Abstract
Alzheimer's disease (AD) is the most common dementia and the trigger of its pathological cascade is widely believed to be the overproduction and accumulation of β-amyloid protein (Aβ) in the affected brain. However, effective AD remedies are still anxiously awaited. Recent evidence suggests that curcumin may be a potential agent for AD treatment. In this study, we used 5×FAD transgenic mice as an AD model to investigate the effects of curcumin on AD. Our results showed that curcumin administration (150 or 300 mg/kg/day, intragastrically, for 60 days) dramatically reduced Aβ production by downregulating BACE1 expression, preventing synaptic degradation, and improving spatial learning and memory impairment of 5×FAD mice. These findings suggest that curcumin is a potential candidate for AD treatment.
Keywords:
Alzheimer’s disease (AD); Curcumin; β-Amyloid protein (Aβ); β-Site amyloid precursor protein cleavage enzyme 1 (BACE1).
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amyloid Precursor Protein Secretases / antagonists & inhibitors*
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Amyloid Precursor Protein Secretases / biosynthesis*
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Amyloid Precursor Protein Secretases / genetics
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Amyloid beta-Peptides / antagonists & inhibitors*
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Amyloid beta-Peptides / metabolism*
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Animals
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Anti-Inflammatory Agents, Non-Steroidal / pharmacology
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Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
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Aspartic Acid Endopeptidases / antagonists & inhibitors*
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Aspartic Acid Endopeptidases / biosynthesis*
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Aspartic Acid Endopeptidases / genetics
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Curcumin / pharmacology
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Curcumin / therapeutic use*
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Gene Expression
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Male
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Memory Disorders / drug therapy
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Memory Disorders / metabolism*
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Memory Disorders / pathology
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Mice
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Mice, Inbred C57BL
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Mice, Transgenic
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Peptide Fragments / antagonists & inhibitors*
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Peptide Fragments / metabolism*
Substances
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Amyloid beta-Peptides
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Anti-Inflammatory Agents, Non-Steroidal
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Peptide Fragments
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amyloid beta-protein (1-42)
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Amyloid Precursor Protein Secretases
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Aspartic Acid Endopeptidases
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Bace1 protein, mouse
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Curcumin