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Thanks to reviewers-2018 感谢评委-2018
Pub Date : 2019-01-01 DOI: 10.1177/1179069519829632
Julia, Cardinali
Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). Journal of Experimental Neuroscience Volume 13: 1 © The Author(s) 2019 Article reuse guidelines: sagepub.com/journals-permissions DOI: 10.1177/1 79069519829632
知识共享非商业性CC BY-NC:本文在知识共享署名-非商业4.0许可(http://www.creativecommons.org/licenses/by-nc/4.0/)的条款下发布,该许可允许非商业用途,复制和分发作品,无需进一步许可,前提是原始作品的署名与SAGE和开放获取页面(https://us.sagepub.com/en-us/nam/open-access-at-sage)上指定的一致。Journal of Experimental Neuroscience卷13:1©The Author(s) 2019文章重用指南:sagepub.com/journals-permissions DOI: 10.1177/1 79069519829632
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引用次数: 0
ZPR1-Dependent Neurodegeneration Is Mediated by the JNK Signaling Pathway JNK信号通路介导zpr1依赖性神经退行性变
Pub Date : 2019-01-01 DOI: 10.1177/1179069519867915
Xiaoting Jiang, Annapoorna Kannan, L. Gangwani
The zinc finger protein ZPR1 deficiency causes neurodegeneration and results in a mild spinal muscular atrophy (SMA)-like disease in mice with reduced Zpr1 gene dosage. Mutation of the survival motor neuron 1 (SMN1) gene causes SMA. Spinal muscular atrophy is characterized by the degeneration of the spinal cord motor neurons caused by chronic low levels of SMN protein. ZPR1 interacts with SMN and is required for nuclear accumulation of SMN. Patients with SMA express reduced levels of ZPR1. Reduced Zpr1 gene dosage increases neurodegeneration and severity of SMA disease in mice. Mechanisms underlying ZPR1-dependent neurodegeneration are largely unknown. We report that neurodegeneration caused by ZPR1 deficiency is mediated by the c-Jun NH2-terminal kinase (JNK) group of mitogen-activated protein kinases (MAPK). ZPR1-dependent neuron degeneration is mediated by central nervous system (CNS)-specific isoform JNK3. ZPR1 deficiency activates the MAPK signaling cascade, MLK3 → MKK7 → JNK3, which phosphorylates c-Jun and activates caspase-mediated neuron degeneration. Neurons from Jnk3-null mice show resistance to ZPR1-dependent neurodegeneration. Pharmacologic inhibition of JNK reduces degeneration of ZPR1-deficient neurons. These data show that ZPR1-dependent neurodegeneration is mediated by the JNK signaling pathway and suggest that ZPR1 downregulation in SMA may contribute to JNK-mediated neurodegeneration associated with SMA pathogenesis.
锌指蛋白ZPR1缺乏导致ZPR1基因剂量减少的小鼠神经退行性变,并导致轻度脊髓性肌萎缩(SMA)样疾病。存活运动神经元1 (SMN1)基因突变导致SMA。脊髓性肌萎缩症以脊髓运动神经元的退化为特征,是由慢性低水平的SMN蛋白引起的。ZPR1与SMN相互作用,是SMN核积累所必需的。SMA患者ZPR1表达水平降低。减少Zpr1基因剂量增加小鼠神经退行性变和SMA疾病的严重程度。zpr1依赖性神经变性的机制在很大程度上是未知的。我们报道了由ZPR1缺陷引起的神经退行性变是由丝裂原活化蛋白激酶(MAPK)的c-Jun nh2末端激酶(JNK)组介导的。zpr1依赖性神经元变性是由中枢神经系统(CNS)特异性亚型JNK3介导的。ZPR1缺陷激活MAPK信号级联,MLK3→MKK7→JNK3,磷酸化c-Jun并激活caspase介导的神经元变性。jnk3缺失小鼠的神经元显示出对zpr1依赖性神经变性的抗性。JNK的药理学抑制可减少zpr1缺失神经元的变性。这些数据表明ZPR1依赖性神经退行性变是由JNK信号通路介导的,提示SMA中ZPR1的下调可能有助于JNK介导的与SMA发病相关的神经退行性变。
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引用次数: 10
Why Is Mom Stressed: Homeorhesis as the Potential Problem and Nicotinamide Riboside as the Potential Solution 为什么妈妈有压力:同质同源性是潜在的问题,烟酰胺核苷是潜在的解决方案
Pub Date : 2019-01-01 DOI: 10.1177/1179069519869679
C. Brenner
