Silveira Leonardo E, Bond David J, MacMillan Erin Leigh, Kozicky Jan-Marie, Muralidharan Kesavan, Bücker Joana, Rosa Adriane Ribeiro, Kapczinski Flavio, Yatham Lakshmi N
1 Mood Disorders Centre, Department of Psychiatry, University of British Columbia, Vancouver, BC, Canada.
2 Laboratory of Molecular Psychiatry, Centro de Pesquisas Experimentais, Hospital de Clínicas de Porto Alegre, and INCT for Translational Medicine, Porto Alegre, Brazil.
Aust N Z J Psychiatry. 2017 Jan;51(1):65-74. doi: 10.1177/0004867415623859. Epub 2016 Jul 11.
Previous studies reported decreased N-acetyl aspartate and increased Glx (the sum of glutamate plus glutamine) in bipolar disorder. Since these studies included patients at different stages of illness, it is unknown whether these changes have a causal role or a consequence of multiple episodes and treatments. The studies in early-stage bipolar disorder patients have the potential to provide answers to these issues. Therefore, we evaluated N-acetyl aspartate and Glx levels in hippocampi of first-episode bipolar disorder patients and health subjects at baseline and at 12 months, and examined the impact of episode recurrence on these measures.
We used single-voxel proton magnetic resonance spectroscopy to compare the hippocampal neurometabolites ( N-acetyl aspartate and Glx) levels between 41 patients with bipolar disorder following recovery from their first-manic episode and 27 matched healthy subjects at recruitment and 12 months later. We also compared N-acetyl aspartate and Glx levels between patients who had a recurrence of a mood episode and those who did not.
There was no main effect of either group (diagnosis) or time for hippocampal N-acetyl aspartate and Glx levels in bipolar disorder patients and healthy subjects. We also did not find any group-by-time interaction for the levels of these metabolites. There were also no differences in N-acetyl aspartate and Glx between patients who experienced a recurrence of a mood episode and those who did not over 12-month follow-up.
Our data suggest that N-acetyl aspartate and Glx levels are not altered in early stage bipolar disorder. Further, these data suggest that episode recurrence in early stages does not have a significant impact on the levels of these metabolites. These may suggest that there may be an early window for intervention to potentially arrest neuroprogression of the disease.
既往研究报道双相情感障碍患者中N-乙酰天门冬氨酸减少，而Glx（谷氨酸与谷氨酰胺之和）增加。由于这些研究纳入了处于疾病不同阶段的患者，因此尚不清楚这些变化是具有因果作用还是多次发作及治疗的结果。对早期双相情感障碍患者的研究有可能为这些问题提供答案。因此，我们评估了首发双相情感障碍患者和健康受试者在基线及12个月时海马体中N-乙酰天门冬氨酸和Glx水平，并研究了发作复发对这些指标的影响。
我们使用单体素质子磁共振波谱法，比较了41例首次躁狂发作恢复后的双相情感障碍患者与27例匹配的健康受试者在入组时及12个月后的海马神经代谢物（N-乙酰天门冬氨酸和Glx）水平。我们还比较了有情绪发作复发的患者与未复发患者之间的N-乙酰天门冬氨酸和Glx水平。
在双相情感障碍患者和健康受试者中，无论是组（诊断）还是时间，对海马体N-乙酰天门冬氨酸和Glx水平均无主要影响。我们也未发现这些代谢物水平存在任何组×时间交互作用。在12个月的随访中，有情绪发作复发的患者与未复发患者之间的N-乙酰天门冬氨酸和Glx也没有差异。
我们的数据表明，早期双相情感障碍患者的N-乙酰天门冬氨酸和Glx水平未发生改变。此外，这些数据表明早期发作复发对这些代谢物水平没有显著影响。这可能提示可能存在一个早期干预窗口，以潜在地阻止疾病的神经进展。
