首页> 外文期刊>Journal of neural transmission >Glial and neuronal damage markers in patients with anorexia nervosa.
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Glial and neuronal damage markers in patients with anorexia nervosa.

机译:神经性厌食症患者的神经胶质和神经元损伤标志物。

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Anorexia nervosa (AN) commonly arises during adolescence leading to interruptions of somatic and psychological development as well as to atrophic brain changes. It remains unclear whether these brain changes are related to the loss of neurons, glia, neuropil or merely due to fluid shifts. We determined leptin levels and two brain-derived damage markers: glial fibrillary acidic protein (GFAP) and neuron-specific enolase (NSE) of 43 acute AN patients and 50 healthy control woman (HCW). Peripheral GFAP and NSE concentrations of AN patients were not elevated and not different from HCW. Subjects with particularly low leptin concentration, indicating severe malnutrition, did not show abnormal values either. During weight recovery the marker proteins remained unchanged. Our preliminary results are in line with neuroimaging studies supporting the reversibility of brain changes in AN and do not substantiate hypotheses relying on the extensive damage of brain cells as an explanation for cerebral atrophy in AN.
机译:神经性厌食症(AN)通常在青春期出现,导致躯体和心理发育受阻以及脑萎缩。尚不清楚这些脑部变化是否与神经元,神经胶质,神经纤维的丧失有关,还是仅由于体液移位而引起。我们确定了43名急性AN患者和50名健康对照妇女(HCW)的瘦素水平和两个脑源性损伤标记:神经胶质纤维酸性蛋白(GFAP)和神经元特异性烯醇化酶(NSE)。 AN患者的外周血GFAP和NSE浓度没有升高,与HCW没有差异。瘦素浓度特别低的受试者,表明严重营养不良,也未显示异常值。在体重恢复期间,标记蛋白保持不变。我们的初步结果与支持AN中脑部变化可逆性的神经影像学研究相符,并且不能证实依赖于脑细胞广泛损伤作为AN中脑萎缩的解释的假说。

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