Hippocampal subfield abnormalities and memory functioning in children with fetal alcohol Spectrum disorders

Roediger, Donovan J.; Krueger, Alyssa M.; Water, Erik de; Mueller, Bryon A.; Boys, Christopher A.; Hendrickson, Timothy; Schumacher, Mariah J.; Mattson, Sarah N.; Jones, Kenneth Lyons; Lim, Kelvin O.; Wozniak, Jeffrey R.

doi:10.1016/j.ntt.2020.106944

Cited by 20 publications

(20 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The hippocampus has long been suspected to be particularly impacted by PAE, given the learning and memory deficits often observed in human and animal studies [ 58 , 60 , 61 ]. The hippocampus differentiates rapidly during fetal development, which may contribute to its particular vulnerability to insult in PAE.…”

Section: Alcohol’s Effects On the Developing Brain And Cognitionmentioning

confidence: 99%

“…The hippocampus, along with other subcortical structures, including the amygdala and caudate, have been reported to be significantly smaller in children with PAE [ 76 , 77 ], although several studies have failed to find volumetric differences in these structures after correction for total brain volume [ 42 , 78 , 79 , 80 ]. A recent neuroimaging study examined hippocampal subfields and found significant volumetric reductions in 5 out of 10 regions in children with PAE compared to controls [ 60 ]. Importantly, the hippocampus is heavily interconnected with other systems [ 81 , 82 , 83 ], and its integrity is critical to the development, functioning, and organization of other domains.…”

Section: Alcohol’s Effects On the Developing Brain And Cognitionmentioning

confidence: 99%

See 1 more Smart Citation

Prenatal and Postnatal Choline Supplementation in Fetal Alcohol Spectrum Disorder

Ernst

Gimbel²,

Water³

et al. 2022

Nutrients

Self Cite

View full text Add to dashboard Cite

Fetal alcohol spectrum disorder (FASD) is common and represents a significant public health burden, yet very few interventions have been tested in FASD. Cognitive deficits are core features of FASD, ranging from broad intellectual impairment to selective problems in attention, executive functioning, memory, visual–perceptual/motor skills, social cognition, and academics. One potential intervention for the cognitive impairments associated with FASD is the essential nutrient choline, which is known to have numerous direct effects on brain and cognition in both typical and atypical development. We provide a summary of the literature supporting the use of choline as a neurodevelopmental intervention in those affected by prenatal alcohol. We first discuss how alcohol interferes with normal brain development. We then provide a comprehensive overview of the nutrient choline and discuss its role in typical brain development and its application in the optimization of brain development following early insult. Next, we review the preclinical literature that provides evidence of choline’s potential as an intervention following alcohol exposure. Then, we review a handful of existing human studies of choline supplementation in FASD. Lastly, we conclude with a review of practical considerations in choline supplementation, including dose, formulation, and feasibility in children.

show abstract

Section: Alcohol’s Effects On the Developing Brain And Cognitionmentioning

confidence: 99%

Section: Alcohol’s Effects On the Developing Brain And Cognitionmentioning

confidence: 99%

Prenatal and Postnatal Choline Supplementation in Fetal Alcohol Spectrum Disorder

Ernst

Gimbel²,

Water³

et al. 2022

Nutrients

Self Cite

View full text Add to dashboard Cite

show abstract

Section: Morphological Change In Hippocampus: Gfap Dark Cells and Thickness Of Hippocampusmentioning

confidence: 99%

“…The main goal for exercise in the CNS is the hippocampal region, especially the DG region (Roediger et al 2021). Dendritic spine density (Zhao et al 2006) and the rate of neurogenesis increase in this area as a result of exercise (Roediger et al 2021). Although the exact mechanism of these morphological effects needs to be clari ed, it seems that the most important mechanism in this process is to increase the synthesis and availability of neurotrophins, especially BDNF (Nijs et al 2015).…”

Section: Morphological Change In Hippocampus: Gfap Dark Cells and Thickness Of Hippocampusmentioning

confidence: 99%

Swimming Training Modifies Stress-induced Changes in the Hippocampal Morphology and Spatial Memory in Rats

