scholarly journals A genetic mouse model of adult-onset, pervasive central nervous system demyelination with robust remyelination

Brain ◽  
2010 ◽  
Vol 133 (10) ◽  
pp. 3017-3029 ◽  
Author(s):  
Maria Traka ◽  
Kavin Arasi ◽  
Robin L. Avila ◽  
Joseph R. Podojil ◽  
Athena Christakos ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mouse Model ◽  
Adult Onset ◽  
Genetic Mouse Model ◽  
Central Nervous System Demyelination

scholarly journals Large-Scale Phenotyping of an Accurate Genetic Mouse Model of JNCL Identifies Novel Early Pathology Outside the Central Nervous System

PLoS ONE ◽  
2012 ◽  
Vol 7 (6) ◽  
pp. e38310 ◽  
Author(s):  
John F. Staropoli ◽  
Larissa Haliw ◽  
Sunita Biswas ◽  
Lillian Garrett ◽  
Sabine M. Hölter ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mouse Model ◽  
Large Scale ◽  
Genetic Mouse Model ◽  
The Central Nervous System

scholarly journals The Function of Selenium in Central Nervous System: Lessons from MsrB1 Knockout Mouse Models

Molecules ◽  
2021 ◽  
Vol 26 (5) ◽  
pp. 1372
Author(s):  
Tengrui Shi ◽  
Jianxi Song ◽  
Guanying You ◽  
Yujie Yang ◽  
Qiong Liu ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Synaptic Plasticity ◽  
Mouse Model ◽  
Mouse Models ◽  
Knockout Mouse ◽  
Methionine Sulfoxide ◽  
Methionine Sulfoxide Reductase ◽  
Knockout Mouse Model ◽  
The Central Nervous System

MsrB1 used to be named selenoprotein R, for it was first identified as a selenocysteine containing protein by searching for the selenocysteine insert sequence (SECIS) in the human genome. Later, it was found that MsrB1 is homologous to PilB in Neisseria gonorrhoeae, which is a methionine sulfoxide reductase (Msr), specifically reducing L-methionine sulfoxide (L-Met-O) in proteins. In humans and mice, four members constitute the Msr family, which are MsrA, MsrB1, MsrB2, and MsrB3. MsrA can reduce free or protein-containing L-Met-O (S), whereas MsrBs can only function on the L-Met-O (R) epimer in proteins. Though there are isomerases existent that could transfer L-Met-O (S) to L-Met-O (R) and vice-versa, the loss of Msr individually results in different phenotypes in mice models. These observations indicate that the function of one Msr cannot be totally complemented by another. Among the mammalian Msrs, MsrB1 is the only selenocysteine-containing protein, and we recently found that loss of MsrB1 perturbs the synaptic plasticity in mice, along with the astrogliosis in their brains. In this review, we summarized the effects resulting from Msr deficiency and the bioactivity of selenium in the central nervous system, especially those that we learned from the MsrB1 knockout mouse model. We hope it will be helpful in better understanding how the trace element selenium participates in the reduction of L-Met-O and becomes involved in neurobiology.

scholarly journals Microglia control small vessel calcification via TREM2

2021 ◽  
Vol 7 (9) ◽  
pp. eabc4898
Author(s):  
Yvette Zarb ◽  
Sucheta Sridhar ◽  
Sina Nassiri ◽  
Sebastian Guido Utz ◽  
Johanna Schaffenrath ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mouse Model ◽  
Vascular Calcification ◽  
Neurovascular Unit ◽  
Small Vessel ◽  
Vascular Pathology ◽  
Cns Development ◽  
Brain Calcification

