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Author | Tong editor | Wang Sizhen plate making ︱ Cha Jiaxue Demyelination (demyelination) is a common disease in central nervous system diseases, and it is also one of the main pathological manifestations of multiple sclerosis (MS) [
In a healthy CNS, oligodendrocyte precursor cells (OPCs) differentiate to give rise to oligodendrocytes (OLs) and form myelin sheaths to encapsulate target axo.
After demyelination, some OLs die, and some survive the demyelination proce.
Demyelination will cause OPCs to activate and differentiate into new OLs to form myelin sheaths; however, OLs that survive demyelination also have the ability to form myelin sheaths again [
Most of the previous studies focused on OLs newly differentiated from OPCs, and the role of surviving OLs in the remyelination process was uncle.
Recently, the laboratory of David.
Lyons at the Centre for Brain Science, University of Edinburgh, UK, published an article in Nature Neuroscience entitled "New oligodendrocytes exhibit more abundant and accurate myelin regeneration than those that survive demyelinatio.
Brain tissue samples found that surviving OLs could form limited myelin sheaths, and myelin sheaths mistargeted neuronal cell bodies rather than axons with high probability [
First, they constructed a zebrafish model that can be used to study demyelination and regeneration: Tg(mbp:TRPV1-tagRFP.
Capsaicin (capsaicin, Csn) induces demyelinati.
By imaging before and after Csn treatment, it was found that there was obvious demyelination in the zebrafish brain 3-24 hours after Csn treatment, but there was obvious remyelination after 24 hours of treatment (F.
1.
This indicates that the zebrafish model can be used to study the process of demyelination and remyelinati.
In addition, the number of OLs decreased by about 33% after 3 h of Csn treatment (F.
2a–f), indicating that there are many OLs that survived the demyelination proce.
Figure 1 Myelin in the brain before and after Csn treatment (Source: Neely et .
, Nat Neurosci, 2022) Figure 2 The number of OLs was not significantly reduced after Csn treatment (Source: Neely et .
, Nat Neurosci, 2022) Then these What role do surviving OLs play in the remyelination process? The researchers continuously observed OLs in the process of myelin damage by in vivo imagi.
Of the 37 OLs observed, 23 cells survived demyelination, and the remaining 4 cells died during demyelinati.
Of the 23 surviving OLs, 22 cells formed new myelin sheat.
In addition, in these surviving OLs, about 60% of the newly formed myelin sheaths were mistargeted to neuronal cell bodies rather than axons (F.
3a,b), and the error rate was much higher than before demyelination (F.
3.
In addition, the researchers also found that the number of new myelin sheaths formed by surviving OLs was significantly reduced compared to before demyelination (F.
3c), and the distance of newly formed myelin sheaths from the soma of OLs was significantly lower than before demyelinati.
to be closer (F.
3.
These results suggest that the ability of surviving OLs to properly form new myelin sheaths during demyelination is very limit.
Figure 3 Surviving OLs have limited remyelination ability (Source: Neely et .
, Nat Neurosci, 2022) In order to better study the function of these surviving myelin sheaths, researchers observed more surviving OLs for a longer period of ti.
The results showed that when surviving OLs formed myelin sheaths, they could not only form new myelin sheaths in previously myelinated locations, but also in previously unmyelinated locations (F.
4a–.
And most of the remyelination occurred after 1 day of Csn treatment, with complete formation of new myelin sheaths by 3 days of Csn treatment (F.
4d–.
Figure 4 The pattern of myelination by surviving OLs (Source: Neely et .
, Nat Neurosci, 2022) In addition, the researchers also observed the effect of Y27632, which promotes myelination, on surviving O.
It was found that Y27632 significantly promoted myelination under normal conditions (F.
5a), but no increased myelination was observed in OLs that survived demyelination (F.
5.
This further illustrates the limited ability of surviving OLs to form myelin sheat.
