Functional connectivity abnormalities and associated cognitive deficits in fetal alcohol Spectrum disorders (FASD)

Wozniak, Jeffrey R.; Mueller, Bryon A.; Mattson, Sarah N.; Coles, Claire D.; Kable, Julie A.; Jones, Kenneth Lyons; Boys, Christopher J.; Lim, Kelvin O.; Riley, Edward P.; Sowell, Elizabeth R.

doi:10.1007/s11682-016-9624-4

Cited by 55 publications

(48 citation statements)

References 63 publications

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“…Indeed, a recent paper by the same authors compared the ability of the cardiac OR and Bayley Scales of Infant Development (BSID‐II) scores at 6 months of age to predict developmental delay at 12 months of age (Mesa et al., ), concluding that cardiac OR was a more sensitive measure of the risk for developing neurodevelopmental delay following prenatal alcohol exposure. Furthermore, measurement of functional connectivity in whole brain using magnetic resonance imaging (Wozniak et al., ) and imaging of prefrontal cortical activation via functional near‐infrared spectroscopy (Kable and Coles, ) are showing promise as sensitive measures of neurodevelopmental impairments in children with prenatal alcohol exposure. To date, brain imaging has only been applied once to assess pre–post outcomes of an intervention for children with FASD (Soh et al., ).…”

Section: Discussionmentioning

confidence: 99%

Effect of Choline Supplementation on Neurological, Cognitive, and Behavioral Outcomes in Offspring Arising from Alcohol Exposure During Development: A Quantitative Systematic Review of Clinical and Preclinical Studies

Akison

Kuo

Reid

et al. 2018

Alcoholism Clin & Exp Res

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Prenatal alcohol exposure results in cognitive, behavioral, and neurological deficits in offspring. There is an urgent need for safe and effective treatments to overcome these effects. Maternal choline supplementation has been identified as a potential intervention. Our objective was to review preclinical and clinical studies using choline supplementation in known cases of fetal alcohol exposure to determine its effectiveness in ameliorating deficits in offspring. A systematic search of 6 electronic databases was conducted and studies selected by reviewing titles/abstracts against specific inclusion/exclusion criteria. Study characteristics, population demographics, alcohol exposure, and intervention methods were tabulated, and quality of reporting was assessed. Data on cognitive, behavioral, and neurological outcomes were extracted and tabulated. Quantitative analysis was performed to determine treatment effects for individual study outcomes. A total of 189 studies were retrieved following duplicate removal. Of these, 22 studies (2 randomized controlled trials, 2 prospective cohort studies, and 18 preclinical studies) met the full inclusion/exclusion criteria. Choline interventions were administered at different times relative to alcohol exposure, impacting on their success to prevent deficits for specific outcomes. Only 1 clinical study showed significant improvements in information processing in 6-month-old infants from mothers treated with choline during pregnancy. Preclinical studies showed significant amelioration of deficits due to prenatal alcohol exposure across a wide variety of outcomes, including epigenetic/molecular changes, gross motor, memory, and executive function. This review suggests that choline supplementation has the potential to ameliorate specific behavioral, neurological, and cognitive deficits in offspring caused by fetal alcohol exposure, at least in preclinical studies. As only 1 clinical study has shown benefit, we recommend more clinical trials be undertaken to assess the effectiveness of choline in preventing deficits across a wider range of cognitive domains in children.

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Section: Discussionmentioning

confidence: 99%

Effect of Choline Supplementation on Neurological, Cognitive, and Behavioral Outcomes in Offspring Arising from Alcohol Exposure During Development: A Quantitative Systematic Review of Clinical and Preclinical Studies

Akison

Kuo

Reid

et al. 2018

Alcoholism Clin & Exp Res

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“…The current study did not obtain individual MRIs from each infant due to the additional challenge of obtaining infant MRIs, limiting our ability to perform connectivity at the source level. Despite some evidence for altered connectivity in older children with FASD ( Wozniak et al, 2016 ), little evidence indicates effects in infancy. For example, recent rsfMRI functional connectivity studies have assessed the effects of alcohol in conjunction with prenatal cocaine exposure and did not find a significant effect of PAE on infant FNC ( Salzwedel et al, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

Hypersynchrony in MEG spectral amplitude in prospectively-identified 6-month-old infants prenatally exposed to alcohol

