SAN 2026

D-56

Cognition, Behavior, and Memory

Long-Term Effects of Prenatal Ethanol Exposure on the Hippocampal-Dependent Memories: A Systematic Review

María Belén Reniero Paretto*1,2,3, Priscila Germino*1, Victoria Diana1, Sofía Alvite Buján1, Agustina Micaela Nogueira1, Brenda Magalí Gómez Muiño1,4, Giselle Aylén Insfran1, Sonia Jazmín Molina1,2,3 (* equal contribution)

1. Universidad de Buenos Aires. Facultad de Psicología. Cátedra I de Neurofisiología. Escuela de Ayudantes. Buenos Aires, Argentina.
2. Universidad de Buenos Aires. Facultad de Medicina. 1ª Cátedra de Farmacología. Buenos Aires, Argentina.
3. Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) - Universidad de Buenos Aires. Centro de Estudios Farmacológicos y Botánicos (CEFyBO). Buenos Aires, Argentina.
4. Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET). Centro Interdisciplinario de Investigaciones en Psicología Matemática y Experimental "Dr. Horacio J. A. Rimoldi". Buenos Aires, Argentina.


Presenting Author:

María Belén

Reniero Paretto

belenreniero213@gmail.com

Prenatal alcohol exposure (PAE) has detrimental effects on the hippocampus (HC), a structure involved in learning, memory, and spatial navigation processes. Given that PAE may induce damage that persists in the long term, the aim of this review was to examine the effects of PAE on the HC and HC-associated memories in later stages of life. A literature search was conducted in PubMed in May 2026 using terms related to ethanol, prenatal exposure, hippocampus, neurodevelopment, and memory. Data extraction and risk-of-bias assessment followed PRISMA guidelines. The included studies comprised research conducted in animal models that assessed HC-dependent memories using various neuropsychological and behavioral tests, along with their neurobiological correlates. Results showed that PAE negatively affects HC-dependent memories, with effects varying by dose, drinking pattern, frequency, duration, and timing of exposure. Greater alterations were associated with higher ethanol doses and binge-drinking-like exposure, whereas lower doses showed absent or partial effects. Significant behavioral, structural, and molecular differences were found between males and females. These findings highlight the relevance of HC damage as a potential contributor to the cognitive impairment associated with PAE and underscore the need for further research to elucidate how these alterations contribute to cognitive deficits and to improve early detection, diagnosis, and prevention strategies.