FigureMyelin-promoting drugs are ineffective against surviving OLs (Credit: Neely et .
, Nat Neurosci, 2022) Histologically, the researchers observed in the gray matter of postmortem MS patients that the myelin of OLs was mistargeted to NeuN-positive neuronal soma, and this phenomenon is very obvious (F.
6), which may be caused by surviving O.
This suggests that despite remyelin remyelin in MS foci (lesions), there are also mistargeted myelin profil.
Figure 6 Myelin-encapsulated cell bodies also exist in the brains of MS patients (Source: Neely et .
, Nat Neurosci, 2022) At the end of the article, the researchers also observed the ability of new OLs to form myelin sheat.
It was found that the ability of newly differentiated OLs to form myelin was consistent with that before demyelination and stronger than that of surviving OLs (F.
7a,b), and the newly differentiated OLs were able to correctly target axo.
This result also suggests that mistargeting of remyelin in MS is caused by surviving OLs rather than de novo O.
FigureRemyelination of nascent OLs (Source: Neely et .
, Nat Neurosci, 2022) Conclusions and discussions, inspiration and prospec.
In conclusion, this work found that the survival of oligodendrocytes (OLs) after demyelination is limited The remyelination ability and abnormal myelin targeting characteristics were validated to some extent in zebrafish models and human MS sampl.
This work also suggests that nascent OLs may be more potential targets for the treatment of demyelinating lesio.
So how to "manipulate" newborn OLs to effectively alleviate demyelinating lesions? This may be the next challenge for researchers to sol.
Original link: https://d.
org/11038/s41593-021-01009-x Talent recruitment ] Biol Psychiatry︱ Tianming Gao’s team revealed that astrocytes regulate adult hippocampal neurogenesis and memory through acetylcholine receptor M1 [2] Curr Biol︱ Chen Nannan et .
revealed that the translation of synaptic regions caused asymmetric distribution of CaMKII protein, and its The role in memory formation [3] Front Aging Neurosci Review︱Fan Dongsheng’s team focused on the interaction between peripheral and central immune systems in amyotrophic lateral sclerosis [4] NPP︱Lu Wei’s team revealed the phosphorylation modification of the auxiliary subunit of GABAA receptors A new mechanism for regulating neurobehavior【5】Cereb Cortex︱Pattern rigidity, the role of temporal dynamics of ventromedial prefrontal cortex on rumination and depression 【6】Front Aging Neurosci︱PTAFR as a novel biomarker for Alzheimer’s 【7】PNAS︱Feng Guoping’s lab reveals the important role of frontal thalamic circuits in working memory 【8】Mol Psychiatry︱Ye Keqiang’s research group reveals that inflammation-activated C/EBPβ/AEP signaling pathway mediates high-fat diet Induced diabetes and Alzheimer's disease【9】PNAS︱Changhe Wang's research group revealed a new mechanism of synaptic exocytosis-endocytosis balance 【10】Autophagy︱Ye Yihong's research group revealed a new molecule that causes neuronal ceroid lipofuscin deposition Mechanism: DNAJC5/CSPα gene mutation leads to lysosomal homeostasis imbalan.
Recommended for high-quality scientific research training courses [1] Practical training course for academic paper writing (Live: 20221~22) [2] Single-cell sequencing and spatial transcriptomics data analysis Symposium (Tencent Online Conference, June 11-12) [3] Symposium on Patch Clamp and Optogenetics and Calcium Imaging Technology May 21-22 Tencent Conference References (swipe up and down to read) [1] Wolswijk.
Oligodendrocyte survival,loss and birth in lesions of chronic-stage multiple sclerosis [.
Brain, 2000, 123(105-1[2]Xin W,Chan J.
Myelin plasticity: sculpting circuits in learning and memory [.
Nat Rev Neurosci, 2020, 21(12): 682-9[3]Neely SA, Williamson JM, Klingseisen A, et .
New oligodendrocytes exhibit more abundant and accurate myelin regeneration than those that survive demyelination [.
