Functional Impairment of the Nervous System with Glycolipid Deficiencies.
Carbohydrate
Ganglioside
Glycoconjugate
Glycolipid
Glycosphingolipid
Mental health disorder
Neural development
Neural stem cell
Neurodegenerative disease
Neurogenesis
Neurological disorder
Regeneration
Journal
Advances in neurobiology
ISSN: 2190-5215
Titre abrégé: Adv Neurobiol
Pays: United States
ID NLM: 101571545
Informations de publication
Date de publication:
2023
2023
Historique:
pmc-release:
01
01
2024
entrez:
18
10
2022
pubmed:
19
10
2022
medline:
21
10
2022
Statut:
ppublish
Résumé
Patients with nervous system disorders suffer from impaired cognitive, sensory and motor functions that greatly inconvenience their daily life and usually burdens their family and society. It is difficult to achieve functional recovery for the damaged central nervous system (CNS) because of its limited ability to regenerate. Glycosphingolipids (GSLs) are abundant in the CNS and are known to play essential roles in cell-cell recognition, adhesion, signal transduction, and cellular migration, that are crucial in all phases of neurogenesis. Despite intense investigation of CNS regeneration, the roles of GSLs in neural regeneration remain unclear. Here we focus on the respective potentials of glycolipids to promote regeneration and repair of the CNS. Mice lacking glucosylceramide, lactosylceramide or gangliosides show lethal phenotypes. More importantly, patients with ganglioside deficiencies exhibit severe clinical phenotypes. Further, neurodegenerative diseases and mental health disorders are associated with altered GSL expression. Accumulating studies demonstrate that GSLs not only delimit physical regions but also play central roles in the maintenance of the biological functions of neurons and glia. We anticipate that the ability of GSLs to modulate behavior of a variety of molecules will enable them to ameliorate biochemical and neurobiological defects in patients. The use of GSLs to treat such defects in the human CNS will be a paradigm-shift in approach since GSL-replacement therapy has not yet been achieved in this manner clinically.
Identifiants
pubmed: 36255683
doi: 10.1007/978-3-031-12390-0_14
pmc: PMC9793801
mid: NIHMS1855344
doi:
Substances chimiques
Glycolipids
0
Lactosylceramides
0
Glucosylceramides
0
Gangliosides
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
419-448Subventions
Organisme : NINDS NIH HHS
ID : R01 NS100839
Pays : United States
Informations de copyright
© 2023. The Author(s), under exclusive license to Springer Nature Switzerland AG.
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