Department of Psychiatry, The Hospital for Sick Children, Toronto, Ontario, Canada,
Department of Psychiatry, The Hospital for Sick Children, Toronto, Ontario, Canada.
Neuropsychobiology. 2024;83(2):61-72. doi: 10.1159/000538060. Epub 2024 Apr 4.
Neurobiological dysfunction is associated with depression in children and adolescents. While research in adult depression suggests that inflammation may underlie the association between depression and brain alterations, it is unclear if altered levels of inflammatory markers provoke neurobiological dysfunction in early-onset depression. The aim of this scoping review was to provide an overview of existing literature investigating the potential interaction between neurobiological function and inflammation in depressed children and adolescents.
Systematic searches were conducted in six databases. Primary research studies that included measures of both neurobiological functioning and inflammation among children (≤18 years) with a diagnosis of depression were included.
Four studies (240 participants; mean age 16.0 ± 0.6 years, 62% female) meeting inclusion criteria were identified. Studies primarily examined the inflammatory markers interleukin 6, tumor necrosis factor alpha, C-reactive protein, and interleukin 1 beta. Exploratory whole brain imaging and analysis as well as region of interest approaches focused on the anterior cingulate cortex, basal ganglia, and white matter tracts were conducted. Most studies found correlations between neurobiological function and inflammatory markers; however, depressive symptoms were not observed to moderate these effects.
A small number of highly heterogeneous studies indicate that depression may not modulate the association between altered inflammation and neurobiological dysfunction in children and adolescents. Replication in larger samples using consistent methodological approaches (focus on specific inflammatory markers, examine certain brain areas) is needed to advance the knowledge of potential neuro-immune interactions early in the course of depression.
神经生物学功能障碍与儿童和青少年的抑郁症有关。虽然成人抑郁症的研究表明，炎症可能是抑郁症和大脑改变之间关联的基础，但目前尚不清楚炎症标志物水平的改变是否会引发早期抑郁症的神经生物学功能障碍。本综述的目的是提供现有文献的概述，这些文献调查了抑郁儿童和青少年中神经生物学功能和炎症之间潜在的相互作用。
在六个数据库中进行了系统搜索。纳入了包括诊断为抑郁症的儿童（≤18 岁）的神经生物学功能和炎症测量的原始研究。
确定了四项符合纳入标准的研究（240 名参与者；平均年龄 16.0±0.6 岁，62%为女性）。这些研究主要研究了白细胞介素 6、肿瘤坏死因子 alpha、C 反应蛋白和白细胞介素 1 beta 等炎症标志物。进行了探索性的全脑成像和分析以及感兴趣区域的方法，重点是前扣带皮层、基底神经节和白质束。大多数研究发现神经生物学功能与炎症标志物之间存在相关性；然而，抑郁症状并没有观察到调节这些影响。
少数高度异质的研究表明，抑郁症可能不会调节儿童和青少年中炎症改变与神经生物学功能障碍之间的关联。需要在更大的样本中使用一致的方法学方法（关注特定的炎症标志物，检查特定的大脑区域）进行复制，以推进对抑郁早期潜在神经免疫相互作用的认识。
