Abstract
Cognitive abilities decline in normal aging, yet the underlying molecular mechanisms are poorly understood. We found that aging was associated with a decrease in the expression of the DNA methyltransferase Dnmt3a2 in the hippocampus and that rescuing Dnmt3a2 levels restored cognitive functions. Moreover, we found that Dnmt3a2 is an activity-regulated immediate early gene that is partly dependent on nuclear calcium signaling and that hippocampal Dnmt3a2 levels determine cognitive abilities in both young adult and aged mice.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Aging / metabolism*
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Aging / psychology
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Animals
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Cognition / physiology*
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Cognition Disorders / enzymology*
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DNA (Cytosine-5-)-Methyltransferases / biosynthesis*
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DNA (Cytosine-5-)-Methyltransferases / metabolism
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DNA (Cytosine-5-)-Methyltransferases / physiology
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DNA Methylation / physiology
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DNA Methyltransferase 3A
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Hippocampus / enzymology*
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Memory Disorders / enzymology
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Memory, Long-Term / physiology
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Mice
Substances
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DNA (Cytosine-5-)-Methyltransferases
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DNA Methyltransferase 3A