

Keyword(s):

Bipolar Disorder ◽

Genetic Risk ◽

Glycogen Synthase ◽

Glycogen Synthase Kinase ◽

Glycogen Synthase Kinase 3 ◽

High Genetic Risk

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Mapping vulnerability to bipolar disorders

European Psychiatry ◽

10.1016/j.eurpsy.2016.01.164 ◽

2016 ◽

Vol 33 (S1) ◽

pp. S124-S125

Author(s):

M.R. Raposo ◽

M.D. Piqueras ◽

I. Martínez ◽

A.L. Galdámez ◽

A. Gil ◽

...

Keyword(s):

Systematic Review ◽

Bipolar Disorder ◽

Genetic Risk ◽

Bipolar Disorders ◽

Grey Matter Volume ◽

High Genetic Risk ◽

The Subject ◽

Mapping Vulnerability ◽

Competing Interest ◽

Left Insula

IntroductionAlthough early interventions in individuals with bipolar disorder may reduce the associated personal and economic burden, the neurobiologic markers of enhanced risk are unknown.ObjectivesThe objective of this paper is to analyze the existence of neurobiological abnormalities in individuals with genetic risk for developing bipolar disorder (HR)Material and methodsA literature search was performed in the available scientific literature on the subject study object, by searching MEDLINE.ResultsThere were 37 studies included in this systematic review. The overall sample for the systematic review included 1258 controls and 996 HR individuals. No significant differences were detected between HR individuals and controls in the selected ROIs (regions of interest): striatum, amygdala, hippocampus, pituitary and frontal lobe. The HR group showed increased grey matter volume compared with patients with established bipolar disorder. The HR individuals showed increased neural response in the left superior frontal gyrus, medial frontal gyrus and left insula compared with controls. The overall results found no significant differences between individuals at high genetic risk and controls since the magnitude of the association as corresponds to an OR < 1.5 (low association)ConclusionThere is accumulating evidence for the existence of neurobiologic abnormalities in individuals at genetic risk for bipolar disorder at various scales of investigation. The etiopathogenesis of bipolar disorder will be better elucidated by future imaging studies investigating larger and more homogeneous samples and using longitudinal designs to dissect neurobiologic abnormalities that are underlying traits of the illness from those related to psychopathologic states, such as episodes of mood exacerbation or pharmacologic treatment.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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