Strategy to enhance transgene expression in proximity of amyloid plaques in a mouse model of Alzheimer's disease.
Alzheimer Disease
/ pathology
Amyloid beta-Peptides
/ metabolism
Animals
Astrocytes
/ metabolism
Disease Models, Animal
Gene Expression
Gene Transfer Techniques
Glial Fibrillary Acidic Protein
/ genetics
Liver
/ metabolism
Mice
Mice, Transgenic
Plaque, Amyloid
/ metabolism
Promoter Regions, Genetic
Transgenes
TgCRND8 mice
amyloid-beta peptides
astrocytes
focused ultrasound
gene expression
Journal
Theranostics
ISSN: 1838-7640
Titre abrégé: Theranostics
Pays: Australia
ID NLM: 101552395
Informations de publication
Date de publication:
2019
2019
Historique:
received:
15
05
2019
accepted:
29
08
2019
entrez:
23
11
2019
pubmed:
23
11
2019
medline:
29
8
2020
Statut:
epublish
Résumé
Gene therapy can be designed to efficiently counter pathological features characteristic of neurodegenerative disorders. Here, we took advantage of the glial fibrillary acidic protein (GFAP) promoter to preferentially enhance transgene expression near plaques composed of amyloid-beta peptides (Aβ), a hallmark of Alzheimer's disease (AD), in the TgCRND8 mouse model of amyloidosis.
Identifiants
pubmed: 31754385
doi: 10.7150/thno.36718
pii: thnov09p8127
pmc: PMC6857057
doi:
Substances chimiques
Amyloid beta-Peptides
0
Glial Fibrillary Acidic Protein
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
8127-8137Subventions
Organisme : NIBIB NIH HHS
ID : R01 EB003268
Pays : United States
Organisme : CIHR
ID : FRN93603
Pays : Canada
Organisme : CIHR
ID : FRN 119312
Pays : Canada
Informations de copyright
© The author(s).
Déclaration de conflit d'intérêts
Competing Interests: The authors have declared that no competing interest exists.
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