Neuroscience Applied最新文献

英文中文

Weight matters: Higher BMI is associated with changes in the brain connectome in health and depression 体重很重要：较高的体重指数与健康和抑郁时大脑连接体的变化有关

Neuroscience Applied

Pub Date : 2026-01-01 Epub Date: 2026-02-13 DOI: 10.1016/j.nsa.2026.106984

Aicha Bouzouina , Marius Gruber , Tong Zhao , Carmen Schiweck , Mareike Aichholzer , Carmen Uckermark , Luise V. Claaß , Frederike Stein , Nils R. Winter , Susanne Meinert , Kira Flinkenflügel , Dominik Grotegerd , Janik Goltermann , Tiana Borgers , Elisabeth Leehr , Linda Bonnekoh , Florian Thomas-Odenthal , Marc Pawlitzki , Paula Usemann , Lea Teutenberg , Sharmili Edwin Thanarajah

Overweight and obesity are bidirectionally associated with major depressive disorder (MDD). However, the underlying mechanisms remain unknown. Here, we investigated whether the body mass index (BMI) is associated with alterations in the structural brain connectome of healthy participants and MDD patients and if these changes in connectivity are associated with clinical outcomes. We analyzed the association of BMI with structural brain connectivity in 746 MDD patients and 852 healthy controls from the Marburg-Münster Affective Disorders Cohort Study (MACS). The structural connectome was reconstructed using tractography in diffusion-weighted magnetic resonance imaging data. Associations between BMI brain connectivity were examined using network-based statistics (NBS). NBS identified a subnetwork of the brain connectome associated with BMI (F-threshold = 4.0, p_FWE < 0.05). The number of streamlines within this network were positively correlated with BMI (β = 56.122, SE = 5.50, t = 10.204, p < 0.001, R² = 0.206), suggesting that an increase in BMI is linked to enhanced connectivity within the network. This association did not differ between healthy controls and MDD patients. BMI was further associated with depression severity (

τ

_BDI = 0.052, p = 0.002) and anhedonia (

τ

_SHAPS-D = 0.035, p = 0.034) across all participants, independent of diagnostic status. However, after controlling for BMI, connectivity within the BMI-associated subnetwork was not related to depression severity or anhedonia, suggesting that BMI-related brain connectivity alterations do not independently explain clinical symptom severity. Our findings reveal an association between BMI and structural brain connectivity, both in healthy controls and MDD patients. These findings indicate that increased body weight has a significant association with the brain structural connectome.

超重和肥胖与重度抑郁症（MDD）双向相关。然而，其潜在机制尚不清楚。在这里，我们研究了身体质量指数（BMI）是否与健康参与者和重度抑郁症患者的结构脑连接组的改变有关，以及这些连接的变化是否与临床结果有关。我们分析了来自marburg - m nster情感障碍队列研究（MACS）的746名重度抑郁症患者和852名健康对照者的BMI与脑结构连通性的关系。在磁共振弥散加权成像数据中，利用束状图重建结构连接体。使用基于网络的统计（NBS）检查BMI脑连接之间的关联。NBS发现脑连接组的一个子网络与BMI相关（F-threshold = 4.0, pFWE < 0.05）。该网络内流线的数量与BMI呈正相关（β = 56.122, SE = 5.50, t = 10.204, p < 0.001, R2 = 0.206），表明BMI的增加与网络内连接性的增强有关。这种关联在健康对照组和重度抑郁症患者之间没有差异。BMI进一步与所有参与者的抑郁严重程度（τBDI = 0.052, p = 0.002）和享乐缺乏（τSHAPS-D = 0.035, p = 0.034）相关，与诊断状态无关。然而，在控制BMI后，BMI相关子网络内的连通性与抑郁严重程度或快感缺乏无关，这表明BMI相关的脑连通性改变不能独立解释临床症状的严重程度。我们的研究结果揭示了在健康对照和重度抑郁症患者中BMI和大脑结构连接之间的关联。这些发现表明，体重增加与大脑结构连接体有显著关联。