The remodeling of female mammalian physiology to support the development of a fertilized egg into an externally breathing individual and then to provide all the nutrition to this individual while remodeling back to nearly her pregestational state is without parallel in male mammalian physiological transitions. While it is common parlance to refer to postpartum depression as a not infrequent stress in women, the postpartum physiological changes after every birth constitute profound metabolic stresses that are understudied and have important nutritional, behavioral, and neurodevelopmental implications for the maternal and neonatal health of every mammalian species. We discovered that the postpartum liver of a lactating female mouse has a depressed nicotinamide adenine dinucleotide (NAD) metabolome linked to circulation of higher levels of NAD metabolites in support of a >20-fold increase in NAD coenzymes in the mammary. Furthermore, by supporting a new mother’s apparent higher demand for NAD precursors, we increased circulation of prolactin, superinduced mammary biosynthetic programs, increased her time of arched-back nursing, enhanced mammary production of brain-derived neurotrophic factor, promoted postgestational weight loss, advanced the neurobehavioral development of her offspring, and allowed them to mature as stronger and more resilient adults with advantages in hippocampal neurogenesis and body composition. These results show that a new mother’s capacity for biosynthesis and functionally important nurturing is apparently limited by NAD. Here, we discuss homeorhetic flow of resources from a new mother to her offspring in the context of NAD metabolism and suggest avenues for future investigation.
雌性哺乳动物生理上的重塑,以支持受精卵发育成一个体外呼吸的个体,然后为这个个体提供所有的营养,同时重塑到接近妊娠期的状态,这在雄性哺乳动物的生理转变中是无与伦比的。虽然人们通常认为产后抑郁是女性的一种常见压力,但每次分娩后的产后生理变化构成了深刻的代谢压力,这一压力尚未得到充分研究,并且对每种哺乳动物的孕产妇和新生儿健康具有重要的营养、行为和神经发育影响。我们发现,在哺乳期雌性小鼠的产后肝脏中,烟酰胺腺嘌呤二核苷酸(NAD)代谢组被抑制,这与NAD代谢产物的高水平循环有关,从而支持乳腺中NAD辅酶的20倍增加。此外,通过支持新妈妈对NAD前体明显更高的需求,我们增加了催乳素的循环,超诱导乳腺生物合成程序,增加了她的弓背护理时间,增强了乳腺脑源性神经营养因子的产生,促进了妊娠后体重减轻,促进了后代的神经行为发育。并使他们成熟为更强壮、更有弹性的成年人,在海马神经发生和身体组成方面具有优势。这些结果表明,NAD明显限制了新母亲的生物合成能力和功能重要的养育能力。在这里,我们讨论了在NAD代谢的背景下资源从新母亲到她的后代的同源性流动,并提出了未来研究的途径。
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引用次数: 3
Obesity Impairs Mobility and Adult Hippocampal Neurogenesis 肥胖影响运动能力和成年海马神经发生
Pub Date : 2019-01-01 DOI: 10.1177/1179069519883580
A. Bracke, G. Domańska, K. Bracke, S. Harzsch, J. van den Brandt, B. Bröker, O. von Bohlen und Halbach
Currently, it is controversially discussed whether a relationship between obesity and cognition exists. We here analyzed a mouse model of obesity (leptin-deficient mice) to study the effects of obesity on the morphology of the hippocampus (a brain structure involved in mechanisms related to learning and memory) and on behavior. Mice aged 4 to 6 months were analyzed. At this age, the obese mice have nearly double the body weight as controls, but display smaller brains (brain volume is about 10% smaller) as control animals of the same age. Adult hippocampal neurogenesis, a process that is linked to learning and memory, might be disturbed in the obese mice and contribute to the smaller brain volume. Adult hippocampal neurogenesis was examined using specific markers for cell proliferation (phosphohistone H3), neuronal differentiation (doublecortin), and apoptosis (caspase 3). The number of phosphohistone H3 and doublecortin-positive cells was markedly reduced in leptin-deficient mice, but not the number of apoptotic cells, indicating that adult hippocampal neurogenesis on the level of cell proliferation was affected. In addition, dendritic spine densities of pyramidal neurons in the hippocampal area CA1 were analyzed using Golgi impregnation. However, no significant change in dendritic spine densities was noted in the obese mice. Moreover, the performance of the mice was analyzed in the open field as well as in the Morris water maze. In the open field test, obese mice showed reduced locomotor activity, but in the Morris water maze they showed similar performance compared with control animals.
