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DNA methylation in cognition comes of age

Nature Neuroscience volume 15, pages 1061–1062 (2012)Cite this article

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A study reveals that aged mice have decreased hippocampal expression of the DNA methyltransferase Dnmt3a2; re-expression in aged mice reverses memory deficits, and knockdown in young mice impairs memory formation.

“Use it or lose it.” So goes the adage for maintaining neurons and their connections, or synapses, in the brain. Increasing research suggests that active mental stimulation and maintenance of overall general physical health may help reduce age-related cognitive decline in the elderly, particularly the risk of dementia and Alzheimer's disease1,2. Although much effort has been dedicated to elucidating the molecular pathways underlying the normal aging process, much less is known about the enzymes that influence these signaling cascades in neurons. Of particular interest are epigenetic mechanisms that mediate long-lasting effects on gene expression and memory formation3. In this issue of Nature Neuroscience, Oliveira et al.4 find that Dnmt3a2, a DNA methyltransferase (DNMT), is critically involved in age-associated cognitive decline in mice. More intriguingly, upregulating Dnmt3a2 can restore cognitive function.

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Figure 1: Elevating Dnmt3a2 can promote memory formation.

Marina Corral

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Authors and Affiliations

  1. Department of Brain and Cognitive Sciences, Susan C. Su and Li-Huei Tsai are at the Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Howard Hughes Medical Institute, Cambridge, Massachusetts, USA.,

    Susan C Su & Li-Huei Tsai

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  1. Susan C Su
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  2. Li-Huei Tsai
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Correspondence to Li-Huei Tsai.

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Su, S., Tsai, LH. DNA methylation in cognition comes of age. Nat Neurosci 15, 1061–1062 (2012). https://doi.org/10.1038/nn.3169

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