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引用次数: 0

Balanced polyunsaturated fatty acids diet prevents the D-galactose-induced neuroinflammation and cognitive impairments 均衡多不饱和脂肪酸饮食可预防d -半乳糖引起的神经炎症和认知障碍。

Neuroscience Applied

Pub Date : 2026-01-01 Epub Date: 2026-02-12 DOI: 10.1016/j.nsa.2026.106989

Ivan Marniquet, Juliette Dupont-Viratelle, Flavie Crespo, Alexandra Séré, Sophie Layé, Jean-Christophe Delpech

The rapid increase of the population aged 65 and over is associated with a higher prevalence of people suffering from cognitive functions alterations. Those impairments are partly due to environmental risk factors such as nutrition. In this context, nutrition, and more specifically the ratio of n-6/n-3 polyunsaturated fatty acids (n-6/n-3 PUFAs), has been extensively studied in relation to cognitive impairment and showed a potential beneficial effect on cognitive decline during aging. Clinical epidemiological studies showed a positive association between the n-3 PUFA consumption and cognitive abilities during aging. Preclinical studies have also demonstrated that dietary n-3 PUFA deficiency disrupts spatial memory, and induces alterations in neuronal functions and increased neuroinflammation, whereas dietary n-3 PUFA supplementation had beneficial effects on cognitive abilities and neuroinflammation in aged mice.

Here we showed that a balanced n-6/n-3 PUFAs precursors diet is sufficient to prevent the induction of accelerated aging characteristics such as contextual memory deficits, the altered emotionality status as well as the increased hippocampal neuroinflammation induced by D-galactose injections in mice, involving the activation of the AGE-RAGE pathway.

These results highlight the protective effects of a balanced n-6/n-3 PUFAs precursors on accelerated aging induced inflammatory, cognitive and emotional-like alterations.

65岁及以上人口的快速增长与认知功能改变患者的高患病率有关。这些损伤部分是由于营养等环境风险因素造成的。在这种背景下，营养，更具体地说是n-6/n-3多不饱和脂肪酸（n-6/n-3 PUFAs）的比例，已经被广泛研究与认知障碍的关系，并显示出对衰老过程中认知能力下降的潜在有益影响。临床流行病学研究表明，n-3 PUFA摄入量与老年认知能力呈正相关。临床前研究还表明，饮食中n-3 PUFA缺乏会破坏空间记忆，导致神经元功能改变和神经炎症增加，而饮食中n-3 PUFA补充对老年小鼠的认知能力和神经炎症有有益影响。在这里，我们发现平衡的n-6/n-3 PUFAs前体饮食足以防止诱导加速衰老特征，如上下文记忆缺陷，情绪状态的改变以及d -半乳糖注射诱导的小鼠海马神经炎症的增加，包括AGE-RAGE通路的激活。这些结果强调了平衡的n-6/n-3 PUFAs前体对加速衰老引起的炎症、认知和情绪样改变的保护作用。

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引用次数: 0

Adult separation anxiety and insomnia symptoms in individuals with mood and anxiety disorders 情绪和焦虑障碍患者的成人分离焦虑和失眠症状

Neuroscience Applied

Pub Date : 2026-01-01 Epub Date: 2025-12-01 DOI: 10.1016/j.nsa.2025.106877

Stefano Pini , Daniela Tramontano , Benedetta Nardi , Laura Palagini , Barbara Milrod , David S. Baldwin , Katharina Domschke , Miriam Schiele , Chiara Bonelli , Federico Giovannoni , Gabriele Massimetti , Liliana Dell’Osso , Barbara Carpita

