Accumulation of amyloid-β in the brain of mouse models of Alzheimer's disease is modified by altered gene expression in the presence of human apoE isoforms during aging.
Humans
Mice
Animals
Alzheimer Disease
/ metabolism
Apolipoprotein E4
/ genetics
Apolipoprotein E3
/ genetics
Mice, Transgenic
Apolipoproteins E
/ metabolism
Amyloid beta-Peptides
/ metabolism
Amyloid beta-Protein Precursor
/ genetics
Brain
/ metabolism
Aging
/ genetics
Protein Isoforms
/ genetics
Gene Expression
Alzheimer's disease
Amyloid-β
Apolipoprotein E
Brain aging
Gene expression
Journal
Neurobiology of aging
ISSN: 1558-1497
Titre abrégé: Neurobiol Aging
Pays: United States
ID NLM: 8100437
Informations de publication
Date de publication:
03 2023
03 2023
Historique:
received:
14
06
2022
revised:
30
11
2022
accepted:
04
12
2022
pubmed:
14
1
2023
medline:
1
2
2023
entrez:
13
1
2023
Statut:
ppublish
Résumé
Apolipoprotein E4 (apoE4) is a risk factor for Alzheimer's disease (AD). Here, we investigated brain amyloid-β (Aβ) accumulation throughout the aging process in an amyloid precursor protein (APP) knock-in (KI) mouse model of AD that expresses human APP
Identifiants
pubmed: 36638682
pii: S0197-4580(22)00257-3
doi: 10.1016/j.neurobiolaging.2022.12.003
pii:
doi:
Substances chimiques
Apolipoprotein E4
0
Apolipoprotein E3
0
Apolipoproteins E
0
Amyloid beta-Peptides
0
Amyloid beta-Protein Precursor
0
Protein Isoforms
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
63-74Informations de copyright
Copyright © 2022 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Disclosure statement All authors report no conflict of interest.