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Functional dysconnection in the prefrontal–amygdala circuitry in unaffected siblings of patients with bipolar I disorder
Author(s) -
Li ChengTa,
Tu PeiChi,
Hsieh JenChuen,
Lee HsinChen,
Bai YaMei,
Tsai ChiaFen,
Wang ShyhJen,
Hsu JuWei,
Huang KaiLin,
Hong ChenJee,
Su TungPing
Publication year - 2015
Publication title -
bipolar disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.285
H-Index - 129
eISSN - 1399-5618
pISSN - 1398-5647
DOI - 10.1111/bdi.12321
Subject(s) - amygdala , hypoactivity , dorsolateral prefrontal cortex , bipolar disorder , functional magnetic resonance imaging , psychology , neuroscience , prefrontal cortex , medicine , cognition
Objectives Bipolar I disorder ( BD ) is a highly heritable disorder characterized by mood swings between high‐energy and low‐energy states. Amygdala hyperactivity and cortical inhibitory hypoactivity [e.g., of the dorsolateral prefrontal cortex (dl PFC )] have been found in patients with BD , as evidenced by their abnormal resting‐state functional connectivity ( FC ) and glucose utilization ( GU ). However, it has not been determined whether functional abnormalities of the dl PFC –amygdala circuit exist in unaffected, healthy siblings of the patients with BD ( BD sib). Methods Twenty euthymic patients with BD , 20 unaffected matching BD sib of the patient group, and 20 well‐matched healthy control subjects were recruited. We investigated seed‐based FC (seeds: dl PFC ) with resting‐state functional magnetic resonance imaging and GU in the regions of interest (e.g., dl PFC and amygdala) using 18 F‐fluorodeoxyglucose positron emission tomography. Results The FC in the dl PFC (right)–amygdala circuit was statistically abnormal in patients with BD and BD sib, but only the patients with BD demonstrated hypoactive GU bilaterally in the dl PFC and hyperactive GU bilaterally in the amygdala. Facilitating differentiation between the BD groups, the altered FC between dl PFC (right) and amygdala (left) was even more prominent in the patients with BD (p < 0.05). Conclusions There was a dysfunctional connection with intact GU in the dl PFC –amygdala circuit of the BD sib, which highlights the vulnerability in families with BD . Diminished top‐down control from the bilateral dl PFC , which prevents adequate inhibition of limbic hyperactivity, might mediate the development of BD .