Stephen

Flynn

Kabella

et al. 2018

NeuroImage: Clinical

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Early identification of children who experience developmental delays due to prenatal alcohol exposure (PAE) remains a challenge for individuals who do not exhibit facial dysmorphia. It is well-established that children with PAE may still exhibit the cognitive and behavioral difficulties, and individuals without facial dysmorphia make up the majority of individuals affected by PAE. This study employed a prospective cohort design to capture alcohol consumption patterns during pregnancy and then followed the infants to 6 months of age. Infants were assessed using magnetoencephalography to capture neurophysiological indicators of brain development and the Bayley Scales of Infant Development-III to measure behavioral development. To account for socioeconomic and family environmental factors, we employed a two-by-two design with pregnant women who were or were not using opioid maintenance therapy (OMT) and did or did not consume alcohol during pregnancy. Based on prior studies, we hypothesized that infants with PAE would exhibit broad increased spectral amplitude relative to non-PAE infants. We also hypothesized that the developmental shift from low to high frequency spectral amplitude would be delayed in infants with PAE relative to controls. Our results demonstrated broadband increased spectral amplitude, interpreted as hypersynchrony, in PAE infants with no significant interaction with OMT. Unlike prior EEG studies in neonates, our results indicate that this hypersynchrony was highly lateralized to left hemisphere and primarily focused in temporal/lateral frontal regions. Furthermore, there was a significant positive correlation between estimated number of drinks consumed during pregnancy and spectral amplitude revealing a dose-response effect of increased hypersynchrony corresponding to greater alcohol consumption. Contrary to our second hypothesis, we did not see a significant group difference in the contribution of low frequency to high frequency amplitude at 6 months of age. These results provide new evidence that hypersynchrony, previously observed in neonates prenatally exposed to high levels of alcohol, persists until 6 months of age and this measure is detectable with low to moderate exposure of alcohol with a dose-response effect. These results indicate that hypersynchrony may provide a sensitive early marker of prenatal alcohol exposure in infants up to 6 months of age.

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“…Fetal alcohol spectrum disorder (FASD), which occurs as a result of prenatal alcohol exposure, can have a multitude of effects on the developing fetus, ranging from craniofacial abnormalities [13] to dysregulation of physiological systems [14,15], as well as behavioral [16] and cognitive dysfunction [17]. FASD is arguably the most common neurodevelopmental disorder, with current US prevalence estimated at 1.1 to 5.0% [18], compared to 1.4% for ASD [19]; however, FASD has received very little research attention-particularly in the context of immune function-making evidence for immune dysfunction limited (reviewed in [20]).…”

Section: Introductionmentioning

confidence: 99%

Immune network dysregulation associated with child neurodevelopmental delay: modulatory role of prenatal alcohol exposure

Bodnar

Wertelecki

Yevtushok

et al. 2020

J Neuroinflammation

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Background: Evidence suggests that cytokine imbalances may be at the root of deficits that occur in numerous neurodevelopmental disorders, including schizophrenia and autism spectrum disorder. Notably, while clinical studies have demonstrated maternal cytokine imbalances with alcohol consumption during pregnancy-and data from animal models have identified immune disturbances in alcohol-exposed offspring-to date, immune alterations in alcohol-exposed children have not been explored. Thus, here we hypothesized that perturbations in the immune environment as a result of prenatal alcohol exposure will program the developing immune system, and result in immune dysfunction into childhood. Due to the important role of cytokines in brain development/function, we further hypothesized that child immune profiles might be associated with their neurodevelopmental status. Methods: As part of a longitudinal study in Ukraine, children of mothers reporting low/no alcohol consumption or moderate-to-heavy alcohol consumption during pregnancy were enrolled in the study and received neurodevelopmental assessments. Group stratification was based on maternal alcohol consumption and child neurodevelopmental status resulting in the following groups: A/TD, alcohol-consuming mother, typically developing child; A/ND, alcohol-consuming mother, neurodevelopmental delay in the child; C/TD, control mother (low/no alcohol consumption), typically development child; and C/ND, control mother, neurodevelopmental delay in the child. Forty cytokines/chemokines were measured in plasma and data were analyzed using regression and constrained principle component analysis. Results: Analyses revealed differential cytokine network activity associated with both prenatal alcohol exposure and neurodevelopmental status. Specifically, alcohol-exposed children showed activation of a cytokine network including eotaxin-3, eotaxin, and bFGF, irrespective of neurodevelopmental status. However, another cytokine network was differentially activated based on neurodevelopmental outcome: A/TD showed activation of MIP-1β, MDC, and MCP-4, and inhibition of CRP and PlGF, with opposing pattern of activation/inhibition detected in the A/ND group. By contrast, in the absence of alcohol-exposure, activation of a network including IL-2, TNF-β, IL-10, and IL-15 was associated with neurodevelopmental delay.

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Functional connectivity abnormalities and associated cognitive deficits in fetal alcohol Spectrum disorders (FASD)

Cited by 55 publications

References 63 publications

Effect of Choline Supplementation on Neurological, Cognitive, and Behavioral Outcomes in Offspring Arising from Alcohol Exposure During Development: A Quantitative Systematic Review of Clinical and Preclinical Studies

Effect of Choline Supplementation on Neurological, Cognitive, and Behavioral Outcomes in Offspring Arising from Alcohol Exposure During Development: A Quantitative Systematic Review of Clinical and Preclinical Studies

Hypersynchrony in MEG spectral amplitude in prospectively-identified 6-month-old infants prenatally exposed to alcohol

Immune network dysregulation associated with child neurodevelopmental delay: modulatory role of prenatal alcohol exposure

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