Epigenetic mechanisms: A possible link between autism spectrum disorders and fetal alcohol spectrum disorders

Varadinova, Miroslava; Boyadjieva, Nadka

doi:10.1016/j.phrs.2015.09.011

Cited by 17 publications

(23 citation statements)

References 162 publications

(167 reference statements)

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“…Taken together, it appears that the immediate effects of prenatal alcohol exposure are to decrease global DNA methylation and MeCP2 levels [129,159,160,161,162,164,189,190], while the longer lasting effects, observed during adolescence or adulthood, are an increase in DNA methylation and MeCP2 levels [165,166,168,171,172]. Based on the neurodevelopmental literature, a global reduction in DNA methylation and MeCP2 levels might be expected to promote astrocyte differentiation, and possibly delay or decrease neurogenesis [72,89].…”

Section: Fasd and Dna Methylationmentioning

confidence: 99%

Chromatin Switches during Neural Cell Differentiation and Their Dysregulation by Prenatal Alcohol Exposure

Gavin

Grayson

Varghese

et al. 2017

Genes

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Prenatal alcohol exposure causes persistent neuropsychiatric deficits included under the term fetal alcohol spectrum disorders (FASD). Cellular identity emerges from a cascade of intrinsic and extrinsic (involving cell-cell interactions and signaling) processes that are partially initiated and maintained through changes in chromatin structure. Prenatal alcohol exposure influences neuronal and astrocyte development, permanently altering brain connectivity. Prenatal alcohol exposure also alters chromatin structure through histone and DNA modifications. However, the data linking alcohol-induced differentiation changes with developmental alterations in chromatin structure remain to be elucidated. In the first part of this review, we discuss the sequence of chromatin structural changes involved in neural cell differentiation during normal development. We then discuss the effects of prenatal alcohol on developmental histone modifications and DNA methylation in the context of neurogenesis and astrogliogenesis. We attempt to synthesize the developmental literature with the FASD literature, proposing that alcohol-induced changes to chromatin structure account for altered neurogenesis and astrogliogenesis as well as altered neuron and astrocyte differentiation. Together these changes may contribute to the cognitive and behavioral abnormalities in FASD. Future studies using standardized alcohol exposure paradigms at specific developmental stages will advance the understanding of how chromatin structural changes impact neural cell fate and maturation in FASD.

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Section: Fasd and Dna Methylationmentioning

confidence: 99%

Chromatin Switches during Neural Cell Differentiation and Their Dysregulation by Prenatal Alcohol Exposure

Gavin

Grayson

Varghese

et al. 2017

Genes

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“…Another recent animal study supports the concept that acute prenatal ethanol exposure reduces the number of nephrons, which effects later adult renal function . On the other hand, there might be overlapping influences between several polygenic, epigenetic, and environmental factors in developmental paths that engender both malformations and organ malfunction resulting in disease during adulthood . All this follows the framework first outlined by David Barker hypothesis on developmental origins of health and disease .…”

Section: Discussionmentioning

confidence: 99%

Maternal alcohol consumption during pregnancy and its association with offspring renal function at 30 years: Observation from a birth cohort study

et al. 2018

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“…FASD defects range from macroscopic structural abnormalities to subtle neurobehavioral disabilities . In addition, FASD children might share autistic traits . Secondary disabilities also occur, with the marked incidence of MDD and anxiety disorders, as well as vulnerability to addiction …”

Section: Genome‐wide Epigenetic Investigations and Insights Into Epigmentioning

confidence: 99%

“…The most significant canonical pathways involved govern synaptic plasticity, with prominent DMRs associated to genes involved in glutamatergic transmission and Hippo signaling (Table ). All these pathways are implicated in several NPDs displaying endophenotypes similar to FASD, such as ASDs, BPD and SCZ . Other epigenetic actors affecting histone methylation and miRNAs are also at play in the short‐ and long‐term consequences of PAE.…”

Section: Genome‐wide Epigenetic Investigations and Insights Into Epigmentioning

confidence: 99%

“…60,61 In addition, FASD children might share autistic traits. 62 Secondary disabilities also occur, with the marked incidence of MDD and anxiety disorders, as well as vulnerability to addiction. 59,63 In line with these neuropsychiatric traits, transcriptomic alterations of the GABAergic, glutamatergic, endocannabinoid and retinoic acid pathways occur during neurodevelopment and persist after prenatal [64][65][66][67][68] Differential DNA methylomic profiles are among the most studied epigenetic marks in PAE studies, including ex vivo cell systems or mouse models of chronic voluntary or binge-like drinking by pregnant mothers, or FASD patients.…”

Section: General Epigenetic Mechanismsmentioning

confidence: 99%

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The impact of epigenomic next‐generation sequencing approaches on our understanding of neuropsychiatric disorders

2017

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Patients suffering from psychiatric disorders have a life span burden, which represents an enormous human, family, social, and economical cost. Several concepts have revolutionized our way of appraising neuropsychiatric disorders (NPDs). They result from a combination of genetic factors and environmental insults, and their etiology finds roots in the neurodevelopmental period. As epigenetic mechanisms tightly control brain development, exposure to adverse conditions disturbing the epigenetic landscape of the fetal brain increases the risk of developing NPDs, due to the persistence of abnormal epigenetic signatures, at distance from the initial stimulus. Here, we review these concepts and discuss recent results based on next-generation sequencing (NGS) approaches that have shed light on the mechanisms that underlie the emergence of NPDs, highlighting the importance of epigenetic phenomena. Because epigenetic mechanisms are potentially reversible, unraveling the epigenetic contribution to the etiology of NPDs is key to the design of future therapeutic strategies. Early diagnosis of patients prone to NPDs for early intervention represents a challenge that waits for biomarkers of vulnerability, and could be decisive for improving the outcome and prognosis of "at-risk" patients.

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Epigenetic mechanisms: A possible link between autism spectrum disorders and fetal alcohol spectrum disorders

Cited by 17 publications

References 162 publications

Chromatin Switches during Neural Cell Differentiation and Their Dysregulation by Prenatal Alcohol Exposure

Chromatin Switches during Neural Cell Differentiation and Their Dysregulation by Prenatal Alcohol Exposure

Maternal alcohol consumption during pregnancy and its association with offspring renal function at 30 years: Observation from a birth cohort study

The impact of epigenomic next‐generation sequencing approaches on our understanding of neuropsychiatric disorders

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