# Fetal alcohol exposure and cerebrovascular development

> **NIH NIH R01** · UNIVERSITY OF SOUTH FLORIDA · 2022 · $309,713

## Abstract

In the United States, fetal alcohol spectrum disorders (FASD) represent the leading preventable cause of birth
defects and neurodevelopmental delay with life-long implications. FASD affects an estimated 40,000 infants in
the US each year, with 2-5% of younger school-age children having FASD. Currently, prediction of FASD
during pregnancy is not available, and there are no readily available cures against FASD. It is widely believed
that early detection of FASD and its subsequent intervention strategies are critical to allow earliest and most
effective therapeutic interventions. While fetal alcohol exposure targets multiple organs and systems, the brain
constitutes the most severely affected organ, exhibiting both structural and functional abnormalities. As
neuronal development critically depends on the oxygen delivery, nutritional supply and waste removal by
cerebral circulation, recent studies have been paying increasing attention to the fetal cerebral circulation as a
critical target of maternal alcohol consumption. However, the timing and mechanisms that govern fetal
cerebrovascular response to alcohol remain elusive. One of the major obstacles that preclude rapid
advancement of the studies on fetal cerebral circulation is lack of high-resolution imaging technique that would
be suitable for imaging of small lab animal species. Current proposal is put forth by the collaborating teams of
bioengineers and cerebrovascular physiologists with the overall goal of delivering a high-speed 3D
photoacoustic tomography (PAT) that will allow non-invasive, simultaneous visualization of all the embryos in a
mouse utero and track their development into adulthood longitudinally to study the association between alcohol
exposure-induced changes in fetal hemodynamics and cerebrovascular outcome after birth. Another obstacle
to developing effective treatments to alleviate symptoms and develop preventive measures against FASD is a
relatively limited knowledge on relevant targets for alcohol, including targets within fetal cerebral arteries. In
this regard, current proposal will focus on cerebral artery mitochondria. Critical role of mitochondria in
regulating cerebral artery function is well documented, and there is no doubt that mitochondrial is one of the
major sensors for alcohol as shown in liver and neurons. In our recent pioneered work we documented
persistent up-regulation of fetal cerebral artery proteome in response to alcohol exposure during mid-
pregnancy. However, systematic studies on cerebral artery mitochondria alterations in response to prenatal
alcohol exposure remain to be performed and the role of alcohol targeting of fetal cerebral artery mitochondria
remains to be established. To overcome these obstacles in the field, we propose to complete three related
Aims: (1) We will optimize a high-speed PAT system for 3D high-resolution brain imaging of rodents; (2) We
will develop advanced software for improved PAT 3D image reconstruction and analysis; (...

## Key facts

- **NIH application ID:** 10359771
- **Project number:** 5R01AA028200-02
- **Recipient organization:** UNIVERSITY OF SOUTH FLORIDA
- **Principal Investigator:** Anna Bukiya
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $309,713
- **Award type:** 5
- **Project period:** 2021-03-01 → 2026-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10359771

## Citation

> US National Institutes of Health, RePORTER application 10359771, Fetal alcohol exposure and cerebrovascular development (5R01AA028200-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10359771. Licensed CC0.

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