Nat Neurosci, 2022, 25(4): 415-2 End of this paper
In a healthy CNS, oligodendrocyte precursor cells (OPCs) differentiate to give rise to oligodendrocytes (OLs) and form myelin sheaths to encapsulate target axo.
After demyelination, some OLs die, and some survive the demyelination proce.
Demyelination will cause OPCs to activate and differentiate into new OLs to form myelin sheaths; however, OLs that survive demyelination also have the ability to form myelin sheaths again [
Most of the previous studies focused on OLs newly differentiated from OPCs, and the role of surviving OLs in the remyelination process was uncle.
Recently, the laboratory of David.
Lyons at the Centre for Brain Science, University of Edinburgh, UK, published an article in Nature Neuroscience entitled "New oligodendrocytes exhibit more abundant and accurate myelin regeneration than those that survive demyelinatio.
Brain tissue samples found that surviving OLs could form limited myelin sheaths, and myelin sheaths mistargeted neuronal cell bodies rather than axons with high probability [
First, they constructed a zebrafish model that can be used to study demyelination and regeneration: Tg(mbp:TRPV1-tagRFP.
Capsaicin (capsaicin, Csn) induces demyelinati.
By imaging before and after Csn treatment, it was found that there was obvious demyelination in the zebrafish brain 3-24 hours after Csn treatment, but there was obvious remyelination after 24 hours of treatment (F.
1.
This indicates that the zebrafish model can be used to study the process of demyelination and remyelinati.
In addition, the number of OLs decreased by about 33% after 3 h of Csn treatment (F.
2a–f), indicating that there are many OLs that survived the demyelination proce.
Figure 1 Myelin in the brain before and after Csn treatment (Source: Neely et .
, Nat Neurosci, 2022) Figure 2 The number of OLs was not significantly reduced after Csn treatment (Source: Neely et .
, Nat Neurosci, 2022) Then these What role do surviving OLs play in the remyelination process? The researchers continuously observed OLs in the process of myelin damage by in vivo imagi.
Of the 37 OLs observed, 23 cells survived demyelination, and the remaining 4 cells died during demyelinati.
Of the 23 surviving OLs, 22 cells formed new myelin sheat.
In addition, in these surviving OLs, about 60% of the newly formed myelin sheaths were mistargeted to neuronal cell bodies rather than axons (F.
3a,b), and the error rate was much higher than before demyelination (F.
3.
In addition, the researchers also found that the number of new myelin sheaths formed by surviving OLs was significantly reduced compared to before demyelination (F.
3c), and the distance of newly formed myelin sheaths from the soma of OLs was significantly lower than before demyelinati.
to be closer (F.
3.
These results suggest that the ability of surviving OLs to properly form new myelin sheaths during demyelination is very limit.
Figure 3 Surviving OLs have limited remyelination ability (Source: Neely et .
, Nat Neurosci, 2022) In order to better study the function of these surviving myelin sheaths, researchers observed more surviving OLs for a longer period of ti.
The results showed that when surviving OLs formed myelin sheaths, they could not only form new myelin sheaths in previously myelinated locations, but also in previously unmyelinated locations (F.
4a–.
And most of the remyelination occurred after 1 day of Csn treatment, with complete formation of new myelin sheaths by 3 days of Csn treatment (F.
4d–.
Figure 4 The pattern of myelination by surviving OLs (Source: Neely et .
, Nat Neurosci, 2022) In addition, the researchers also observed the effect of Y27632, which promotes myelination, on surviving O.
It was found that Y27632 significantly promoted myelination under normal conditions (F.
5a), but no increased myelination was observed in OLs that survived demyelination (F.
5.
This further illustrates the limited ability of surviving OLs to form myelin sheat.
FigureMyelin-promoting drugs are ineffective against surviving OLs (Credit: Neely et .
