Linking immune-mediated damage to neurodegeneration in multiple sclerosis: could network-based MRI help?
Linking immune-mediated damage to neurodegeneration in multiple sclerosis: could network-based MRI help?
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DOI：
10.1093/braincomms/fcab237
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发表时间：
2021
影响因子：
4.8
通讯作者：
Ciccarelli O
中科院分区：
文献类型：
--
作者：
Groppa S;Gonzalez-Escamilla G;Eshaghi A;Meuth SG;Ciccarelli O
炎症性脱髓鞘是多发性硬化症初始阶段的特征，而进行性轴突和神经元损失同时存在，并显着导致长期身体和认知障碍。从涉及炎症性脱髓鞘或神经变性的多发性硬化症病理学的二元观点到大脑重组的综合动态模型的概念转变的需求尚未得到满足，在该模型中，神经胶质-神经元相互作用、突触改变和灰质病理学是在全脑水平上纵向设想的。功能和结构 MRI 可以描绘复发、缓解或疾病进展的网络标志，这可能与炎症发作、修复和神经变性背后的病理生理学相关。在这里，我们的目标是将多发性硬化症灰质回路动力学的最新发现统一在分子和病理生理学标志的框架内，并结合疾病相关的网络重组，同时强调动物模型（体内和离体）和人类临床数据（成像和组织学）的进展。我们认为，基于 MRI 的大脑网络表征对于更好地描述正在进行的病理学和详细阐述特定机制至关重要，这些机制可用于准确建模和预测整个疾病阶段的疾病过程。格罗帕、冈萨雷斯-埃斯卡米拉等人。提议通过共同解决脱髓鞘、小胶质细胞和可能是代偿性或适应不良的网络重组问题，结束多发性硬化症作为神经炎症或神经退行性的二元观点。所有这些都根据疾病进展和 MRI 可量化的病理过程（包括 GM 病变和萎缩）呈现。
Inflammatory demyelination characterizes the initial stages of multiple sclerosis, while progressive axonal and neuronal loss are coexisting and significantly contribute to the long-term physical and cognitive impairment. There is an unmet need for a conceptual shift from a dualistic view of multiple sclerosis pathology, involving either inflammatory demyelination or neurodegeneration, to integrative dynamic models of brain reorganization, where, glia-neuron interactions, synaptic alterations and grey matter pathology are longitudinally envisaged at the whole-brain level. Functional and structural MRI can delineate network hallmarks for relapses, remissions or disease progression, which can be linked to the pathophysiology behind inflammatory attacks, repair and neurodegeneration. Here, we aim to unify recent findings of grey matter circuits dynamics in multiple sclerosis within the framework of molecular and pathophysiological hallmarks combined with disease-related network reorganization, while highlighting advances from animal models (in vivo and ex vivo) and human clinical data (imaging and histological). We propose that MRI-based brain networks characterization is essential for better delineating ongoing pathology and elaboration of particular mechanisms that may serve for accurate modelling and prediction of disease courses throughout disease stages. Groppa, Gonzalez-Escamilla et al. propose to end the dualistic view of multiple sclerosis as either neuroinflammatory or neurodegenerative, by conjointly addressing demyelination, microglia and network reorganization that can be compensatory or maladaptive. All presented in the light of disease progression and MRI quantifiable pathological processes, including GM lesions and atrophy.
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