In Alzheimer's disease, amyloid beta accumulation is a protective mechanism that ultimately fails.
Alzheimer's disease
[11C]Pittsburgh compound B
[18F]fluorodeoxyglucose
amyloid beta
blood-brain barrier
cerebral blood flow
cerebral glucose metabolism
positron emission tomography
Journal
Alzheimer's & dementia : the journal of the Alzheimer's Association
ISSN: 1552-5279
Titre abrégé: Alzheimers Dement
Pays: United States
ID NLM: 101231978
Informations de publication
Date de publication:
08 Jun 2022
08 Jun 2022
Historique:
revised:
19
04
2022
received:
26
05
2021
accepted:
25
04
2022
pubmed:
9
6
2022
medline:
9
6
2022
entrez:
8
6
2022
Statut:
aheadofprint
Résumé
Here, we claim that amyloid beta (Aβ) accumulation is a protective mechanism that ultimately fails. We predict that more Aβ accumulates in regions with higher rates of glucose metabolism, reaching a maximum followed by progression of pathology. Aβ accumulation is characteristic of Alzheimer's disease (AD) but the accumulation does not correlate with cognitive decline, unlike the rates of glucose metabolism. We compared averaged and individual estimates of regional binding potentials of [ The claim explains the cognitive decline in some patients at a significantly lower level of Aβ deposition than in other patients, as well as the presence of cognitively healthy individuals with high Aβ accumulation. With further support of the hypothesis, the significance of Aβ accumulation in brains of patients with AD may require revision.
Sections du résumé
HYPOTHESIS AND PREDICTIONS
UNASSIGNED
Here, we claim that amyloid beta (Aβ) accumulation is a protective mechanism that ultimately fails. We predict that more Aβ accumulates in regions with higher rates of glucose metabolism, reaching a maximum followed by progression of pathology.
BACKGROUND
BACKGROUND
Aβ accumulation is characteristic of Alzheimer's disease (AD) but the accumulation does not correlate with cognitive decline, unlike the rates of glucose metabolism.
STRATEGY
METHODS
We compared averaged and individual estimates of regional binding potentials of [
SIGNIFICANCE
CONCLUSIONS
The claim explains the cognitive decline in some patients at a significantly lower level of Aβ deposition than in other patients, as well as the presence of cognitively healthy individuals with high Aβ accumulation. With further support of the hypothesis, the significance of Aβ accumulation in brains of patients with AD may require revision.
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Novo Nordisk Scandinavia and Aarhus University
ID : NOVA
Organisme : Novo Nordisk Scandinavia and Aarhus University
ID : AUFF-E-2016-9-27
Organisme : Jaschafonden, Skibsreder Per Henriksen R og Hustrus Fond
Informations de copyright
© 2022 The Authors. Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association.
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