目前,人们对肥胖与认知之间是否存在关系进行了有争议的讨论。我们在此分析了一种肥胖小鼠模型(瘦素缺乏小鼠),以研究肥胖对海马体形态(一种参与学习和记忆机制的大脑结构)和行为的影响。4-6岁的小鼠 月进行分析。在这个年龄,肥胖小鼠的体重几乎是对照组的两倍,但与同龄的对照动物相比,它们的大脑较小(大脑体积约小10%)。成年海马神经发生是一个与学习和记忆有关的过程,肥胖小鼠可能会受到干扰,导致大脑体积变小。使用细胞增殖(磷酸组蛋白H3)、神经元分化(双皮质素)和凋亡(胱天蛋白酶3)的特异性标记物检测成年海马神经发生。在瘦素缺乏的小鼠中,磷酸组蛋白H3和双皮质素阳性细胞的数量显著减少,但凋亡细胞的数量没有减少,这表明成年海马神经发生在细胞增殖水平上受到了影响。此外,用高尔基体浸渍法分析了海马CA1区锥体神经元的树突棘密度。然而,肥胖小鼠的树突棘密度没有显著变化。此外,还分析了小鼠在开阔场地和Morris水迷宫中的表现。在野外试验中,肥胖小鼠的运动活性降低,但在莫里斯水迷宫中,与对照动物相比,它们表现出相似的表现。
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引用次数: 21
Diffusion Tensor Imaging of the Evolving Response to Mild Traumatic Brain Injury in Rats 大鼠轻度颅脑损伤演化反应的张量扩散成像
Pub Date : 2019-01-01 DOI: 10.1177/1179069519858627
W. S. Hoogenboom, Todd G Rubin, Kenny Q. Ye, Min-Hui Cui, Kelsey C Branch, Jinyuan Liu, C. Branch, M. Lipton
Mild traumatic brain injury (mTBI), also known as concussion, is a serious public health challenge. Although most patients recover, a substantial minority suffers chronic disability. The mechanisms underlying mTBI-related detrimental effects remain poorly understood. Although animal models contribute valuable preclinical information and improve our understanding of the underlying mechanisms following mTBI, only few studies have used diffusion tensor imaging (DTI) to study the evolution of axonal injury following mTBI in rodents. It is known that DTI shows changes after human concussion and the role of delineating imaging findings in animals is therefore to facilitate understanding of related mechanisms. In this work, we used a rodent model of mTBI to investigate longitudinal indices of axonal injury. We present the results of 45 animals that received magnetic resonance imaging (MRI) at multiple time points over a 2-week period following concussive or sham injury yielding 109 serial observations. Overall, the evolution of DTI metrics following concussive or sham injury differed by group. Diffusion tensor imaging changes within the white matter were most noticeable 1 week following injury and returned to baseline values after 2 weeks. More specifically, we observed increased fractional anisotropy in combination with decreased radial diffusivity and mean diffusivity, in the absence of changes in axial diffusivity, within the white matter of the genu corpus callosum at 1 week post-injury. Our study shows that DTI can detect microstructural white matter changes in the absence of gross abnormalities as indicated by visual screening of anatomical MRI and hematoxylin and eosin (H&E)-stained sections in a clinically relevant animal model of mTBI. Whereas additional histopathologic characterization is required to better understand the neurobiological correlates of DTI measures, our findings highlight the evolving nature of the brain’s response to injury following concussion.
