Epigenetic mechanisms in neurological disease
Open accessAbstract
The exploration of brain epigenomes, which consist of various types of DNA methylation and covalent histone modifications, is providing new and unprecedented insights into the mechanisms of neural development, neurological disease and aging. Traditionally, chromatin defects in the brain were considered static lesions of early development that occurred in the context of rare genetic syndromes, but it is now clear that mutations and maladaptations of the epigenetic machinery cover a much wider continuum that includes adult-onset neurodegenerative disease. Here, we describe how recent advances in neuroepigenetics have contributed to an improved mechanistic understanding of developmental and degenerative brain disorders, and we discuss how they could influence the development of future therapies for these conditions.
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Several neurological disorders, including Rhett Syndrome, Smith-Magenis syndrome and schizophrenia, are characterized by dysregulation of L1 activity.
“several neurological disorders, including Rhett Syndrome, Smith–Magenis syndrome and schizophrenia are characterized by dysregulation of L1 activity27,45,47.”
From SIRT6 represses LINE1 retrotransposons by ribosylating KAP1 but this repression fails with stress and age (2014) · cites this paper as [47]
In “Mutations affecting DNA methylation and neurological disease” (page unavailable), the review links Rett syndrome to MeCP2 defects and reports de-repression of retrotransposons in MeCP2-deficient neuronal chromatin. It does not establish dysregulated L1 activity as a characteristic of Smith–Magenis syndrome or schizophrenia; its mention of schizophrenia concerns MECP2 variants, not L1 activity. (LLM, conf=0.82)
Experimental — accuracy not yet measuredMonogenetic brain disorders exist in which the phenotype is driven by mutations in genes encoding epigenetic modifiers, such as Rett Syndrome.
“For example, there are monogenetic brain disorders in which the phenotype is driven by mutations in genes encoding epigenetic modifiers, such as Rett Syndrome (see ref 38 for review).”
From Epigenetics and depression (2019) · cites this paper as [38]
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- Authors
- Jakovcevski, M., & Akbarian, S.
- Affiliations
- University of Massachusetts Chan Medical School (US)
- Corresponding author
- Akbarian, Schahram
- Venue
- Nature Medicine
- Published
- 2012-08
- Volume
- 18
- Issue
- 8
- Pages
- 1194-1204
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC3596876
- OpenAlex
- W2012089320
- Cited by
- 450
- References
- 155
- Citations by year
- 2026: 18 · 2025: 20 · 2024: 25 · 2023: 16 · 2022: 26 · 2021: 18 · 2020: 27 · 2019: 28 · 2018: 33 · 2017: 57 · 2016: 44 · 2015: 48 · 2014: 48 · 2013: 34 · 2012: 5
- FWCI
- 3.98
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Autism Speaks
- National Institutes of Health
- Defense Advanced Research Projects Agency
- National Institute of Mental Health (P50MH096890, R01MH086509, R01MH093332)
- National Institute on Drug Abuse
- National Institute of Neurological Disorders and Stroke (R21NS076958)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- neuroepigenetics, epigenetic mechanisms, neurodevelopmental disorders, neurodegenerative diseases, DNA methylation, histone modifications, chromatin, epigenetic therapy, aging, adult-onset neurodegeneration
- MeSH terms
- Animals, Chromatin, Histones, Humans, Nervous System Diseases, DNA Methylation, Epigenesis, Genetic, Mice
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