BDNF DNA methylation changes as a biomarker of psychiatric disorders: literature review and open access database analysis

Zheleznyakova, Galina Yurevna; Cao, Hao; Schiöth, Helgi B.

doi:10.1186/s12993-016-0101-4

Cited by 95 publications

(69 citation statements)

References 70 publications

(98 reference statements)

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“…Aberrant DNA methylation has been implicated in a plethora of studies in neuropsychiatric diseases including schizophrenia, bipolar, and major depression disorders (Bayraktar & Kreutz, 2018;Mill et al, 2008;Murgatroyd et al, 2009). One of the hallmarks of schizophrenia is a down-regulation of BDNF expression that is associated with the enrichment of 5-methylcytosine at gene regulatory domains within the Bdnf promoter (Zheleznyakova et al, 2016). Moreover, elevated hippocampal DNMT3a expression has been reported in the postmortem brain of schizophrenia patients (Zhubi et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Synaptic control of DNA-methylation involves activity-dependent degradation of DNMT3a1 in the nucleus

Bayraktar

Yuanxiang

Gomes

et al. 2019

Preprint

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DNA-methylation is a crucial epigenetic mark for activity-dependent gene expression in neurons. Very little is known how synaptic signals impact promoter methylation in neuronal nuclei. In this study we show that protein levels of the principal de novo DNA-methyltransferase in neurons, DNMT3a1, are tightly controlled by activation of N-methyl-D-aspartate receptors (NMDAR) containing the GluN2A subunit.Interestingly, synaptic NMDAR drive degradation of the methyltransferase in a neddylation-dependent manner. Inhibition of neddylation, the conjugation of the small ubiquitin-like protein NEDD8 to lysine residues, interrupts degradation of DNMT3a1 and results in deficits of promoter methylation of activity-dependent genes, synaptic plasticity as well as memory formation. In turn, the underlying molecular pathway is triggered by the induction of synaptic plasticity and in response to object location learning. Collectively the data show that GluN2A containing NMDAR control synapseto-nucleus signaling that links plasticity-relevant signals to activity-dependent DNAmethylation involved in memory formation.

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Section: Discussionmentioning

confidence: 99%

Synaptic control of DNA-methylation involves activity-dependent degradation of DNMT3a1 in the nucleus

Bayraktar

Yuanxiang

Gomes

et al. 2019

Preprint

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“…The regulation of BDNF by DNA methylation and non-coding RNA in neurological diseases has been reviewed in References [44,45]. However, the change of histone modifications that affect BDNF expression in neurological diseases is an under-investigated area of research.…”

Section: Epigenetics In Neurological Diseasesmentioning

confidence: 99%

Epigenetic Regulation of BDNF Gene during Development and Diseases

Chen

2017

IJMS

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Brain-derived neurotrophic factor (BDNF) is required for the development of the nervous system, proper cognitive function and memory formation. While aberrant expression of BDNF has been implicated in neurological disorders, the transcriptional regulation of BDNF remains to be elucidated. In response to different stimuli, BDNF expression can be initiated from different promoters. Several studies have suggested that the expression of BDNF is regulated by promoter methylation. An emerging theme points to the possibility that histone modifications at the BDNF promoters may link to the neurological pathology. Thus, understanding the epigenetic regulation at the BDNF promoters will shed light on future therapies for neurological disorders. The present review summarizes the current knowledge of histone modifications of the BDNF gene in neuronal diseases, as well as the developmental regulation of the BDNF gene based on data from the Encyclopedia of DNA Elements (ENCODE).

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“…It has a critical role in development [12] and due to its stability and ease of measurement is widely investigated both to understand mechanisms driving disease states, as well as for its potential to be used as a biomarker for numerous health and disease outcomes [13,14,15,16,17,18]. DNA methylation marks have been associated with diseases such as cancer, and therefore show promise for use as independent biomarkers.…”

Section: Epigeneticsmentioning

confidence: 99%

Cord Blood DNA Methylation Biomarkers for Predicting Neurodevelopmental Outcomes

Hodyl

Roberts

Bianco‐Miotto

2016

Genes

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Adverse environmental exposures in pregnancy can significantly alter the development of the fetus resulting in impaired child neurodevelopment. Such exposures can lead to epigenetic alterations like DNA methylation, which may be a marker of poor cognitive, motor and behavioral outcomes in the infant. Here we review studies that have assessed DNA methylation in cord blood following maternal exposures that may impact neurodevelopment of the child. We also highlight some key studies to illustrate the potential for DNA methylation to successfully identify infants at risk for poor outcomes. While the current evidence is limited, in that observations to date are largely correlational, in time and with larger cohorts analyzed and longer term follow-up completed, we may be able to develop epigenetic biomarkers that not only indicate adverse early life exposures but can also be used to identify individuals likely to be at an increased risk of impaired neurodevelopment even in the absence of detailed information regarding prenatal environment.

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BDNF DNA methylation changes as a biomarker of psychiatric disorders: literature review and open access database analysis

Cited by 95 publications

References 70 publications

Synaptic control of DNA-methylation involves activity-dependent degradation of DNMT3a1 in the nucleus

Synaptic control of DNA-methylation involves activity-dependent degradation of DNMT3a1 in the nucleus

Epigenetic Regulation of BDNF Gene during Development and Diseases

Cord Blood DNA Methylation Biomarkers for Predicting Neurodevelopmental Outcomes

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