, Nat Neurosci, 2022) Histologically, the researchers observed in the gray matter of postmortem MS patients that the myelin of OLs was mistargeted to NeuN-positive neuronal soma, and this phenomenon is very obvious (F.
6), which may be caused by surviving O.
This suggests that despite remyelin remyelin in MS foci (lesions), there are also mistargeted myelin profil.
Figure 6 Myelin-encapsulated cell bodies also exist in the brains of MS patients (Source: Neely et .
, Nat Neurosci, 2022) At the end of the article, the researchers also observed the ability of new OLs to form myelin sheat.
It was found that the ability of newly differentiated OLs to form myelin was consistent with that before demyelination and stronger than that of surviving OLs (F.
7a,b), and the newly differentiated OLs were able to correctly target axo.
This result also suggests that mistargeting of remyelin in MS is caused by surviving OLs rather than de novo O.
FigureRemyelination of nascent OLs (Source: Neely et .
, Nat Neurosci, 2022) Conclusions and discussions, inspiration and prospec.
In conclusion, this work found that the survival of oligodendrocytes (OLs) after demyelination is limited The remyelination ability and abnormal myelin targeting characteristics were validated to some extent in zebrafish models and human MS sampl.
This work also suggests that nascent OLs may be more potential targets for the treatment of demyelinating lesio.
So how to "manipulate" newborn OLs to effectively alleviate demyelinating lesions? This may be the next challenge for researchers to sol.
Original link: https://d.
org/11038/s41593-021-01009-x Talent recruitment ] Biol Psychiatry︱ Tianming Gao’s team revealed that astrocytes regulate adult hippocampal neurogenesis and memory through acetylcholine receptor M1 [2] Curr Biol︱ Chen Nannan et .
revealed that the translation of synaptic regions caused asymmetric distribution of CaMKII protein, and its The role in memory formation [3] Front Aging Neurosci Review︱Fan Dongsheng’s team focused on the interaction between peripheral and central immune systems in amyotrophic lateral sclerosis [4] NPP︱Lu Wei’s team revealed the phosphorylation modification of the auxiliary subunit of GABAA receptors A new mechanism for regulating neurobehavior【5】Cereb Cortex︱Pattern rigidity, the role of temporal dynamics of ventromedial prefrontal cortex on rumination and depression 【6】Front Aging Neurosci︱PTAFR as a novel biomarker for Alzheimer’s 【7】PNAS︱Feng Guoping’s lab reveals the important role of frontal thalamic circuits in working memory 【8】Mol Psychiatry︱Ye Keqiang’s research group reveals that inflammation-activated C/EBPβ/AEP signaling pathway mediates high-fat diet Induced diabetes and Alzheimer's disease【9】PNAS︱Changhe Wang's research group revealed a new mechanism of synaptic exocytosis-endocytosis balance 【10】Autophagy︱Ye Yihong's research group revealed a new molecule that causes neuronal ceroid lipofuscin deposition Mechanism: DNAJC5/CSPα gene mutation leads to lysosomal homeostasis imbalan.
Recommended for high-quality scientific research training courses [1] Practical training course for academic paper writing (Live: 20221~22) [2] Single-cell sequencing and spatial transcriptomics data analysis Symposium (Tencent Online Conference, June 11-12) [3] Symposium on Patch Clamp and Optogenetics and Calcium Imaging Technology May 21-22 Tencent Conference References (swipe up and down to read) [1] Wolswijk.
Oligodendrocyte survival,loss and birth in lesions of chronic-stage multiple sclerosis [.
Brain, 2000, 123(105-1[2]Xin W,Chan J.
Myelin plasticity: sculpting circuits in learning and memory [.
Nat Rev Neurosci, 2020, 21(12): 682-9[3]Neely SA, Williamson JM, Klingseisen A, et .
New oligodendrocytes exhibit more abundant and accurate myelin regeneration than those that survive demyelination [.
Nat Neurosci, 2022, 25(4): 415-2 End of this paper