The Diagnostic and Statistical Manual for Mental disorder (DSM-5) identifies severe sleep disruption as one of the clinical features and diagnostic criteria for Separation Anxiety Disorder (SAD), with one diagnostic criterion being a persistent reluctance or refusal to sleep away from home or to go to sleep without being near a central attachment figure. While SAD is commonly associated with childhood, it can also present in adulthood (A-SAD), especially in individuals with mood and anxiety disorders. During this phase of an individual's life, A-SAD may prominently interfere with daily activities, as well as with sleep. This study aims to evaluate the impact of symptoms of SAD on sleep in a large cohort of patients with mood and anxiety disorders. A total of 404 consecutively recruited outpatients with mood or anxiety disorders were assessed with the Structured Clinical Interview for Separation Anxiety Disorder (SCI-SAS), the Adult Separation Anxiety (ASA-27), and the Hamilton Rating Scales for Depression (HAM–D) and Anxiety (HAM-A). Insomnia symptom scores were calculated using nine items that encompass the definition of sleep disturbances from the Mood Spectrum–Self Report (MOODS-SR). Overall, 91 patients were diagnosed with A-SAD only, 33 with childhood-onset SAD (C-SAD), 79 with both A-SAD and C-SAD, and 201 had no history of SAD. No significant differences were found in HAM-A and HAM-D scores between the four groups, nor in the frequency of their primary diagnosis (anxiety disorders, major depression, or bipolar disorder). However, sleep disturbance scores were significantly higher in participants with A-SAD, with or without C-SAD, compared to only C-SAD or no SAD. Regression analyses revealed that ASA-27 total score was a significant predictor of sleep disturbances (p < .002), while HAM-A and HAM-D scores were not. While sleep disturbances are often linked to anxiety and depressive symptoms, these findings suggest that adult separation anxiety contributes independently to sleep impairment in individuals with mood and anxiety disorders. This highlights the importance of assessing and addressing separation anxiety in clinical practice when treating sleep-related complaints in this population.

《精神障碍诊断与统计手册》（DSM-5）将严重睡眠中断确定为分离焦虑障碍（SAD）的临床特征和诊断标准之一，其中一个诊断标准是持续不愿或拒绝离家睡觉，或者在没有中心依恋对象的情况下睡觉。虽然SAD通常与童年有关，但它也可能出现在成年期（A-SAD），特别是在患有情绪和焦虑障碍的个体中。在个体生命的这一阶段，A-SAD可能显著地干扰日常活动和睡眠。本研究旨在评估SAD症状对一大群情绪和焦虑障碍患者睡眠的影响。采用分离焦虑障碍结构化临床访谈（SCI-SAS）、成人分离焦虑量表（ASA-27）和汉密尔顿抑郁量表（HAM-D）和焦虑量表（HAM-A）对404例连续招募的情绪或焦虑障碍门诊患者进行评估。失眠症状的评分是根据情绪谱自我报告（mods - sr）中包含睡眠障碍定义的9个项目来计算的。总体而言，91例患者仅诊断为A-SAD， 33例为儿童期发病的SAD (C-SAD)， 79例同时患有A-SAD和C-SAD， 201例无SAD病史。四组之间的HAM-A和HAM-D评分没有显著差异，他们的主要诊断（焦虑症、重度抑郁症或双相情感障碍）的频率也没有显著差异。然而，与只有C-SAD或没有SAD的参与者相比，伴有或不伴有C-SAD的A-SAD参与者的睡眠障碍得分明显更高。回归分析显示ASA-27总分是睡眠障碍的显著预测因子（p < .002），而HAM-A和HAM-D评分则不是。虽然睡眠障碍通常与焦虑和抑郁症状有关，但这些发现表明，成人分离焦虑对患有情绪和焦虑障碍的个体的睡眠障碍有独立的影响。这突出了在临床实践中评估和解决分离焦虑的重要性，当治疗这一人群的睡眠相关投诉时。

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引用次数: 0

Machine learning-based identification of neural markers for transdiagnostic psychopathology across development 基于机器学习的跨发育跨诊断精神病理学神经标记物识别

