Long-Term Caloric Restriction Attenuates β-Amyloid Neuropathology and Is Accompanied by Autophagy in APPswe/PS1delta9 Mice.
Alzheimer Disease
/ diet therapy
Amyloid beta-Peptides
/ metabolism
Animal Nutritional Physiological Phenomena
Animals
Aspartic Acid
/ analogs & derivatives
Autophagy
/ physiology
Calcium-Binding Proteins
/ metabolism
Caloric Restriction
/ methods
Cerebral Cortex
/ metabolism
Creatine
/ metabolism
Disease Models, Animal
Fluorodeoxyglucose F18
Glucose
/ metabolism
Hippocampus
/ diagnostic imaging
Magnetic Resonance Spectroscopy
Maze Learning
Mice
Mice, Inbred C3H
Mice, Inbred C57BL
Mice, Transgenic
Microfilament Proteins
/ metabolism
Neurons
/ physiology
Plaque, Amyloid
/ diet therapy
Positron Emission Tomography Computed Tomography
Radiopharmaceuticals
APPswe/PS1delta9
[18F]FDG-PET/CT
amyloid β
autophagy
caloric restriction
iba1
Journal
Nutrients
ISSN: 2072-6643
Titre abrégé: Nutrients
Pays: Switzerland
ID NLM: 101521595
Informations de publication
Date de publication:
18 Mar 2021
18 Mar 2021
Historique:
received:
04
02
2021
revised:
09
03
2021
accepted:
16
03
2021
entrez:
3
4
2021
pubmed:
4
4
2021
medline:
8
5
2021
Statut:
epublish
Résumé
Caloric restriction (CR) slows the aging process, extends lifespan, and exerts neuroprotective effects. It is widely accepted that CR attenuates β-amyloid (Aβ) neuropathology in models of Alzheimer's disease (AD) by so-far unknown mechanisms. One promising process induced by CR is autophagy, which is known to degrade aggregated proteins such as amyloids. In addition, autophagy positively regulates glucose uptake and may improve cerebral hypometabolism-a hallmark of AD-and, consequently, neural activity. To evaluate this hypothesis, APPswe/PS1delta9 (tg) mice and their littermates (wild-type, wt) underwent CR for either 16 or 68 weeks. Whereas short-term CR for 16 weeks revealed no noteworthy changes of AD phenotype in tg mice, long-term CR for 68 weeks showed beneficial effects. Thus, cerebral glucose metabolism and neuronal integrity were markedly increased upon 68 weeks CR in tg mice, indicated by an elevated hippocampal fluorodeoxyglucose [
Identifiants
pubmed: 33803798
pii: nu13030985
doi: 10.3390/nu13030985
pmc: PMC8003277
pii:
doi:
Substances chimiques
Aif1 protein, mouse
0
Amyloid beta-Peptides
0
Calcium-Binding Proteins
0
Microfilament Proteins
0
Radiopharmaceuticals
0
Fluorodeoxyglucose F18
0Z5B2CJX4D
Aspartic Acid
30KYC7MIAI
N-acetylaspartate
997-55-7
Glucose
IY9XDZ35W2
Creatine
MU72812GK0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Deutsche Forschungsgemeinschaft
ID : KU3280/1-2
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