轻度创伤性脑损伤(mTBI),也称为脑震荡,是一个严重的公共卫生挑战。尽管大多数病人都能康复,但仍有相当一部分人患有慢性残疾。mtbi相关有害影响的潜在机制仍然知之甚少。尽管动物模型提供了有价值的临床前信息,并提高了我们对mTBI后潜在机制的理解,但只有很少的研究使用弥散张量成像(DTI)来研究啮齿动物mTBI后轴突损伤的演变。众所周知,DTI在人类脑震荡后表现出变化,因此描述动物成像结果的作用是促进对相关机制的理解。在这项工作中,我们使用啮齿动物模型mTBI研究轴索损伤的纵向指标。我们介绍了45只动物在脑震荡或假性损伤后2周内的多个时间点接受磁共振成像(MRI)的结果,产生了109个系列观察结果。总体而言,各组脑震荡或假性损伤后DTI指标的演变有所不同。损伤后1周白质内弥散张量成像变化最为明显,2周后恢复到基线值。更具体地说,我们观察到,在损伤后1周,膝胼胝体白质内的分数各向异性增加,同时径向弥散性和平均弥散性降低,而轴向弥散性没有变化。我们的研究表明,DTI可以在没有明显异常的情况下检测到mTBI动物模型中解剖MRI和苏木精和伊红(H&E)染色切片的视觉筛查显示的微结构白质变化。虽然需要额外的组织病理学特征来更好地理解DTI测量的神经生物学相关性,但我们的研究结果强调了脑震荡后大脑对损伤反应的进化性质。
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引用次数: 21
Suppression of MAP4K4 Signaling Ameliorates Motor Neuron Degeneration in Amyotrophic Lateral Sclerosis-Molecular Studies Toward New Therapeutics 抑制MAP4K4信号可改善肌萎缩侧索硬化症患者的运动神经元退化——新疗法的分子研究
Pub Date : 2019-01-01 DOI: 10.1177/1179069519862798
M. Watts, Chen Wu, L. Rubin
Amyotrophic lateral sclerosis (ALS), the most common motor neuron (MN) disease of adults, is characterized by the degeneration of upper MNs in the motor cortex and lower MNs in the brain stem and spinal cord. Our recent work suggests that a MAP kinase family member, MAP4K4 (mitogen-activated protein kinase kinase kinase kinase 4), regulates MN degeneration in ALS. Activation of MAP4K4 occurs prior to MN death and inhibition of MAP4K4 improves neurite integrity and neuronal viability in a cell autonomous manner. The mechanism through which MAP4K4 reduction specifically modulates MN viability can be attributed to the attenuation of the c-Jun apoptotic pathway, as well as to the activation of FoxO1-mediated autophagy that reduces the accumulation of protein aggregates. We additionally show the feasibility of MAP4K4 as a drug target using a MAP4K4-specific inhibitor, which improves the survival of both primary and induced pluripotent stem cell (iPSC)-derived MNs. Our studies are thus far the first to highlight a MAP4K4-initiated signaling cascade that contributes to MN degeneration in ALS, providing a new mechanism underlying MN death in disease and a druggable target for new therapeutics. We propose exciting future directions and unexplored avenues based upon this work.
肌萎缩性侧索硬化症(ALS)是成人最常见的运动神经元(MN)疾病,其特征是运动皮层上部MN和脑干和脊髓下部MN的退化。我们最近的研究表明,MAP激酶家族成员MAP4K4(丝裂原激活蛋白激酶激酶激酶激酶4)调节ALS患者的MN变性。MAP4K4的激活发生在MN死亡之前,抑制MAP4K4以细胞自主的方式改善神经突的完整性和神经元的活力。MAP4K4减少特异性调节MN活力的机制可归因于c-Jun凋亡途径的衰减,以及fox01介导的自噬的激活,从而减少蛋白质聚集体的积累。此外,我们还利用MAP4K4特异性抑制剂证明了MAP4K4作为药物靶点的可行性,该抑制剂可提高原代和诱导多能干细胞(iPSC)衍生的MNs的存活率。到目前为止,我们的研究首次强调了map4k4启动的信号级联导致ALS患者MN变性,为MN在疾病中死亡提供了新机制,并为新疗法提供了可药物靶点。基于这项工作,我们提出了令人兴奋的未来方向和未探索的途径。
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引用次数: 13
Neurological Disease Modelling for Spinocerebellar Ataxia Using Zebrafish 利用斑马鱼建立脊髓小脑共济失调的神经系统疾病模型
Pub Date : 2019-01-01 DOI: 10.1177/1179069519880515
K. Namikawa, A. Dorigo, R. Köster
The cerebellum integrates sensory information and motor actions. Increasing experimental evidence has revealed that these functions as well as the cerebellar cytoarchitecture are highly conserved in zebrafish compared with mammals. However, the potential of zebrafish for modelling human cerebellar diseases remains to be addressed. Spinocerebellar ataxias (SCAs) represent a group of genetically inherited cerebellar diseases leading to motor discoordination that is most often caused by affected cerebellar Purkinje cells (PCs). Towards modelling SCAs in zebrafish we identified a small-sized PC-specific regulatory element that was used to develop coexpression vectors with tunable expression strength. These vectors allow for in vivo imaging of SCA-affected PCs by high-resolution fluorescence imaging. Next, zebrafish with SCA type 13 (SCA13) transgene expression were established, revealing that SCA13-induced cell-autonomous PC degeneration results in eye movement deficits. Thus, SCA13 zebrafish mimic the neuropathology of an SCA-affected brain as well as the involved loss of motor control and hence provide a powerful approach to unravel SCA13-induced cell biological pathogenic and cytotoxic mechanisms.
