Abstract
Previously, we showed that blueberry (BB) supplementation reversed the deleterious effects of aging on motor behavior and neuronal signaling in senescent rodents. We now report that BB-fed (from 4 months of age) APP + PS1 transgenic mice showed no deficits in Y-maze performance (at 12 months of age) with no alterations in amyloid beta burden. It appeared that the protective mechanisms are derived from BB-induced enhancement of memory-associated neuronal signaling (e.g. extracellular signal-regulated kinase) and alterations in neutral sphingomyelin-specific phospholipase C activity. Thus, our data indicate for the first time that it may be possible to overcome genetic predispositions to Alzheimer disease through diet.
MeSH terms
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Alzheimer Disease / drug therapy*
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Alzheimer Disease / genetics
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Alzheimer Disease / physiopathology
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Amyloid beta-Peptides / analysis
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Amyloid beta-Protein Precursor / genetics
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Animals
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Behavior, Animal*
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Blueberry Plants*
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Brain / enzymology
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Diet*
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Disease Models, Animal
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Fruit*
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GTP Phosphohydrolases / metabolism
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Genetic Predisposition to Disease
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Membrane Proteins / genetics
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Memory
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Mice
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Mice, Inbred C57BL
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Mice, Inbred DBA
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Mice, Transgenic
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Mitogen-Activated Protein Kinases / metabolism
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Neurons / physiology
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Phytotherapy
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Plant Extracts / therapeutic use
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Presenilin-1
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Protein Kinase C / metabolism
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Protein Kinase C-alpha
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Signal Transduction*
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Sphingomyelins / metabolism
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Type C Phospholipases / metabolism
Substances
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Amyloid beta-Peptides
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Amyloid beta-Protein Precursor
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Membrane Proteins
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Plant Extracts
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Presenilin-1
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Sphingomyelins
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Prkca protein, mouse
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Protein Kinase C
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Protein Kinase C-alpha
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Mitogen-Activated Protein Kinases
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Type C Phospholipases
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GTP Phosphohydrolases