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  • In this study our goal was to detect alteration

    2018-11-14

    In this study, our goal was to detect alteration of CT in the unmedicated adult MDD and BD-II patients who were in a depressive episode, and compare to the healthy controls to assess morphometric differences and similarities that may reflect common and/or distinct XL184 regions in affective disorders. Considering the similarities and differences in the clinical symptoms and brain alterations revealed in previous studies (de Almeida & Phillips, 2013; Lan et al., 2014), we hypothesized that depressive episode unmedicated adult MDD and BD-II patients would not only have CT abnormalities that they shared in common but also abnormalities in CT that are specific to each disease. Considering the similarities and differences in clinical symptoms and brain alterations revealed in previous studies (de Almeida & Phillips, 2013; Lan et al., 2014), we hypothesized that the depressive unmedicated adult MDD and BD-II patients would not only have CT abnormalities that they shared in common but also abnormalities in CT that are specific to each disorder. And these abnormal regions would likely be the key brain structures involving in depression symptoms, such as the limbic and prefrontal regions. In addition, as BD is considered to have more complexity and severity than MDD, we supposed that the BD patients had more widespread CT abnormalities than the MDD patients.
    Methods and Materials
    Results
    Discussion
    Limitations There are several limitations to be addressed in this study. First, the samples of patients may not fully represent the MDD and BD populations. A previous study indicated that, due to the potential instability of the diagnosis, based on an epidemiological study, approximately 1–5% of MDD subjects will develop BD more than one year after their initial identification (Whiteford et al., 2013). Second, multiple recurrent episodes of conditions in the BD and MDD patients may have impacted the observed morphometric abnormalities. Third, the MDD group showed not only significantly lower in the years of education than the controls, but also significantly higher YMRS score than the BD patients. These may potentially have biased the observed morphometric abnormalities. Therefore, we assessed if the cortical thickness difference was associated with YMRS score or years of education, and found that cortical thickness in these clusters had no significant correlations with years of education or YMRS score. In addition, changes to cortical thickness by some confounders cannot be considered in this study, such as IQ, medication history and rapid cycling in BD patients. Furthermore, the significant results of correlation didn\'t survive after the FDR correction. A future replication study that examines the CT using FreeSurfer by separating first-episode and recurrent episodes of BD or MDD patients in a larger matched sample would be beneficial for elucidating the underlying neurobiological differences between BD and MDD patients. Last but not least, because we carried out a cross-sectional study, we cannot infer whether the abnormal CT in the patients was caused by the brain disorders or whether the patients had innate abnormal brain structures (e.g., neural disposition, genetic origins). A longitudinal study is needed to find evidence for disorder-induced CT changes.
    Conclusion
    Conflicts of Interest
    Author Contributions
    Acknowledgments
    Introduction Obesity is a typical lifestyle-related disease (Stein and Colditz, 2004). The disrupted balance between energy intake and energy expenditure causes obesity, which is defined as the excess accumulation of fat mass (Friedman, 2009). Diet-induced obesity is associated with inflammation not only in the peripheral tissues but also in the hypothalamus (De Souza et al., 2005), by which energy balance is primarily regulated (Morton et al., 2006). The consumption of a high-fat diet (HFD) increases the expression levels of tumor necrosis factor-alpha (TNFα) and interleukin-6 (IL-6) in the arcuate nucleus and lateral hypothalamus (Thaler et al., 2012; De Souza et al., 2005), leading to leptin resistance (De Souza et al., 2005; Zhang et al., 2008; De Git and Adan, 2015). The hypothalamic inflammation induced by a HFD is reported to occur prior to substantial body weight gain, suggesting that it might play a causal role in obesity (Valdearcos et al., 2014; Thaler et al., 2012; De Git and Adan, 2015). Recent studies suggest that glial cells, including microglia, are involved in the inflammatory processes in response to a HFD (De Git and Adan, 2015; Argente-Arizon et al., 2015), although the precise mechanisms by which glial cells regulate hypothalamic inflammation remain to be elucidated.