Explicating the role of amygdala substructure alterations in the link between hypoleptinemia and rumination in anorexia nervosa

IF 5.3 2区医学 Q1 PSYCHIATRY

Acta Psychiatrica Scandinavica Pub Date : 2023-09-08 DOI:10.1111/acps.13607

Marie-Louis Wronski, Charlotte Hohnemann, Fabio Bernardoni, Klaas Bahnsen, Arne Doose, Dominic Arold, Katrin Borucki, Laura M. Holsen, Elizabeth A. Lawson, Franziska Plessow, Kerstin Weidner, Veit Roessner, Stefan Diestel, Joseph A. King, Maria Seidel, Stefan Ehrlich

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引用次数: 0

Abstract

Objective

The amygdaloid complex plays a pivotal role in emotion processing and has been associated with rumination transdiagnostically. In anorexia nervosa (AN), we previously observed differential reductions of amygdala nuclei volumes (rostral-medial cluster substantially affected) and, in another study, elevated food−/weight-related rumination. Both amygdala volumes and rumination frequency correlated with characteristically suppressed leptin levels in AN. Thus, we hypothesized that amygdala nuclei alterations might be associated with AN-related rumination and potentially mediate the leptin-rumination relationship in AN.

Methods

Rumination (food−/weight-related) was assessed using ecological momentary assessment for a 14-day period. We employed frequentist and Bayesian linear mixed effects models in females with AN (n = 51, 12–29 years, majority admitted to inpatient treatment) and age-matched healthy females (n = 51) to investigate associations between rostral-medial amygdala nuclei volume alterations (accessory basal, cortical, medial nuclei, corticoamygdaloid transitions) and rumination. We analyzed mediation effects using multi-level structural equation models.

Results

Reduced right accessory basal and cortical nuclei volumes predicted more frequent weight-related rumination in AN; both nuclei fully mediated the effect of leptin on weight-related rumination. In contrast, we found robust evidence for the absence of amygdala nuclei volume effects on rumination in healthy females.

Conclusion

This study provides first evidence for the relevance of specific amygdala substructure reductions regarding cognitive symptom severity in AN and points toward novel mechanistic insight into the relationship between hypoleptinemia and rumination, which might involve the amygdaloid complex. Our findings in AN may have important clinical value with respect to understanding the beneficial neuropsychiatric effects of leptin (treatment) in AN and potentially other psychiatric conditions such as depression.

Abstract Image

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解释杏仁核亚结构改变在神经性厌食症的低肽血症和反刍之间的联系中的作用

目的杏仁核复合体在情绪加工中起关键作用，并与反刍相关。在神经性厌食症(AN)中，我们之前观察到杏仁核体积的差异减少(喙侧-内侧簇受到严重影响)，在另一项研究中，食物/体重相关反刍增加。杏仁核体积和反刍频率与AN中特征性抑制的瘦素水平相关。因此，我们假设杏仁核的改变可能与AN相关的反刍有关，并可能介导AN中瘦素与反刍的关系。方法采用生态瞬时评价法对14 d的反刍(与食物/体重相关)进行评价。我们在AN女性(n = 51, 12-29岁，大多数住院治疗)和年龄匹配的健康女性(n = 51)中采用频率和贝叶斯线性混合效应模型来研究杏仁核喙侧-内侧核体积改变(附属基底核、皮质核、内侧核、皮质杏仁核转换)与反刍之间的关系。采用多层次结构方程模型分析中介效应。结果右侧副基底核和皮质核体积的减小预示着AN患者体重相关反刍的频率增加;两个核完全介导瘦素对体重相关反刍的影响。相反，我们发现了强有力的证据，证明杏仁核体积对健康女性反刍没有影响。结论本研究首次证实了AN患者杏仁核亚结构特异性减少与认知症状严重程度之间的相关性，并为探究低肽血症与反刍之间的关系提供了新的机制见解，其中可能涉及杏仁核复合体。我们在AN方面的研究结果可能具有重要的临床价值，有助于理解瘦素(治疗)在AN和潜在的其他精神疾病(如抑郁症)中的有益神经精神作用。

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来源期刊

Acta Psychiatrica Scandinavica 医学-精神病学

CiteScore

11.20

自引率

3.00%

发文量

135

审稿时长

6-12 weeks

期刊介绍： Acta Psychiatrica Scandinavica acts as an international forum for the dissemination of information advancing the science and practice of psychiatry. In particular we focus on communicating frontline research to clinical psychiatrists and psychiatric researchers. Acta Psychiatrica Scandinavica has traditionally been and remains a journal focusing predominantly on clinical psychiatry, but translational psychiatry is a topic of growing importance to our readers. Therefore, the journal welcomes submission of manuscripts based on both clinical- and more translational (e.g. preclinical and epidemiological) research. When preparing manuscripts based on translational studies for submission to Acta Psychiatrica Scandinavica, the authors should place emphasis on the clinical significance of the research question and the findings. Manuscripts based solely on preclinical research (e.g. animal models) are normally not considered for publication in the Journal.