小脑整合感觉信息和运动动作。越来越多的实验证据表明,与哺乳动物相比,斑马鱼的这些功能以及小脑细胞结构都是高度保守的。然而,斑马鱼模拟人类小脑疾病的潜力仍有待解决。脊髓小脑共济失调(SCAs)代表了一组遗传遗传性小脑疾病,导致运动失调,最常由受影响的小脑浦肯野细胞(PCs)引起。为了模拟斑马鱼的sca,我们确定了一个小尺寸的pc特异性调控元件,用于开发具有可调表达强度的共表达载体。这些载体允许通过高分辨率荧光成像对受sca影响的pc进行体内成像。接下来,建立SCA13型(SCA13)转基因表达的斑马鱼,揭示SCA13诱导的细胞自主PC变性导致眼动障碍。因此,SCA13斑马鱼模拟了sca影响的大脑的神经病理学以及相关的运动控制丧失,因此为揭示SCA13诱导的细胞生物学致病和细胞毒性机制提供了有力的方法。
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引用次数: 8
A Further Analysis and Commentary on: Profiling Changes in Cortical Astroglial Cells Following Chronic Stress 对慢性应激后皮质星形胶质细胞图谱变化的进一步分析和评述
Pub Date : 2019-01-01 DOI: 10.1177/1179069519870182
Gianfilippo Coppola, G. Rurak, Stephanie Simard, N. Salmaso
The neuroplasticity hypothesis of depression proposes that major depressive disorders are related to decreased hippocampal and cortical neural plasticity, which is reversed by antidepressant treatment. Astroglial cells have emerged as key mediators of neural plasticity and are involved in the cause and treatment of depression and anxiety-like behaviors. One of the ways that astroglia modulate neuroplasticity is through the formation and maintenance of perineuronal nets (PNNs). Perineuronal nets are important extracellular matrix components that respond to stress and are implicated in anxiety-like behaviors. Normally, astroglial cells continuously turnover PNNs by degrading and donating PNN proteins; however, chronic stress slows PNN protein degradation and increases cortical PNN expression overall. In this report, we used weighted gene co-expression network analysis and eigengene analysis to further delineate the pathways and key regulators involved in the astroglial-PNN relationship following chronic stress. Our analyses indicate that chronic variable stress induces the expression of PNNs through inhibition of trophic pathways and key transcription factors in astroglial cells. These data further support the integral role of astroglial cells in the neuroplasticity hypothesis of depression through their modulation of anxiety-like behaviors and PNNs.
抑郁症的神经可塑性假说认为,重度抑郁症与海马和皮层神经可塑性降低有关,而抗抑郁药物治疗可逆转这种可塑性。星形胶质细胞已成为神经可塑性的关键介质,并参与抑郁和焦虑样行为的病因和治疗。星形胶质细胞调节神经可塑性的途径之一是通过形成和维持神经周围网络(pnn)。神经周围网络是重要的细胞外基质成分,对压力作出反应,并涉及焦虑样行为。正常情况下,星形胶质细胞通过降解和供体PNN蛋白不断地更新PNN;然而,慢性应激减缓了PNN蛋白的降解,并增加了皮层PNN的表达。在本报告中,我们使用加权基因共表达网络分析和特征基因分析来进一步描绘慢性应激后星形胶质细胞- pnn关系的途径和关键调节因子。我们的分析表明,慢性可变应激通过抑制星形胶质细胞的营养通路和关键转录因子来诱导PNNs的表达。这些数据进一步支持星形胶质细胞通过调节焦虑样行为和pnn在抑郁症的神经可塑性假说中的整体作用。
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引用次数: 4
Assessment of Improvement in Oxidative Stress Indices with Resocialization in Memory Retrieval in Y-Maze in Male Rats. 再社会化对y型迷宫记忆提取中氧化应激指标改善的评价。
Pub Date : 2018-12-26 eCollection Date: 2018-01-01 DOI: 10.1177/1179069518820323
Hamidreza Famitafreshi, Morteza Karimian

Introduction: Memory deficit is an important issue in some psychiatric diseases either as a primary symptom or as a comorbid symptom. Factors that determine the decline or improvement of memory are an important subject to reduce the severity of these diseases.

