scholarly journals Embryonic Exposure to 2,2′,3,5′,6‐pentachlorobiphenyl (PCB‐95) Causes Developmental Malformations in Zebrafish

2019 ◽  
Vol 39 (1) ◽  
pp. 162-170 ◽  
Author(s):  
Prabha Ranasinghe ◽  
Robert J. Thorn ◽  
Renee Seto ◽  
Robbert Creton ◽  
William C. Bridges ◽  
...  
Keyword(s):  
Embryonic Exposure ◽  
Developmental Malformations

scholarly journals Developmental malformations in Huntington disease: neuropathologic evidence of focal neuronal migration defects in a subset of adult brains

2021 ◽  
Vol 141 (3) ◽  
pp. 399-413 ◽  
Author(s):  
R. A. Hickman ◽  
P. L. Faust ◽  
M. K. Rosenblum ◽  
K. Marder ◽  
M. F. Mehler ◽  
...  
Keyword(s):  
New York ◽  
Huntington Disease ◽  
Trinucleotide Repeat ◽  
Validation Cohort ◽  
Hypothalamic Hamartoma ◽  
Discovery Cohort ◽  
Brain Bank ◽  
Neuronal Precursors ◽  
Neurodevelopmental Abnormalities ◽  
Developmental Malformations

AbstractNeuropathologic hallmarks of Huntington Disease (HD) include the progressive neurodegeneration of the striatum and the presence of Huntingtin (HTT) aggregates that result from abnormal polyQ expansion of the HTT gene. Whether the pathogenic trinucleotide repeat expansion of the HTT gene causes neurodevelopmental abnormalities has garnered attention in both murine and human studies; however, documentation of discrete malformations in autopsy brains of HD individuals has yet to be described. We retrospectively searched the New York Brain Bank (discovery cohort) and an independent cohort (validation cohort) to determine whether developmental malformations are more frequently detected in HD versus non-HD brains and to document their neuropathologic features. One-hundred and thirty HD and 1600 non-HD whole brains were included in the discovery cohort and 720 HD and 1989 non-HD half brains were assessed in the validation cohort. Cases with developmental malformations were found at 6.4–8.2 times greater frequency in HD than in non-HD brains (discovery cohort: OR 8.68, 95% CI 3.48–21.63, P=4.8 × 10-5; validation cohort: OR 6.50, 95% CI 1.83–23.17, P=0.0050). Periventricular nodular heterotopias (PNH) were the most frequent malformations and contained HTT and p62 aggregates analogous to the cortex, whereas cortical malformations with immature neuronal populations did not harbor such inclusions. HD individuals with malformations had heterozygous HTT CAG expansions between 40 and 52 repeats, were more frequently women, and all were asymmetric and focal, aside from one midline hypothalamic hamartoma. Using two independent brain bank cohorts, this large neuropathologic series demonstrates an increased occurrence of developmental malformations in HD brains. Since pathogenic HTT gene expansion is associated with genomic instability, one possible explanation is that neuronal precursors are more susceptible to somatic mutation of genes involved in cortical migration. Our findings further support emerging evidence that pathogenic trinucleotide repeat expansions of the HTT gene may impact neurodevelopment.

scholarly journals Diving into the world of alcohol teratogenesis: a review of zebrafish models of fetal alcohol spectrum disorder

2018 ◽  
Vol 96 (2) ◽  
pp. 88-97 ◽  
Author(s):  
Yohaan Fernandes ◽  
Desire M. Buckley ◽  
Johann K. Eberhart
Keyword(s):  
Fetal Alcohol Spectrum Disorder ◽  
Model Organism ◽  
Spectrum Disorder ◽  
Structural Defects ◽  
Craniofacial Skeleton ◽  
Fetal Alcohol ◽  
Embryonic Exposure ◽  
Fetal Alcohol Spectrum ◽  
The Brain ◽  
Insight Into

The term fetal alcohol spectrum disorder (FASD) refers to the entire suite of deleterious outcomes resulting from embryonic exposure to alcohol. Along with other reviews in this special issue, we provide insight into how animal models, specifically the zebrafish, have informed our understanding of FASD. We first provide a brief introduction to FASD. We discuss the zebrafish as a model organism and its strengths for alcohol research. We detail how zebrafish has been used to model some of the major defects present in FASD. These include behavioral defects, such as social behavior as well as learning and memory, and structural defects, disrupting organs such as the brain, sensory organs, heart, and craniofacial skeleton. We provide insights into how zebrafish research has aided in our understanding of the mechanisms of ethanol teratogenesis. We end by providing some relatively recent advances that zebrafish has provided in characterizing gene-ethanol interactions that may underlie FASD.

Embryonic exposure to pentabromobenzene inhibited the inflation of posterior swim bladder in zebrafish larvae

2020 ◽  
Vol 259 ◽  
pp. 113923 ◽  
Author(s):  
Wei Peng ◽  
Sitian Liu ◽  
Yongyong Guo ◽  
Lihua Yang ◽  
Bingsheng Zhou
Keyword(s):  
Swim Bladder ◽  
Zebrafish Larvae ◽  
Embryonic Exposure
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