How Alcohol Alters the Brain Cells That Command Our Mind

For decades, it was believed that the brain was composed almost exclusively of neurons, while other cells (glial cells) were seen merely as support. However, recent studies reveal that astrocytes—star-shaped cells—are in fact the active conductors of brain communication, controlling plasticity and the development of the mind.¹ These cells play a decisive role in mental health and are severely harmed by alcohol consumption at all stages of life.

The vulnerability of astrocytes begins very early, since during pregnancy exposure to alcohol interferes with the maturation of these cells.² This process compromises the proper formation of synapses and the blood–brain barrier, directly contributing to the cognitive deficits observed in Fetal Alcohol Syndrome (FAS). During adolescence,³ the impact continues, with alcohol reducing the physical proximity between the processes of these cells and neurons, which impairs the efficiency of connections in the hippocampus—a region vital for the formation of new memories and learning—and in the prefrontal cortex, which acts as the command center for decision-making and impulse control.

In adults with alcohol dependence, astrocytes undergo a profound change known as reactivity, altering their molecular structure and beginning to produce inflammatory substances.² One of the most striking effects of this alteration occurs in the extracellular matrix, where these cells create networks that surround neurons.⁴ Excessive alcohol consumption can make these networks too rigid, trapping neural circuits and promoting behavioral inflexibility and compulsive drinking.

Despite this damage, science is beginning to see new hope for future treatments in these cells. Research in animals indicates that manipulating specific genes within astrocytes—such as through the use of PPAR-γ receptors⁵—can protect memory and learning against the toxic effects of ethanol. Understanding how these cells communicate with the rest of the brain may therefore represent a new frontier for restoring functions lost to alcoholism.

The consequences of this cellular dysregulation extend beyond microscopic biology, manifesting as profound damage to overall health and the integrity of human behavior. Gestational exposure to alcohol is the most common and preventable cause of intellectual disability worldwide, resulting in permanent structural abnormalities and lifelong impairments in cognition and social adaptability. In adulthood, the reduction in the number and density of these cells helps explain the cognitive decline and loss of brain volume observed in individuals with alcohol use disorders. Understanding this relationship is essential, as it suggests that the future of alcoholism treatment may lie in the restoration of these cells.

References

1. Chung, W. S., Baldwin, K. T., & Allen, N. J. (2024). Astrocyte Regulation of Synapse Formation, Maturation, and Elimination. Cold Spring Harbor perspectives in biology, 16(8), a041352. https://doi.org/10.1101/cshperspect.a041352
2. Guizzetti, M., Mangieri, R. A., Ezerskiy, L. A., Hashimoto, J. G., Bajo, M., Farris, S. P., Homanics, G. E., Lasek, A. W., Mayfield, R. D., Messing, R. O., & Roberto, M. (2026). Astrocytes and Alcohol Throughout the Lifespan. Biological psychiatry, 99(1), 9–20. https://doi.org/10.1016/j.biopsych.2025.04.013
3. Healey, K. L., Bell, A., Scofield, M. D., & Swartzwelder, H. S. (2022). Adolescent intermittent ethanol exposure reduces astrocyte-synaptic proximity in the adult medial prefrontal cortex in rats: Reversal by gabapentin. Addiction neuroscience, 4, 100047. https://doi.org/10.1016/j.addicn.2022.100047
4. Soles, A., Selimovic, A., Sbrocco, K., Ghannoum, F., Hamel, K., Moncada, E. L., Gilliat, S., & Cvetanovic, M. (2023). Extracellular Matrix Regulation in Physiology and in Brain Disease. International journal of molecular sciences, 24(8), 7049. https://doi.org/10.3390/ijms24087049
5. Garcia-Baos, A., Pastor, A., Gallego-Landin, I. et al. The role of PPAR-γ in memory deficits induced by prenatal and lactation alcohol exposure in mice. Mol Psychiatry28, 3373–3383 (2023). https://doi.org/10.1038/s41380-023-02191-z