Division of Psychological and Social Medicine and Developmental Neurosciences, Translational Developmental Neuroscience Section, Faculty of Medicine, Technische Universität Dresden, Dresden, Germany.
Department of Child and Adolescent Psychiatry, Eating Disorder Research and Treatment Center, Faculty of Medicine, Technische Universität Dresden, Dresden, Germany.
Psychol Med. 2023 Nov;53(15):7053-7061. doi: 10.1017/S0033291723000387. Epub 2023 Mar 27.
Anorexia nervosa (AN) is characterized by severe emaciation and drastic reductions of brain mass, but the underlying mechanisms remain unclear. The present study investigated the putative association between the serum-based protein markers of brain damage neurofilament light (NF-L), tau protein, and glial fibrillary acidic protein (GFAP) and cortical thinning in acute AN.
Blood samples and magnetic resonance imaging scans were obtained from 52 predominantly adolescent, female patients with AN before and after partial weight restoration (increase in body mass index >14%). The effect of marker levels before weight gain and change in marker levels on cortical thickness (CT) was modeled at each vertex of the cortical surface using linear mixed-effect models. To test whether the observed effects were specific to AN, follow-up analyses exploring a potential general association of marker levels with CT were conducted in a female healthy control (HC) sample ( = 147).
In AN, higher baseline levels of NF-L, an established marker of axonal damage, were associated with lower CT in several regions, with the most prominent clusters located in bilateral temporal lobes. Tau protein and GFAP were not associated with CT. In HC, no associations between damage marker levels and CT were detected.
A speculative interpretation would be that cortical thinning in acute AN might be at least partially a result of axonal damage processes. Further studies should thus test the potential of serum NF-L to become a reliable, low-cost and minimally invasive marker of structural brain alterations in AN.
神经性厌食症(AN)的特征是严重消瘦和大脑质量的急剧减少,但潜在的机制仍不清楚。本研究调查了脑损伤的血清蛋白标志物神经丝轻链(NF-L)、tau 蛋白和胶质纤维酸性蛋白(GFAP)与急性 AN 皮质变薄之间的潜在关联。
从 52 名主要为青少年女性的 AN 患者中获得了血液样本和磁共振成像扫描,这些患者在部分体重恢复(体重指数增加>14%)前后。使用线性混合效应模型,在皮质表面的每个顶点,对体重增加前标志物水平和标志物水平变化对皮质厚度(CT)的影响进行建模。为了测试观察到的影响是否特定于 AN,在女性健康对照组(HC)样本(=147)中进行了后续分析,以探索标志物水平与 CT 之间的潜在一般关联。
在 AN 中,较高的 NF-L 基线水平(一种公认的轴突损伤标志物)与几个区域的 CT 降低相关,最显著的簇位于双侧颞叶。Tau 蛋白和 GFAP 与 CT 无相关性。在 HC 中,未发现损伤标志物水平与 CT 之间存在相关性。
一种推测的解释是,急性 AN 中的皮质变薄至少部分可能是轴突损伤过程的结果。因此,进一步的研究应该测试血清 NF-L 作为 AN 结构性脑改变可靠、低成本和微创标志物的潜力。