Fetal alcohol spectrum disorders and cognitive functions of young children

Bakoyiannis, Ioannis; Gkioka, Eleana; Pergialiotis, Vasilios; Mastroleon, Ioanna; Prodromidou, Anastasia; Vlachos, Georgios; Perrea, Despina

doi:10.1515/revneuro-2014-0029

Cited by 27 publications

(14 citation statements)

References 94 publications

(96 reference statements)

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“…When a pregnant woman abuses alcohol, her exposed children are at a high risk for developing fetal alcohol spectrum disorders (FASDs), which are developmental disorders which can be characterized by diverse symptoms, including delayed growth, craniofacial abnormalities, intellectual impairment, anxiety, depression, and social impairment (Bakoyiannis et al, 2014; Driscoll, Streissguth, & Riley, 1990; Kelly, Day, & Streissguth, 2000). The occurrence and severity of symptoms depend on the duration and developmental timing of alcohol exposure (Alfonso-Loeches & Guerri, 2011).…”

Section: Alcohol-related Pathologymentioning

confidence: 99%

Alcohol effects on the epigenome in the germline: Role in the inheritance of alcohol-related pathology

Chastain

Sarkar

2017

Alcohol

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Excessive alcohol exposure has severe health consequences, and clinical and animal studies have demonstrated that disruptions in the epigenome of somatic cells, such as those in brain, are an important factor in the development of alcohol-related pathologies, such as alcohol-use disorders (AUDs) and fetal alcohol spectrum disorders (FASDs). It is also well known that alcohol-related health problems are passed down across generations in human populations, but the complete mechanisms for this phenomenon are currently unknown. Recent studies in animal models have suggested that epigenetic factors are also responsible for the transmission of alcohol-related pathologies across generations. Alcohol exposure has been shown to induce changes in the epigenome of sperm of exposed male animals, and these epimutations are inherited in the offspring. This paper reviews evidence for multigenerational and transgenerational epigenetic inheritance of alcohol-related pathology through the germline. We also review the literature on the epigenetic effects of alcohol exposure on somatic cells in brain, and its contribution to AUDs and FASDs. We note gaps in knowledge in this field, such as the lack of clinical studies in human populations and the lack of data on epigenetic inheritance via the female germline, and we suggest future research directions.

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Section: Alcohol-related Pathologymentioning

confidence: 99%

Alcohol effects on the epigenome in the germline: Role in the inheritance of alcohol-related pathology

Chastain

Sarkar

2017

Alcohol

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“…Perinatal drinking is associated with many adverse fetal health effects [72-74], including fetal alcohol spectrum disorders [75,76], neurodevelopmental outcomes [77], and central nervous system deficits. Additionally, drinking while pregnant is associated with long-term effects such as speech and language outcomes [78], cognitive and behavioral challenges [79,80], and executive functioning deficits in children [81], and psychosocial consequences in adulthood [82]. …”

Section: Alcoholmentioning

confidence: 99%

Substance Use in the Perinatal Period

Forray

Foster

2015

Curr Psychiatry Rep

115

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Perinatal substance use remains a major public health problem and is associated with a number of deleterious maternal and fetal effects. Polysubstance use in pregnancy is common, and can potentiate adverse maternal and fetal outcomes. Tobacco is the most commonly used substance in pregnancy, followed by alcohol and illicit substances. The treatments for perinatal substance use are limited and consist mostly of behavioral and psychosocial interventions. Of these contingency management has shown the most efficacy. More recently, novel interventions such as progesterone for postpartum cocaine use have shown promise. The purpose of this review is to examine the recent literature on the use of tobacco, alcohol, cannabis, stimulants, and opioids in the perinatal period, their effects on maternal and fetal health and current treatments.

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“…Based also on the four‐digit method of diagnosis (Astley ), there are also a number of other subtypes with evolving nomenclature and definitions settled on partial expressions of FAS, including partial fetal alcohol syndrome, alcohol‐related neurodevelopmental disorder, alcohol‐related birth defects, and fetal alcohol effect (Bakoyiannis et al . ).…”

Section: Introductionmentioning

confidence: 97%

Paternal alcohol exposure in mice alters brain NGF and BDNF and increases ethanol-elicited preference in male offspring

et al. 2015

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Ethanol (EtOH) exposure during pregnancy induces cognitive and physiological deficits in the offspring. However, the role of paternal alcohol exposure (PAE) on offspring EtOH sensitivity and neurotrophins has not received much attention. The present study examined whether PAE may disrupt nerve growth factor (NGF) and/or brain-derived neurotrophic factor (BDNF) and affect EtOH preference/rewarding properties in the male offspring. CD1 sire mice were chronically addicted for EtOH or administered with sucrose. Their male offsprings when adult were assessed for EtOH preference by a conditioned place preference paradigm. NGF and BDNF, their receptors (p75 NTR , TrkA and TrkB), dopamine active transporter (DAT), dopamine receptors D1 and D2, pro-NGF and pro-BDNF were also evaluated in brain areas. PAE affected NGF levels in frontal cortex, striatum, olfactory lobes, hippocampus and hypothalamus. BDNF alterations in frontal cortex, striatum and olfactory lobes were found. PAE induced a higher susceptibility to the EtOH rewarding effects mostly evident at the lower concentration (0.5 g/kg) that was ineffective in non-PAE offsprings. Moreover, higher ethanol concentrations (1.5 g/kg) produced an aversive response in PAE animals and a significant preference in non-PAE offspring. PAE affected also TrkA in the hippocampus and p75 NTR in the frontal cortex. DAT was affected in the olfactory lobes in PAE animals treated with 0.5 g/kg of ethanol while no differences were found on D1/D2 receptors and for pro-NGF or pro-BDNF. In conclusion, this study shows that: PAE affects NGF and BDNF expression in the mouse brain; PAE may induce ethanol intake preference in the male offspring.

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Fetal alcohol spectrum disorders and cognitive functions of young children

Cited by 27 publications

References 94 publications

Alcohol effects on the epigenome in the germline: Role in the inheritance of alcohol-related pathology

Alcohol effects on the epigenome in the germline: Role in the inheritance of alcohol-related pathology

Substance Use in the Perinatal Period

Paternal alcohol exposure in mice alters brain NGF and BDNF and increases ethanol-elicited preference in male offspring

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