Emerging Roles of Exosomes in Huntington's Disease.
Huntington’s disease
biomarker
exosome
extracellular vesicle
huntingtin
neurodegeneration
polyQ
therapy
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
15 Apr 2021
15 Apr 2021
Historique:
received:
30
03
2021
revised:
12
04
2021
accepted:
13
04
2021
entrez:
30
4
2021
pubmed:
1
5
2021
medline:
14
5
2021
Statut:
epublish
Résumé
Huntington's disease (HD) is a rare hereditary autosomal dominant neurodegenerative disorder, which is caused by expression of mutant huntingtin protein (mHTT) with an abnormal number of glutamine repeats in its N terminus, and characterized by intracellular mHTT aggregates (inclusions) in the brain. Exosomes are small extracellular vesicles that are secreted generally by all cell types and can be isolated from almost all body fluids such as blood, urine, saliva, and cerebrospinal fluid. Exosomes may participate in the spreading of toxic misfolded proteins across the central nervous system in neurodegenerative diseases. In HD, such propagation of mHTT was observed both in vitro and in vivo. On the other hand, exosomes might carry molecules with neuroprotective effects. In addition, due to their capability to cross blood-brain barrier, exosomes hold great potential as sources of biomarkers available from periphery or carriers of therapeutics into the central nervous system. In this review, we discuss the emerging roles of exosomes in HD pathogenesis, diagnosis, and therapy.
Identifiants
pubmed: 33920936
pii: ijms22084085
doi: 10.3390/ijms22084085
pmc: PMC8071291
pii:
doi:
Substances chimiques
Huntingtin Protein
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Grantová Agentura České Republiky
ID : 19-01747S
Organisme : Ministerstvo Školství, Mládeže a Tělovýchovy
ID : LTC18079
Organisme : European Cooperation in Science and Technology (COST)
ID : CA16119
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