The brain after COVID-19: Compensatory neurogenesis or persistent neuroinflammation?
The brain after COVID-19: Compensatory neurogenesis or persistent neuroinflammation?
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DOI：
10.1016/j.eclinm.2020.100684
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发表时间：
2021-01
影响因子：
15.1
通讯作者：
Fieremans E
中科院分区：
文献类型：
--
作者：
Goldberg E;Podell K;Sodickson DK;Fieremans E
吕一平等人报道，与健康对照组相比，急性疾病三个月后康复的COVID-19患者大脑灰质体积增加，基于mri的白质水扩散测量值也发生了变化。他们认为，神经发生和肥大导致了体积增大，而髓鞘再生通路限制了患者的扩散。如果这些解释是正确的，那么它们表明，在COVID-19恢复过程中，大脑的代偿机制是强有力的、反直觉的。然而，该研究的方法和结果都允许其他解释。这些样本的年龄和性别是匹配的，但与微观结构和体积变量[2]相关的教育或病前神经认知变量则不匹配。这使得患者样本可能比对照样本包含更大、更相互关联的发病前大脑。局部体积增加和弥漫性降低可能反映了持续的神经炎症，而不是神经发生。病毒性神经感染引起炎症状态，激活几种中枢神经系统细胞类型并引起水肿[3]，导致局部脑容量短暂增加。分数各向异性（FA）的增加和弥散性的降低可能反映轴突变性[4]或小胶质细胞增生和炎症[5]，而不是髓鞘再生。细胞毒性水肿可限制扩散；血管源性水肿可导致FA可逆性增加。总的来说，DTI对微观结构的变化是敏感的，但不是特定的。
Yiping Lu et al.[1] report increased grey matter volumes and changes in MRI-based measures of water diffusion in white matter in the brains of recovered COVID-19 patients three months after acute illness, compared to healthy controls. They propose that neurogenesis and hypertrophy caused volumetric enlargement, and pathway remyelination restricted diffusion in the patients. If valid, these explanations suggest vigorous and counter-intuitive compensatory brain mechanisms during recovery from COVID-19. However, both the methodology and the findings of the study allow alternative explanations.The samples were matched for age and sex, but not for educational or premorbid neurocognitive variables known to correlate with microstructural and volumetric variables [2]. This allows the possibility that the patient sample included larger and more interconnected premorbid brains than the control sample. Regional volume increase and decreased diffusivity may reflect persistent neuroinflammation rather than neurogenesis. Viral neuroinfections cause inflammatory states, activating several CNS cell types and causing edema [3], leading to transient increases in regional brain volume. Instead of remyelination, increased fractional anisotropy (FA) and decreased diffusivity may reflect axonal degeneration [4] or microgliosis and inflammation [5]. Cytotoxic edema may restrict diffusion; vasogenic edema may lead to reversible increases in FA. Overall, DTI is sensitive but not specific to changes in microstructure.
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影响因子：
15.1
作者：
Lu, Yiping;Li, Xuanxuan;Yin, Bo
通讯作者：
Yin, Bo
影响因子：
5.7
作者：
Song, SK;Sun, SW;Neufeld, AH
通讯作者：
Neufeld, AH
影响因子：
5.7
作者：
Guglielmetti C;Veraart J;Roelant E;Mai Z;Daans J;Van Audekerke J;Naeyaert M;Vanhoutte G;Delgado Y Palacios R;Praet J;Fieremans E;Ponsaerts P;Sijbers J;Van der Linden A;Verhoye M
通讯作者：
Verhoye M
影响因子：
3.2
作者：
Marques, Paulo Cesar Goncalves;Soares, Jose Miguel Montenegro;Sousa, Nuno Jorge Carvalho
通讯作者：
Sousa, Nuno Jorge Carvalho