DNA methylation impacts on learning and memory in aging
Open accessAbstract
Learning and memory are two of the fundamental cognitive functions that confer us the ability to accumulate knowledge from our experiences. Although we use these two mental skills continuously, understanding the molecular basis of learning and memory is very challenging. Methylation modification of DNA is an epigenetic mechanism that plays important roles in regulating gene expression, which is one of the key processes underlying the functions of cells including neurons. Interestingly, a genome-wide decline in DNA methylation occurs in the brain during normal aging, which coincides with a functional decline in learning and memory with age. It has been speculated that DNA methylation in neurons might be involved in memory coding. However, direct evidence supporting the role of DNA methylation in memory formation is still under investigation. This particular function of DNA methylation has not drawn wide attention despite several important studies that have provided supportive evidence for the epigenetic control of memory formation. To facilitate further exploration of the epigenetic basis of memory function, we will review existing studies on DNA methylation that are related to the development and function of the nervous system. We will focus on studies illustrating how DNA methylation regulates neural activities and memory formation via the control of gene expression in neurons, and relate these studies to various age-related neurological disorders that affect cognitive functions.
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Epigenetic mechanisms are proposed to play crucial roles in ageing and age-related neurodegeneration.
“Epigenetic mechanisms are furthermore proposed to play crucial roles in ageing and age-related neurodegeneration 18, 19.”
From Resilience in mental health: linking psychological and neurobiological perspectives. (2013) · cites this paper as [19]
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- Authors
- Liu, L., van Groen, T., Kadish, I., & Tollefsbol, T. O.
- Affiliations
- University of Alabama at Birmingham (US)
- Corresponding author
- Liu, Liang
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2009-04
- Volume
- 30
- Issue
- 4
- Pages
- 549-560
- ISSN
- 0197-4580 (ISSN-L)
- PMC
- PMC2656583
- OpenAlex
- W1976478257
- Cited by
- 152
- References
- 137
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 4 · 2023: 7 · 2022: 7 · 2021: 5 · 2020: 4 · 2019: 8 · 2018: 4 · 2017: 12 · 2016: 5 · 2015: 6 · 2014: 11 · 2013: 14 · 2012: 12
- FWCI
- 0.79
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R01CA129415)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- DNA methylation, learning and memory, brain aging, epigenetics, gene expression regulation, neurons, memory formation, age-related neurological disorders, cognitive decline, brain development
- MeSH terms
- Aging, Animals, Gene Expression Regulation, Humans, Learning, Learning Disabilities, Memory, Memory Disorders, DNA Methylation, Neurodegenerative Diseases, Epigenesis, Genetic
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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