Safari¹,

Jahromi²,

Aligholi³

et al. 2021

Preprint

View full text Add to dashboard Cite

This study assessed the effect of swimming training on morphology (Glial fibrillary acidic protein (GFAP), dark cells and thickness of CA1 and DG) of the hippocampus and spatial memory performance in young male rats exposed to chronic stress. Adult male wistar rats were randomly assigned to five groups: swimming training (ST); exposure to chronic mild stress (CS); exposure to chronic mild stress followed by swimming training (CS + ST); exposure to chronic mild stress followed by a recovery period (CS + recovery); control group with no exercise or stress intervention. Spatial memory was measured by Morris Water Maze (MWM). Results: The lowest GFAP and number of dark cells, the highest thickness of CA1, DG, and spatial memory performance were observed in the ST group. In the CS + ST group, swimming training reduced GFAP and the number of dark cells, increased thickness of CA1 and DG, and memory performance, compared to control and CS + Recovery. In the CS group, GFAP and the number of dark cells were highest and thickness of CA1 and DG were lowest among the study groups. In the CS + Recovery group, GFAP, and the number of dark cells were lower, compared to the CS group. Conclusion: swimming training could attenuate astrogliosis and the number of dark cells in both stressed and non-stressed rats and its effect on non-stressed rats was more prominent than in stressed rats. Among young male rates, swimming training could improve stress-induced spatial memory performance and hippocampal morphology.

show abstract

“…During this period, the prefrontal cortex and hippocampus, along with other brain regions, go through a transient period of mass neurodevelopment and rapid growth (growth spurt) [6][7][8]. Maternal alcohol consumption during this period leads, among other issues, to anatomical abnormalities, depressive-like behaviors, and learning and memory impairments in children [9].…”

Section: Introductionmentioning

confidence: 99%

Aversive Learning Deficits and Depressive-Like Behaviors Are Accompanied by an Increase in Oxidative Stress in a Rat Model of Fetal Alcohol Spectrum Disorders: The Protective Effect of Rapamycin

Łopatyńska-Mazurek

Komsta

Gibuła‐Tarłowska

et al. 2021

IJMS

View full text Add to dashboard Cite

Fetal alcohol spectrum disorders (FASDs) are one of the most common consequences of ethanol exposure during pregnancy. In adulthood, these disorders can be manifested by learning and memory deficits and depressive-like behavior. Ethanol-induced oxidative stress may be one of the factors that induces FASD development. The mammalian target of the Rapamycin (mTOR) signaling pathway that acts via two distinct multiprotein complexes, mTORC1 and mTORC2, can affect oxidative stress. We investigated whether mTOR-dependent or mTOR-independent mechanisms are engaged in this phenomenon. Thus, Rapamycin—a selective inhibitor of mTORC1, Torin-2—a non-selective mTORC1/mTORC2 inhibitor, and FK-506—a drug that impacts oxidative stress in an mTOR-independent manner were used. Behavioral tests were performed in adult (PND60-65) rats using a passive avoidance (PA) task (aversive learning and memory) and forced swimming test (FST) (depressive-like behaviors). In addition, the biochemical parameters of oxidative stress, such as lipid peroxidation (LPO), as well as apurinic/apyrimidinic (AP)-sites were determined in the hippocampus and prefrontal cortex in adult (PND65) rats. The rat FASD model was induced by intragastric ethanol (5 g/kg/day) administration at postnatal day (PND)4–9 (an equivalent to the third trimester of human pregnancy). All substances (3 mg/kg) were given 30 min before ethanol. Our results show that neonatal ethanol exposure leads to deficits in context-dependent fear learning and depressive-like behavior in adult rats that were associated with increased oxidative stress parameters in the hippocampus and prefrontal cortex. Because these effects were completely reversed by Rapamycin, an mTORC1 inhibitor, this outcome suggests its usefulness as a preventive therapy in disorders connected with prenatal ethanol exposure.

show abstract

Hippocampal subfield abnormalities and memory functioning in children with fetal alcohol Spectrum disorders

Cited by 20 publications

References 61 publications

Prenatal and Postnatal Choline Supplementation in Fetal Alcohol Spectrum Disorder

Prenatal and Postnatal Choline Supplementation in Fetal Alcohol Spectrum Disorder

Swimming Training Modifies Stress-induced Changes in the Hippocampal Morphology and Spatial Memory in Rats

Aversive Learning Deficits and Depressive-Like Behaviors Are Accompanied by an Increase in Oxidative Stress in a Rat Model of Fetal Alcohol Spectrum Disorders: The Protective Effect of Rapamycin

Contact Info

Product

Resources

About