AbstractAlcohol intake by women before planning a preg-nancy, during pregnancy, and/or during lactation induces brain, behavioral, and physical abnormalities in the fetus, which are known as fetal alcohol spectrum disorders. Thanks to the availability of animal models, some cellular and bio-chemical processes affecting offspring exposed to ethanol during early development have been extensively investigated. Ethanol effects may bemitigated or increased if offspring also are exposed to either positive or adverse conditions during early life. These environmental conditions may have an im-pact on neuronal and behavioral development and may in-crease the risk of developing neuropsychiatric symptoms. Indeed, brain development largely is modifiable by experi-ences, and neuroplasticity is particularly evident during early phases of life. Molecular mediators for brain development and synaptic plasticity are neurotrophins, such as nerve growth factor and brain-derived neurotrophic factor. Early ethanol exposure not only affects the fetal brain directly, but it also leads to long-lasting consequences that emerge during adult-hood and aging. Although the mechanisms responsible for these abnormalities in the fetus are unclear, it is hypothesized that ethanol might damage the central nervous system through oxidative stress processes by increasing free-radical produc-tion and decreasing cellular antioxidant ability. Ethanol’sef-fects on animal models have been investigated in detail; however, only few studies have investigated the consequences of early wine consumption. Wine contains several concentrations of ethanol and is consumed largely by Medi-terranean populations. We recently compared the conse-quences of early exposure to ethanol or red wine (at the same ethanol concentration) administered during different stages of development in animal models. Our studies show a series of behavioral and neurologic abnormalities in juvenile, adult, and aged offspring of mice exposed to ethanol. A much smaller number of changes (if any) were evidenced as a consequence of early exposure to red wine. Antioxidant com-pounds measurable in red wine may have mitigated the tox-icity associated with ethanol in the fetus. These “protective” mechanisms inmice pre- and postnatally exposed to red wine, compared with the ethanol group, remain unknown. As a whole, our data should not be interpreted as encouraging women to consume red wine before or during pregnancy and/or lactation. Indeed, in these cases, alcohol intake abso-lutely must be avoided. KeywordsAnimal models. Fetal alcohol syndrome (FAS). Neurodevelopment. Neuroplasticity. Behavior