Neuroscience Applied

Pub Date : 2026-01-01 Epub Date: 2026-01-02 DOI: 10.1016/j.nsa.2025.105574

J. von Trott , S. Mena , F. Coutts , L. Berger , C. Vetter , P.A. Lalousis , N. Koutsouleris

引用次数: 0

A role for Glycine Transporter-2 inhibitors in regulating accumbal dopamine levels and voluntary alcohol intake in rats 甘氨酸转运蛋白-2抑制剂在调节大鼠伏隔多巴胺水平和自愿酒精摄入中的作用

Neuroscience Applied

Pub Date : 2026-01-01 Epub Date: 2026-01-02 DOI: 10.1016/j.nsa.2025.105540

Y. Olsson , K. Danielsson , A. Domi , H. Lidö , M. Ericson , B. Söderpalm

引用次数: 0

Plasma-based metabolomic and lipidomic analyses reveal the potential biomarker LPE 16:0 as predictor for treatment outcome in a depression study 在一项抑郁症研究中，基于血浆代谢组学和脂质组学分析揭示了LPE 16:0作为治疗结果预测因子的潜在生物标志物

Neuroscience Applied

Pub Date : 2026-01-01 Epub Date: 2026-01-02 DOI: 10.1016/j.nsa.2025.105581

C. Hohoff , S.M. Wissing , L. Steinbach , H. Althaus , T. Lange , S. Schuchardt , E. Van Assche , B.T. Baune

引用次数: 0

INTENSIFY prior to therapy resistance - PsychSTRATA as an innovative project for identifying and stratifying therapy resistance 在治疗抵抗之前加强- PsychSTRATA作为一个创新项目，用于识别和分层治疗抵抗

Neuroscience Applied

Pub Date : 2026-01-01 Epub Date: 2026-01-02 DOI: 10.1016/j.nsa.2025.105584

S. Fromme , C. Okhuijsen-Pfeifer , I. Winter-van Rossum , B.T. Baune

引用次数: 0

A multimodal observational case-control study exploring gut microbiota – hippocampus alterations in high positive schizotypy individuals from the general population 一项多模式观察性病例对照研究，探索普通人群中高阳性分裂型个体的肠道微生物群-海马体改变

Neuroscience Applied

Pub Date : 2026-01-01 Epub Date: 2026-01-02 DOI: 10.1016/j.nsa.2025.105585

G.C. Iseli , J.F.V. Castellanos , D. Coynel , J. Stone , M. Zurita Soler , P. Allen , F. Zelaya , M. Derrien , U.E. Lang , M. Debbané , U. Ettinger , J. Raes , A. Schmidt

引用次数: 0

Factor analysis of the Hungarian version of the alcohol relapse risk scale: a recommendation of a shortened version 匈牙利版酒精复发风险量表的因素分析：推荐缩短版

Neuroscience Applied

Pub Date : 2026-01-01 Epub Date: 2026-01-02 DOI: 10.1016/j.nsa.2025.105546

O. Bagi , F.F. Farkas , J. Gajdics , B.K. Kádár , B. Andó , B.A. Lázár , I.K. Pribék

引用次数: 0

Early transcriptomic changes predict long-term treatment outcome of ketamine versus midazolam in patients with treatment-resistant depression in the KADS study 在KADS研究中，早期转录组变化可预测治疗难治性抑郁症患者氯胺酮与咪达唑仑的长期治疗结果

Neuroscience Applied

Pub Date : 2026-01-01 Epub Date: 2026-01-02 DOI: 10.1016/j.nsa.2025.105591

S.M. Wissing , C. Hohoff , E. Van Assche , T. Lange , L. Steinbach , D. Barton , M. Berk , G.L. Carter , V. Dong , P.B. Fitzgerald , V. Galvez , N. Glozier , P. Glue , M.L. Hackett , D. Hadzi-Pavlovic , A.J. Harvey , S. Hood , D.M. Martin , P.B. Mitchell , N. Mills , B.T. Baune

引用次数: 0

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