Microglia participate in central nervous system (CNS) development and homeostasis and are often implicated in modulating disease processes. However, less is known about the role of microglia in the biology of the neurovascular unit (NVU). In particular, data are scant on whether microglia are involved in CNS vascular pathology. In this study, we use a mouse model of primary familial brain calcification, Pdgfbret/ret, to investigate the role of microglia in calcification of the NVU. We report that microglia enclosing vessel calcifications, coined calcification-associated microglia, display a distinct activation phenotype. Pharmacological ablation of microglia with the CSF1R inhibitor PLX5622 leads to aggravated vessel calcification. Mechanistically, we show that microglia require functional TREM2 for controlling vascular calcification. Our results demonstrate that microglial activity in the setting of pathological vascular calcification is beneficial. In addition, we identify a previously unrecognized function of microglia in halting the expansion of vascular calcification.

scholarly journals A neonatal mouse model of central nervous system infections caused by Coxsackievirus B5

2018 ◽  
Vol 7 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Qunying Mao ◽  
Xiaotian Hao ◽  
Yalin Hu ◽  
Ruixiao Du ◽  
Shuhui Lang ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mouse Model ◽  
Neonatal Mouse ◽  
Central Nervous System Infections

scholarly journals Morbillivirus Infection of the Mouse Central Nervous System Induces Region-Specific Upregulation of MMPs and TIMPs Correlated to Inflammatory Cytokine Expression

2001 ◽  
Vol 75 (17) ◽  
pp. 8268-8282 ◽  
Author(s):  
Seng-Thuon Khuth ◽  
Hideo Akaoka ◽  
Axel Pagenstecher ◽  
Olivier Verlaeten ◽  
Marie-Françoise Belin ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mouse Model ◽  
Neurological Disorders ◽  
Dynamic Balance ◽  
Brain Structures ◽  
Cytokine Expression ◽  
Tissue Inhibitors Of Metalloproteinases ◽  
Cns Infection ◽  
Necrosis Factor Alpha

ABSTRACT Viral infection of the central nervous system (CNS) can result in perturbation of cell-to-cell communication involving the extracellular matrix (ECM). ECM integrity is maintained by a dynamic balance between the synthesis and proteolysis of its components, mainly as a result of the action of matrix metalloproteinases (MMPs) and the tissue inhibitors of metalloproteinases (TIMPs). An MMP/TIMP imbalance may be critical in triggering neurological disorders, in particular in virally induced neural disorders. In the present study, a mouse model of brain infection using a neurotropic strain of canine distemper virus (CDV) was used to study the effect of CNS infection on the MMP/TIMP balance and cytokine expression. CDV replicates almost exclusively in neurons and has a unique pattern of expression (cortex, hypothalamus, monoaminergic nuclei, hippocampus, and spinal cord). Here we show that although several mouse brain structures were infected, they exhibited a differential pattern in terms of MMP, TIMP, and cytokine expression, exemplified by (i) a large increase in pro-MMP9 levels, in particular in the hippocampus, which occurred mainly in neurons and was associated with in situ gelatinolytic activity, (ii) specific and significant upregulation of MT1-MMP mRNA expression in the cortex and hypothalamus, (iii) an MMP/TIMP imbalance, suggested by the upregulation of TIMP-1 mRNA in the cortex, hippocampus, and hypothalamus and of TIMP-3 mRNA in the cortex, and (iv) a concomitant region-specific large increase in expression of Th1-like cytokines, such as gamma interferon, tumor necrosis factor alpha, and interleukin 6 (IL-6), contrasting with weaker induction of Th2-like cytokines, such as IL-4 and IL-10. These data indicate that an MMP/TIMP imbalance in specific brain structures, which is tightly associated with a local inflammatory process as shown by the presence of immune infiltrating cells, differentially impairs CNS integrity and may contribute to the multiplicity of late neurological disorders observed in this viral mouse model.

Anomalies Characteristic of Central Nervous System Demyelination

2018 ◽  
Vol 36 (1) ◽  
pp. 59-68 ◽  
Author(s):  
Christine Lebrun ◽  
Orhun H. Kantarci ◽  
Aksel Siva ◽  
Daniel Pelletier ◽  
Darin T. Okuda
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Central Nervous System Demyelination
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