Prenatal alcohol exposure (PAE) is recognized as a leading preventable cause of birth defects, giving rise to a continuum of cognitive, behavioral, and physical impairments collectively referred to as Fetal Alcohol Spectrum Disorders (FASD). While PAE affects multiple developing organ systems, the fetal brain is particularly vulnerable, exhibiting enduring structural and functional abnormalities in response to alcohol exposure. Recent research highlights mitochondrial dysfunction as an important mechanism in the pathogenesis of alcohol-related neurodevelopmental deficits. Mitochondria are highly susceptible to alcohol-induced damage, and mounting evidence demonstrates mitochondrial impairments across various organ systems following PAE—focusing growing attention on its specific effects within the developing central nervous system. This chapter explores the essential roles of mitochondria throughout key stages of neurodevelopment and evaluates how PAE disrupts mitochondrial function in different organ systems. Special emphasis is placed on the developing brain, with a focus on its three primary cellular populations: neurons, glial cells, and the cerebral vasculature. Current findings indicate that fetal mitochondria are particularly sensitive to alcohol exposure, resulting in altered mitochondrial morphology, increased production of reactive oxygen species (ROS), elevated oxidative stress, and impaired cellular respiration. Taken together, these data underscore mitochondria as a critical and vulnerable target of PAE—especially in the developing brain—where mitochondrial dysfunction contributes to the neurodevelopmental deficits’ characteristic of FASD. Advancing our understanding of these mechanisms opens the door to mitochondria-targeted interventions, offering promising therapeutic avenues to protect mitochondrial function and mitigate the long-term consequences of prenatal alcohol exposure.