Long-term alterations to DNA methylation as a biomarker of prenatal alcohol exposure: From mouse models to human children with fetal alcohol spectrum disorders

Alcohol ◽  
2017 ◽  
Vol 60 ◽  
pp. 67-75 ◽  
Author(s):  
Benjamin I. Laufer ◽  
Eric J. Chater-Diehl ◽  
Joachim Kapalanga ◽  
Shiva M. Singh
2013 ◽  
Vol 2 (3) ◽  
pp. 37-49 ◽  
Author(s):  
Therese M Grant ◽  
Natalie Novick Brown ◽  
J. Christopher Graham ◽  
Nancy Whitney ◽  
Dan Dubovsky ◽  
...  

Grant, T., Novick Brown, N., Graham, J., Whitney, N., Dubovsky, D. , & Nelson, L. (2013). Screening in treatment programs for Fetal Alcohol Spectrum Disorders that could affect therapeutic progress. The International Journal Of Alcohol And Drug Research, 2(3), 37-49. doi:10.7895/ijadr.v2i3.116 (http://dx.doi.org/10.7895/ijadr.v2i3.116)Aims: While structured intake interviews are the standard of care in substance abuse treatment programs, these interviews often do not screen for cognitive impairments, such as those found in fetal alcohol spectrum disorders (FASD) and other brain-based developmental disorders. The research reported here supports a brief interview protocol, the Life History Screen (LHS), that screens clients unobtrusively for adverse life-course outcomes typically found in FASD, so as to guide follow-up assessments and treatment planning.Design: Two-group observational study.Setting: A three-year case management intervention program in Washington State for high-risk women who abuse alcohol and/or drugs during pregnancy.Participants: Group 1: No prenatal alcohol exposure (N = 463); Group 2: Diagnosed with FASD (Fetal Alcohol Syndrome, Alcohol Related Neurodevelopmental Disorder, fetal alcohol effects, or static encephalopathy) by a qualified physician (N = 25), or suspected of having FASD (reported prenatal alcohol exposure and displayed behaviors consistent with a clinical diagnosis of FASD) (N = 61).Measures: The Addiction Severity Index (ASI) was administered to participants at intake. We analyzed eleven ASI items that corresponded to questions on the LHS in order to assess the potential of the LHS for identifying adults with possible FASD. The Life History Screen itself was not administered.Findings: Analysis of group differences between the diagnosed FASD and suspected FASD groups supported our decision to collapse the two groups for the main analysis. The Life History Screen shows promise as an efficient pre-treatment screen, in that core items are significantly associated with FASD group membership on factors involving childhood history, maternal drinking, education, substance use, employment, and psychiatric symptomatology.Conclusions: The Life History Screen may have utility as a self-report measure that can be used at the outset of treatment to identify clients with cognitive impairments and learning disabilities due to prenatal alcohol exposure.


2013 ◽  
Vol 49 (1) ◽  
pp. 84-95 ◽  
Author(s):  
Svetlana Popova ◽  
Aleksandra Yaltonskaya ◽  
Vladimir Yaltonsky ◽  
Yaroslav Kolpakov ◽  
Ilya Abrosimov ◽  
...  

2021 ◽  
pp. 153537022098039
Author(s):  
Erin Mathews ◽  
Kevyn Dewees ◽  
Deborah Diaz ◽  
Carlita Favero

Fetal Alcohol Spectrum Disorders (FASDs) describe a range of deficits, affecting physical, mental, cognitive, and behavioral function, arising from prenatal alcohol exposure. FASD causes widespread white matter abnormalities, with significant alterations of tracts in the cerebral cortex, cerebellum, and hippocampus. These brain regions present with white-matter volume reductions, particularly at the midline. Neural pathways herein are guided primarily by three guidance cue families: Semaphorin/Neuropilin, Netrin/DCC, and Slit/Robo. These guidance cue/receptor pairs attract and repulse axons and ensure that they reach the proper target to make functional connections. In several cases, these signals cooperate with each other and/or additional molecular partners. Effects of alcohol on guidance cue mechanisms and their associated effectors include inhibition of growth cone response to repellant cues as well as changes in gene expression. Relevant to the corpus callosum, specifically, developmental alcohol exposure alters GABAergic and glutamatergic cell populations and glial cells that serve as guidepost cells for callosal axons. In many cases, deficits seen in FASD mirror aberrancies in guidance cue/receptor signaling. We present evidence for the need for further study on how prenatal alcohol exposure affects the formation of neural connections which may underlie disrupted functional connectivity in FASD.


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