Therapeutic Assay with the Non-toxic C-Terminal Fragment of Tetanus Toxin (TTC) in Transgenic Murine Models of Prion Disease.
Autophagy
Neurodegeneration
Prion
Prion diseases
Tetanus toxin
Journal
Molecular neurobiology
ISSN: 1559-1182
Titre abrégé: Mol Neurobiol
Pays: United States
ID NLM: 8900963
Informations de publication
Date de publication:
Oct 2021
Oct 2021
Historique:
received:
13
04
2021
accepted:
08
07
2021
pubmed:
21
7
2021
medline:
4
2
2022
entrez:
20
7
2021
Statut:
ppublish
Résumé
The non-toxic C-terminal fragment of the tetanus toxin (TTC) has been described as a neuroprotective molecule since it binds to Trk receptors and activates Trk-dependent signaling, activating neuronal survival pathways and inhibiting apoptosis. Previous in vivo studies have demonstrated the ability of this molecule to increase mice survival, inhibit apoptosis and regulate autophagy in murine models of neurodegenerative diseases such as amyotrophic lateral sclerosis and spinal muscular atrophy. Prion diseases are fatal neurodegenerative disorders in which the main pathogenic event is the conversion of the cellular prion protein (PrP
Identifiants
pubmed: 34283400
doi: 10.1007/s12035-021-02489-5
pii: 10.1007/s12035-021-02489-5
pmc: PMC8497292
doi:
Substances chimiques
Tetanus Toxin
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
5312-5326Subventions
Organisme : European Regional Development Fund
ID : POCTEFA 2014-2020
Informations de copyright
© 2021. The Author(s).
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