Home > Publications Database > Long-Term Caloric Restriction Attenuates β-Amyloid Neuropathology and Is Accompanied by Autophagy in APPswe/PS1delta9 Mice. > print

001     156008
005     20240328115555.0
024 7 _ |a 10.3390/nu13030985
|2 doi
024 7 _ |a pmid:33803798
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024 7 _ |a pmc:PMC8003277
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037 _ _ |a DZNE-2021-01140
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Müller, Luisa
|0 0000-0001-7942-3273
|b 0
245 _ _ |a Long-Term Caloric Restriction Attenuates β-Amyloid Neuropathology and Is Accompanied by Autophagy in APPswe/PS1delta9 Mice.
260 _ _ |a Basel
|c 2021
|b MDPI
336 7 _ |a article
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336 7 _ |a ARTICLE
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336 7 _ |a JOURNAL_ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a 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 [18F] ([18F]FDG) uptake and increased N-acetylaspartate-to-creatine ratio using positron emission tomography/computer tomography (PET/CT) imaging and magnet resonance spectroscopy (MRS). Improved neuronal activity and integrity resulted in a better cognitive performance within the Morris Water Maze. Moreover, CR for 68 weeks caused a significant increase of LC3BII and p62 protein expression, showing enhanced autophagy. Additionally, a significant decrease of Aβ plaques in tg mice in the hippocampus was observed, accompanied by reduced microgliosis as indicated by significantly decreased numbers of iba1-positive cells. In summary, long-term CR revealed an overall neuroprotective effect in tg mice. Further, this study shows, for the first time, that CR-induced autophagy in tg mice accompanies the observed attenuation of Aβ pathology.
536 _ _ |a 353 - Clinical and Health Care Research (POF4-353)
|0 G:(DE-HGF)POF4-353
|c POF4-353
|f POF IV
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
650 _ 7 |a APPswe/PS1delta9
|2 Other
650 _ 7 |a [18F]FDG-PET/CT
|2 Other
650 _ 7 |a amyloid β
|2 Other
650 _ 7 |a autophagy
|2 Other
650 _ 7 |a caloric restriction
|2 Other
650 _ 7 |a iba1
|2 Other
650 _ 7 |a Aif1 protein, mouse
|2 NLM Chemicals
650 _ 7 |a Amyloid beta-Peptides
|2 NLM Chemicals
650 _ 7 |a Calcium-Binding Proteins
|2 NLM Chemicals
650 _ 7 |a Microfilament Proteins
|2 NLM Chemicals
650 _ 7 |a Radiopharmaceuticals
|2 NLM Chemicals
650 _ 7 |a Fluorodeoxyglucose F18
|0 0Z5B2CJX4D
|2 NLM Chemicals
650 _ 7 |a Aspartic Acid
|0 30KYC7MIAI
|2 NLM Chemicals
650 _ 7 |a N-acetylaspartate
|0 997-55-7
|2 NLM Chemicals
650 _ 7 |a Glucose
|0 IY9XDZ35W2
|2 NLM Chemicals
650 _ 7 |a Creatine
|0 MU72812GK0
|2 NLM Chemicals
650 _ 2 |a Alzheimer Disease: diet therapy
|2 MeSH
650 _ 2 |a Alzheimer Disease: pathology
|2 MeSH
650 _ 2 |a Amyloid beta-Peptides: metabolism
|2 MeSH
650 _ 2 |a Animal Nutritional Physiological Phenomena
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Aspartic Acid: analogs & derivatives
|2 MeSH
650 _ 2 |a Aspartic Acid: metabolism
|2 MeSH
650 _ 2 |a Autophagy: physiology
|2 MeSH
650 _ 2 |a Calcium-Binding Proteins: metabolism
|2 MeSH
650 _ 2 |a Caloric Restriction: methods
|2 MeSH
650 _ 2 |a Cerebral Cortex: metabolism
|2 MeSH
650 _ 2 |a Creatine: metabolism
|2 MeSH
650 _ 2 |a Disease Models, Animal
|2 MeSH
650 _ 2 |a Fluorodeoxyglucose F18
|2 MeSH
650 _ 2 |a Glucose: metabolism
|2 MeSH
650 _ 2 |a Hippocampus: diagnostic imaging
|2 MeSH
650 _ 2 |a Hippocampus: metabolism
|2 MeSH
650 _ 2 |a Magnetic Resonance Spectroscopy
|2 MeSH
650 _ 2 |a Maze Learning
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Mice, Inbred C3H
|2 MeSH
650 _ 2 |a Mice, Inbred C57BL
|2 MeSH
650 _ 2 |a Mice, Transgenic
|2 MeSH
650 _ 2 |a Microfilament Proteins: metabolism
|2 MeSH
650 _ 2 |a Neurons: physiology
|2 MeSH
650 _ 2 |a Plaque, Amyloid: diet therapy
|2 MeSH
650 _ 2 |a Plaque, Amyloid: pathology
|2 MeSH
650 _ 2 |a Positron Emission Tomography Computed Tomography
|2 MeSH
650 _ 2 |a Radiopharmaceuticals
|2 MeSH
700 1 _ |a Power Guerra, Nicole
|b 1
700 1 _ |a Stenzel, Jan
|b 2
700 1 _ |a Rühlmann, Claire
|b 3
700 1 _ |a Lindner, Tobias
|0 0000-0001-7826-3132
|b 4
700 1 _ |a Krause, Bernd J
|b 5
700 1 _ |a Vollmar, Brigitte
|b 6
700 1 _ |a Teipel, Stefan
|0 P:(DE-2719)2000026
|b 7
|u dzne
700 1 _ |a Kuhla, Angela
|b 8
770 _ _ |a Calorie Restriction’s Effects on Health and Disease: From Basic Research to Human Health
773 _ _ |a 10.3390/nu13030985
|g Vol. 13, no. 3, p. 985 -
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|n 3
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|t Nutrients
|v 13
|y 2021
|x 2072-6643
856 4 _ |y OpenAccess
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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