Magnetic Resonance Imaging of Brain Anomalies in Fetal Alcohol Syndrome

Swayze, Victor W.; Johnson, Virginia P.; Hanson, James W.; Piven, Joseph; Sato, Yutaka; Giedd, Jay N.; Mosnik, Diane; Andreasen, Nancy C.

doi:10.1542/peds.99.2.232

Cited by 236 publications

(158 citation statements)

References 82 publications

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“…Our data identify tPA as a key regulator of the neurotoxic effects of alcohol in a murine model of FAS. Imaging studies of humans with FAS show microencephaly (28), reductions in cortical gray matter (29), decreased basal ganglia size (30), and abnormal development or absence of the corpus callosum (31). In our experiments, WT mice showed >100-fold increase in FJB staining in the thalamus and cortex after ethanol exposure.…”

Section: Discussionmentioning

confidence: 49%

Tissue plasminogen activator is required for the development of fetal alcohol syndrome in mice

Noel

Norris

Strickland

2011

Proc. Natl. Acad. Sci. U.S.A.

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Ethanol exposure during developmental synaptogenesis can lead to brain defects referred to as fetal alcohol syndrome (FAS), which can include mental health problems such as cognitive deficits and mental retardation. In FAS, widespread neuronal death and brain mass loss precedes behavioral and cognitive impairments in adulthood. Because tissue plasminogen activator (tPA) has been implicated in neurodegeneration, we examined whether it mediates FAS. Neonatal WT and tPA −/− mice were injected with ethanol to mimic FAS in humans. In WT mice, ethanol elicited caspase-3 activation, significant forebrain neurodegeneration, and decreased contextual fear conditioning in adults. However, tPA-deficient mice were protected from these neurotoxicities, and this protection could be abrogated by exogenous tPA. Selective pharmacological modulators of NMDA and GABA A receptor pathways revealed that the effects of tPA were mediated by the NR2B subunit of the NMDA receptor. This study identifies tPA as a critical signaling component in FAS.

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Section: Discussionmentioning

confidence: 49%

Tissue plasminogen activator is required for the development of fetal alcohol syndrome in mice

Noel

Norris

Strickland

2011

Proc. Natl. Acad. Sci. U.S.A.

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“…The significant association between alcohol exposure during pregnancy and CH that was consistently reported by several of the identified studies 7,25,27 is somewhat unsurprising given its known teratogenic potential.…”

mentioning

confidence: 78%

Maternal environmental risk factors for congenital hydrocephalus: a systematic review

Kalyvas

Κalamatianos

Pantazi

et al. 2016

FOC

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OBJECTIVE Congenital hydrocephalus (CH) is one of the most frequent CNS congenital malformations, representing an entity with serious pathological consequences. Although several studies have previously assessed child-related risk factors associated with CH development, there is a gap of knowledge on maternal environmental risk factors related to CH. The authors have systematically assessed extrinsic factors in the maternal environment that potentially confer an increased risk of CH development. METHODS The Cochrane Library, MEDLINE, and EMBASE were systematically searched for works published between 1966 and December 2015 to identify all relevant articles published in English. Only studies that investigated environmental risk factors concerning the mother—either during gestation or pregestationally—were included. RESULTS In total, 13 studies (5 cohorts, 3 case series, 3 case-control studies, 1 meta-analysis, and 1 case report) meeting the inclusion criteria were identified. Maternal medication or alcohol use during gestation; lifestyle modifiable maternal pathologies such as obesity, diabetes, or hypertension; lack of prenatal care; and a low socioeconomic status were identified as significant maternal environmental risk factors for CH development. Maternal infections and trauma to the mother during pregnancy have also been highlighted as potential mother-related risk factors for CH. CONCLUSIONS Congenital hydrocephalus is an important cause of serious infant health disability that can lead to health inequalities among adults. The present study identified several maternal environmental risk factors for CH, thus yielding important scientific information relevant to prevention of some CH cases. However, further research is warranted to confirm the impact of the identified factors and examine their underlying behavioral and/or biological basis, leading to the generation of suitable prevention strategies.

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“…Abnormalities included hippocampal commissure agenesis [23], callosal malformation, cavum septi pellucidi and cavum vergae [58]. The corpus callosum, the biggest white matter structure in the brain, which connects the two cerebral hemispheres, has been examined in many PAE investigations.…”

Section: Accepted Manuscriptmentioning

confidence: 99%

“…The superior posterior region between the isthmus and splenium was also more severely displaced as compared to the more anterior part [59]. It should be noted that the decreased thickness and area of the corpus callosum were associated with decreased palpebral fissure length, a FASD facial characteristic [58;63], and the severity of midline structural malformations correlated with the severity of facial anomalies in individuals with FASD [58].…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Radiological studies of fetal alcohol spectrum disorders in humans and animal models: An updated comprehensive review

Nguyen

Chong

Tieng

et al. 2017

Magnetic Resonance Imaging

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Magnetic Resonance Imaging of Brain Anomalies in Fetal Alcohol Syndrome

Cited by 236 publications

References 82 publications

Tissue plasminogen activator is required for the development of fetal alcohol syndrome in mice

Tissue plasminogen activator is required for the development of fetal alcohol syndrome in mice

Maternal environmental risk factors for congenital hydrocephalus: a systematic review

Radiological studies of fetal alcohol spectrum disorders in humans and animal models: An updated comprehensive review

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