scholarly journals Central nervous system inflammation is a hallmark of pathogenesis in mouse models of GM1 and GM2 gangliosidosis

Brain ◽  
2003 ◽  
Vol 126 (4) ◽  
pp. 974-987 ◽  
Author(s):  
M. Jeyakumar
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mouse Models ◽  
Gm2 Gangliosidosis ◽  
Central Nervous System Inflammation

scholarly journals CD93 regulates central nervous system inflammation in two mouse models of autoimmune encephalomyelitis

Immunology ◽  
2018 ◽  
Vol 155 (3) ◽  
pp. 346-355 ◽  
Author(s):  
Mark R. Griffiths ◽  
Marina Botto ◽  
Bryan Paul Morgan ◽  
James W. Neal ◽  
Philippe Gasque
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mouse Models ◽  
Autoimmune Encephalomyelitis ◽  
Central Nervous System Inflammation

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 A cell-based drug delivery platform for treating central nervous system inflammation

2021 ◽  
Author(s):  
Oren Levy ◽  
Veit Rothhammer ◽  
Ivan Mascanfroni ◽  
Zhixiang Tong ◽  
Rui Kuai ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Central Nervous System ◽  
Nervous System ◽  
Central Nervous System Inflammation ◽  
Delivery Platform ◽  
A Cell

scholarly journals Viral pre-challenge increases central nervous system inflammation after intracranial interleukin-1β injection

2014 ◽  
Vol 11 (1) ◽  
Author(s):  
Yvonne Couch ◽  
Andrew E Davis ◽  
Inês Sá-Pereira ◽  
Sandra J Campbell ◽  
Daniel C Anthony
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Interleukin 1Β ◽  
Central Nervous System Inflammation
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