Abstract
Familial risk plays a significant role in the etiology of schizophrenia (SZ). Many studies using neuroimaging have demonstrated structural and functional alterations in relatives of SZ patients, with significant results found in diverse brain regions involving the anterior cingulate cortex (ACC), caudate, dorsolateral prefrontal cortex (DLPFC), and hippocampus. This study investigated whether unaffected relatives of first episode SZ differ from healthy controls (HCs) in effective connectivity measures among these regions. Forty-six unaffected first-degree relatives of first episode SZ patients—according to the DSM-IV—were studied. Fifty HCs were included for comparison. All subjects underwent resting state functional magnetic resonance imaging (fMRI). We used stochastic dynamic causal modeling (sDCM) to estimate the directed connections between the left ACC, right ACC, left caudate, right caudate, left DLPFC, left hippocampus, and right hippocampus. We used Bayesian parameter averaging (BPA) to characterize the differences. The BPA results showed hyperconnectivity from the left ACC to right hippocampus and hypoconnectivity from the right ACC to right hippocampus in SZ relatives compared to HCs. The pattern of anterior cingulate cortico-hippocampal connectivity in SZ relatives may be a familial feature of SZ risk, appearing to reflect familial susceptibility for SZ.
Highlights
It is well established that familial risk plays a significant role in the etiology of schizophrenia (SZ) through family, adoption, twin, and sibling studies
Regions of Interest For each subject, we studied the effective connectivity among seven region of interest (ROI) including the left dorsolateral prefrontal cortex (DLPFC), and the bilateral
The left panel is for first-degree relatives of SZ patients and right panel refers to healthy controls (HCs)
Summary
It is well established that familial risk plays a significant role in the etiology of schizophrenia (SZ) through family, adoption, twin, and sibling studies. A 31% to 58% concordance rate of SZ exists in monozygotic twins (Tsuang, 2000). Effective Connectivity in Unaffected Relatives of Schizophrenia liability to SZ was 81% (95% confidence interval (CI): 73%, 90%) based on results from 12 twin studies of SZ (Sullivan et al, 2003). Brain structural deficits in twins discordant for SZ were more pronounced in monozygotic than in dizygotic twins (Baare et al, 2001; Hulshoff Pol et al, 2004, 2006), suggesting association of cerebral abnormalities with genetic factors for SZ. The question is whether their first-degree relatives present specific alterations of the brain
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