Objective:

Recent studies of patients with bipolar disorder or at high genetic risk reveal structural dysconnections among key brain networks supporting cognitive and affective processes. Understanding the longitudinal trajectories of these networks across the peak age range of bipolar disorder onset could inform mechanisms of illness onset or resilience.

Methods:

Longitudinal diffusion-weighted MRI and phenotypic data were acquired at baseline and after 2 years in 183 individuals ages 12–30 years in two cohorts: 97 unaffected individuals with a first-degree relative with bipolar disorder (the high-risk group) and 86 individuals with no family history of mental illness (the control group). Whole-brain structural networks were derived using tractography, and longitudinal changes in these networks were studied using network-based statistics and mixed linear models.

Results:

Both groups showed widespread longitudinal changes, comprising both increases and decreases in structural connectivity, consistent with a shared neurodevelopmental process. On top of these shared changes, high-risk participants showed weakening of connectivity in a network encompassing the left inferior and middle frontal areas, left striatal and thalamic structures, the left fusiform, and right parietal and occipital regions. Connections among these regions strengthened in the control group, whereas they weakened in the high-risk group, shifting toward a cohort with established bipolar disorder. There was marginal evidence for even greater network weakening in those who had their first manic or hypomanic episode before follow-up.

Conclusions:

Neurodevelopment from adolescence into early adulthood is associated with a substantial reorganization of structural brain networks. Differences in these maturational processes occur in a multisystem network in individuals at high genetic risk of bipolar disorder. This may represent a novel candidate to understand resilience and predict conversion to bipolar disorder.

中文翻译：

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双相情感障碍高遗传风险年轻人结构连接的纵向变化

客观的：

最近对双相情感障碍或高遗传风险患者的研究揭示了支持认知和情感过程的关键大脑网络之间的结构性失联。了解这些网络在双相情感障碍发病高峰年龄范围内的纵向轨迹可以为疾病发病或恢复机制提供信息。

方法：

纵向扩散加权 MRI 和表型数据在基线时和 2 年后在两个队列中的 183 名 12-30 岁的个体中获得：97 名未受影响的个体，其一级亲属患有双相情感障碍（高风险组）和 86 名个体无精神疾病家族史（对照组）。全脑结构网络是使用牵引描记法得出的，并且这些网络中的纵向变化是使用基于网络的统计数据和混合线性模型来研究的。

结果：

两组都表现出广泛的纵向变化，包括结构连接性的增加和减少，这与共同的神经发育过程一致。除了这些共同变化之外，高风险参与者在包括左下额叶和中额叶区域、左纹状体和丘脑结构、左梭形、右顶叶和枕叶区域的网络中表现出连通性减弱。这些区域之间的联系在对照组中得到加强，而在高风险组中则减弱，转向已确定双相情感障碍的队列。有边际证据表明，在随访前首次出现躁狂或轻躁狂发作的人的网络减弱程度更大。

结论：

从青春期到成年早期的神经发育与大脑结构网络的大量重组有关。这些成熟过程的差异发生在双相情感障碍高遗传风险个体的多系统网络中。这可能代表了一个新的候选者来理解复原力并预测转化为双相情感障碍。