N-acetylaspartate normalization in bipolar depression after lamotrigine treatment.

N-acetylaspartate normalization in bipolar depression after lamotrigine treatment.
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DOI:
10.1111/bdi.12285
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发表时间:
2015-06
期刊:
影响因子:
5.4
通讯作者:
Frye MA
Frye MA
中科院分区:
医学2区
文献类型:
--
作者:
Croarkin PE;Thomas MA;Port JD;Baruth JM;Choi DS;Abulseoud OA;Frye MA

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目的观察拉莫三嗪治疗前后双相抑郁症患者神经元活力的一般指标n -乙酰天冬氨酸(NAA)和总NAA (tNAA)与n -乙酰天冬氨酸谷氨酸的联合信号。鉴于NAA是通过乙酰辅酶a - l-天冬氨酸- n -乙酰转移酶将天冬氨酸直接乙酰化合成的,我们假设拉莫三嗪治疗可能与NAA水平升高有关。双相抑郁症患者在基线(n = 15)和拉莫三嗪治疗12周后(n = 10)分别对前扣带进行二维质子磁共振波谱检查。一组年龄匹配的健康对照(n = 9)在基线进行扫描以进行比较。在基线时,双相抑郁症患者的NAA显著降低[平均标准偏差(SD) = 1.13 (0.21);p = 0.02]高于对照组[mean (SD) = 1.37(0.27)]。NAA显著升高[mean (SD) = 1.39 (0.21);p = 0.01]和tNAA [mean (SD) = 1.61 (0.25)];拉莫三嗪治疗12周后P = 0.02]。这些数据表明,双相抑郁症的NAA缺陷在拉莫三嗪治疗后正常化。未来的研究有必要评估基线NAA水平是否是识别拉莫三嗪反应模式的潜在生物标志物,以及这种功能性脑变化是否具有相关的临床反应。
To examine N-acetylaspartate (NAA), a general marker of neuronal viability, and total NAA (tNAA), the combined signal of NAA and N-acetylaspartylglutamate, in bipolar depression before and after lamotrigine treatment. Given that NAA is synthesized through direct acetylation of aspartate by acetyl-coenzyme A-L-aspartate-N-acetyltransferase, we hypothesized that treatment with lamotrigine would be associated with an increase in NAA level. Patients with bipolar depression underwent two-dimensional proton magnetic resonance spectroscopy of the anterior cingulate at baseline (n = 15) and after 12 weeks of lamotrigine treatment (n = 10). A group of age-matched healthy controls (n = 9) underwent scanning at baseline for comparison. At baseline, patients with bipolar depression had significantly lower NAA [mean standard deviation (SD) = 1.13 (0.21); p = 0.02] than controls [mean (SD) = 1.37 (0.27)]. Significant increases in NAA [mean (SD) = 1.39 (0.21); p = 0.01] and tNAA [mean (SD) = 1.61 (0.25); p = 0.02] levels were found after 12 weeks of lamotrigine treatment. These data suggest an NAA deficit in bipolar depression that is normalized after lamotrigine treatment. Future research is warranted to evaluate whether baseline NAA level is a potential biomarker for identifying lamotrigine response patterns and whether this functional brain change has an associated clinical response.