Methods and materials: In this study, 32 male Sprague-Dawley rats were randomly divided into 4 experimental groups: social (control), isolation, resocialization for 3 days, and resocialization for 7 days. Isolation occurred for 14 days. Resocialization groups were resocialized for 3 or 7 days after isolation. In the social group, there was no intervention with normal socializing among the rats. In the isolation group, rats were isolated with no resocialization. In all 4 groups, after performing the Y-maze, the rats' brains were removed to assess oxidative stress status in the hippocampus and prefrontal cortex.

Results: Y-maze performance improved after 3 and 7 days of resocialization. However, oxidative stress status for malondialdehyde, glutathione and nitrite/nitrate returned to normal levels except in 2 experiments after 7 days of resocialization. In addition, in 2 experiments, just glutathione in the prefrontal cortex and nitrite/nitrate in the hippocampus after 3 days of resocialization improved.

Conclusions: A return to normal levels in all types of antioxidant markers in the resocialization groups is not the only factor for improving memory deficits resulting from isolation. Resocialization may also be activating other regulatory mechanisms besides an antioxidant defense.

简介:记忆缺陷在一些精神疾病中是一个重要的问题,无论是作为主要症状还是作为合并症。决定记忆力衰退或改善的因素是降低这些疾病严重程度的重要课题。方法与材料:将32只雄性Sprague-Dawley大鼠随机分为社会(对照组)、隔离、再社会化3 d、再社会化7 d 4个实验组。隔离持续了14天。再社会化组在隔离后进行3天或7天的再社会化。在社交组中,没有干预大鼠之间的正常社交。在隔离组,大鼠被隔离,没有再社会化。在所有四组中,在完成y迷宫后,大鼠的大脑被移除以评估海马和前额皮质的氧化应激状态。结果:再社会化3天和7天后,y型迷宫的表现有所改善。然而,丙二醛、谷胱甘肽和亚硝酸盐的氧化应激状态在7天后恢复到正常水平,只有2个实验例外。此外,在2个实验中,只有前额皮质谷胱甘肽和海马亚硝酸盐/硝酸盐在再社会化3天后有所改善。结论:在再社会化群体中,所有类型的抗氧化标记物恢复到正常水平并不是改善隔离导致的记忆缺陷的唯一因素。除抗氧化防御外,再社会化也可能激活其他调节机制。
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引用次数: 9
An Overlooked Brain Region in the Aetiology of Anorexia Nervosa: The Importance of Behaviourally Driven Neuroimaging Analysis. 神经性厌食症病因学中被忽视的脑区:行为驱动的神经影像学分析的重要性。
Pub Date : 2018-12-20 eCollection Date: 2018-01-01 DOI: 10.1177/1179069518820068
Andrea Phillipou, David Jonathan Castle, Larry Allen Abel, Caroline Gurvich, Susan Lee Rossell

The neurobiological contributions to anorexia nervosa (AN) remain poorly understood, hindering the development of effective neurobiological treatments such as medications and brain stimulation. A large number of studies have been undertaken utilising neuroimaging techniques, such as magnetic resonance imaging (MRI), to gain a better understanding of the brain mechanisms involved in the illness. However, the analyses undertaken by many studies have utilised a whole-brain analytical approach as much of this research has been exploratory in nature. This is, however, problematic as small brain regions that differ between groups may not have the statistical power to produce statistically significant results. This is highlighted in a recent study undertaken by our group utilising diffusion-weighted imaging. In this research, we identified widespread white matter microstructural differences in individuals with AN, but only showed differences in a small brain region (the superior colliculus) when a region-of-interest approach that was driven by behavioural findings was utilised. The importance of hypothesis-driven neuroimaging analyses is discussed in this article.

神经性厌食症(AN)的神经生物学贡献仍然知之甚少,阻碍了有效的神经生物学治疗如药物和脑刺激的发展。大量的研究利用神经成像技术,如磁共振成像(MRI),以更好地了解与疾病有关的大脑机制。然而,许多研究采用了全脑分析方法,因为许多研究本质上是探索性的。然而,这是有问题的,因为各组之间不同的小大脑区域可能没有统计能力产生统计上显著的结果。我们小组最近利用弥散加权成像进行的一项研究强调了这一点。在这项研究中,我们确定了AN患者中广泛存在的白质微观结构差异,但当使用由行为研究结果驱动的兴趣区域方法时,仅显示了小脑区(上丘)的差异。本文讨论了假设驱动的神经影像学分析的重要性。
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引用次数: 3
期刊
Journal of Experimental Neuroscience
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