Aβ-induced vulnerability propagates via the brain's default mode network.
Alzheimer Disease
/ diagnostic imaging
Amyloid beta-Peptides
/ metabolism
Aniline Compounds
Animals
Animals, Genetically Modified
Brain
/ diagnostic imaging
Cognitive Dysfunction
/ diagnostic imaging
Ethylene Glycols
Fluorodeoxyglucose F18
Humans
Magnetic Resonance Imaging
Neural Pathways
/ diagnostic imaging
Neurofibrillary Tangles
/ metabolism
Positron-Emission Tomography
Radiopharmaceuticals
Rats
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
04 06 2019
04 06 2019
Historique:
received:
19
06
2018
accepted:
16
04
2019
entrez:
6
6
2019
pubmed:
6
6
2019
medline:
18
6
2019
Statut:
epublish
Résumé
The link between brain amyloid-β (Aβ), metabolism, and dementia symptoms remains a pressing question in Alzheimer's disease. Here, using positron emission tomography ([
Identifiants
pubmed: 31164641
doi: 10.1038/s41467-019-10217-w
pii: 10.1038/s41467-019-10217-w
pmc: PMC6547716
doi:
Substances chimiques
Amyloid beta-Peptides
0
Aniline Compounds
0
Ethylene Glycols
0
Radiopharmaceuticals
0
Fluorodeoxyglucose F18
0Z5B2CJX4D
florbetapir
6867Q6IKOD
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
2353Subventions
Organisme : Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de Recherche en Santé du Canada)
ID : MOP-11-51-31
Pays : International
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