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Journal of Zhejiang University SCIENCE B 1998 Vol.-1 No.-1 P.

http://doi.org/10.1631/jzus.B2300776


The structure of myelin in the central nervous system and another possible driving force for its formation—myelin compaction


Author(s):  Qi SHAO, Simin CHEN, Tian XU, Yuyu SHI, Zijin SUN, Qingguo WANG, Xueqian WANG, Fafeng CHENG

Affiliation(s):  College of traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing 100029, China; more

Corresponding email(s):   wxqbucm@126.com, fafengcheng@gmail.com

Key Words:  Myelin, Central nervous system, White matter, Myelin compaction


Qi SHAO, Simin CHEN, Tian XU, Yuyu SHI, Zijin SUN, Qingguo WANG, Xueqian WANG, Fafeng CHENG. The structure of myelin in the central nervous system and another possible driving force for its formation—myelin compaction[J]. Journal of Zhejiang University Science B, 1998, -1(-1): .

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%A Qi SHAO
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%A Tian XU
%A Yuyu SHI
%A Zijin SUN
%A Qingguo WANG
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Abstract: 
myelin formation is considered the last true "invention" in the evolution of vertebrate nervous system cell structure. The rapid, jumping pulse propagation achieved by myelin enables the high conduction speed that is the basis of human movement, sensation and cognitive function. As a key structure in the brain, white matter is the gathering place of myelin. However, with age, white matter-associated functions become abnormal, and a large number of myelin sheaths show degenerative changes, causing serious neurological and cognitive disorders. Despite the extensive time and effort invested in exploring myelination and its functions, numerous unresolved issues and challenges persist. In-depth exploration of the functional role of myelin may bring new inspiration for the treatment of central nervous system (CNS) diseases and even mental illnesses. In this study, we conducted a comprehensive examination of the structure and key molecules of the myelin in the CNS, delving into its formation process. Specifically, we propose a new hypothesis regarding the source of power for myelin expansion in which membrane compaction may serve as a driving force for myelin extension. The implications of this hypothesis could provide valuable insights into the pathophysiology of diseases involving myelin malfunction and open new avenues for therapeutic intervention in myelin-related disorders

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