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神经性厌食症部分体重恢复后神经元和神经胶质损伤标志物的纵向差异变化。

Differential longitudinal changes of neuronal and glial damage markers in anorexia nervosa after partial weight restoration.

机构信息

Division of Psychological and Social Medicine and Developmental Neuroscience, Faculty of Medicine, Technische Universität Dresden, Dresden, Germany.

Translational Developmental Neuroscience Section, Eating Disorder Research and Treatment Center, Department of Child and Adolescent Psychiatry, Faculty of Medicine, Technische Universität Dresden, Dresden, Germany.

出版信息

Transl Psychiatry. 2021 Feb 9;11(1):86. doi: 10.1038/s41398-021-01209-w.

Abstract

Atrophic brain changes in acute anorexia nervosa (AN) are often visible to the naked eye on computed tomography or magnetic resonance imaging scans, but it remains unclear what is driving these effects. In neurological diseases, neurofilament light (NF-L) and tau protein have been linked to axonal damage. Glial fibrillary acidic protein (GFAP) has been associated with astroglial injury. In an attempt to shed new light on factors potentially underlying past findings of structural brain alterations in AN, the current study investigated serum NF-L, tau protein, and GFAP levels longitudinally in AN patients undergoing weight restoration. Blood samples were obtained from 54 acutely underweight, predominantly adolescent female AN patients and 54 age-matched healthy control participants. AN patients were studied in the severely underweight state and again after short-term partial weight restoration. Group comparisons revealed higher levels of NF-L, tau protein, and GFAP in acutely underweight patients with AN compared to healthy control participants. Longitudinally, a decrease in NF-L and GFAP but not in tau protein levels was observed in AN patients upon short-term partial weight restoration. These results may be indicative of ongoing neuronal and astroglial injury during the underweight phase of AN. Normalization of NF-L and GFAP but not tau protein levels may indicate an only partial restoration of neuronal and astroglial integrity upon weight gain after initial AN-associated cell damage processes.

摘要

在急性神经性厌食症(AN)中,大脑萎缩的变化在计算机断层扫描或磁共振成像扫描中常常肉眼可见,但尚不清楚是什么导致了这些影响。在神经疾病中,神经丝轻链(NF-L)和tau 蛋白与轴突损伤有关。胶质纤维酸性蛋白(GFAP)与星形胶质细胞损伤有关。为了深入了解潜在的因素,本研究试图对 AN 患者过去发现的结构性脑改变的潜在因素进行新的探索,纵向研究了正在接受体重恢复的 AN 患者的血清 NF-L、tau 蛋白和 GFAP 水平。从 54 名急性体重不足的、以青少年女性为主的 AN 患者和 54 名年龄匹配的健康对照组参与者中采集了血液样本。在极度消瘦状态下对 AN 患者进行了研究,并在短期部分体重恢复后再次进行了研究。组间比较显示,与健康对照组参与者相比,急性消瘦的 AN 患者的 NF-L、tau 蛋白和 GFAP 水平更高。纵向研究显示,在 AN 患者短期部分体重恢复期间,NF-L 和 GFAP 水平下降,但 tau 蛋白水平没有下降。这些结果可能表明在 AN 的消瘦阶段存在持续的神经元和星形胶质细胞损伤。NF-L 和 GFAP 水平的正常化,但 tau 蛋白水平没有正常化,可能表明在初始 AN 相关细胞损伤过程后,体重增加仅部分恢复了神经元和星形胶质细胞的完整性。

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