Summary: A follow-up study from Finland finds that young adults who began heavy alcohol use during adolescence show thinner cortical gray matter and altered neurotransmission patterns compared with peers who drank little or not at all.
Using magnetic resonance imaging (MRI) together with simultaneous transcranial magnetic stimulation and electroencephalography (TMS-EEG), researchers identified reduced cortical thickness and an increased N45 potential—an electrophysiological marker related to inhibitory GABAergic and excitatory glutamatergic activity. The results point to persistent, region-specific brain changes linked to adolescent heavy drinking and emphasize the need for further research into underlying mechanisms.
Key facts
- Adolescent heavy drinking is associated with reduced cortical gray matter thickness in adulthood.
- Young adults with a history of heavy adolescent drinking showed increased N45 potential, indicating altered balance of inhibitory GABA and excitatory glutamate neurotransmission.
- The frontal and parietal lobes were among the brain regions most affected by these structural and functional changes.
Source: University of Eastern Finland
Overview
Adolescence is a critical period of brain development, and exposure to repeated heavy alcohol use during this time can have long-lasting consequences. This Finnish longitudinal study followed participants over roughly a decade—beginning in early to mid-adolescence and continuing into their mid-twenties—to investigate how heavy drinking during adolescence relates to adult brain structure and cortical neurotransmission.
The research team combined high-resolution MRI to quantify gray matter (GM) thickness with TMS-EEG to measure cortical responses. The TMS-evoked N45 potential is interpreted as reflecting a balance between inhibitory GABAergic and excitatory NMDA receptor–mediated glutamatergic activity. By directly correlating GM thickness with electrophysiological measures, the study aimed to clarify how structural brain differences relate to functional neurotransmission among those with a history of heavy adolescent drinking.
Participants included 26 young adults with a sustained history of heavy alcohol consumption beginning in adolescence and 21 control participants who reported little or no alcohol use. All participants were monitored from ages 13–18 through their mid-twenties. Brain structure was assessed using magnetic resonance imaging, and cortical excitability and inhibition were evaluated via simultaneous TMS and EEG recordings.
Compared with the light-drinking control group, the heavy-drinking group showed significantly thinner cortex in several brain regions. Electrophysiologically, the heavy-drinking group exhibited larger N45 amplitudes, particularly over frontal regions. Importantly, among the heavy-drinking participants, thinner gray matter in specific areas correlated with larger frontal N45 amplitudes—an association that was not present in the light-drinking group. The strongest structure-function correlations were observed in the frontal and parietal lobes, including the left superior frontal gyrus, left supramarginal gyrus, and superior parietal regions in both hemispheres.
These findings suggest that long-term heavy alcohol exposure beginning in adolescence is associated with regional cortical thinning and concurrent alterations in the balance of inhibition and excitation in cortical circuits. The frontal and parietal lobes—regions involved in executive functions, attention, and sensory integration—appear particularly vulnerable. While the study establishes robust associations, it does not determine causality, and the authors call for additional research to identify the mechanisms driving these structural and functional changes.
About this neurodevelopment research news
Author: Maj Vuorre
Source: University of Eastern Finland
Contact: Maj Vuorre – University of Eastern Finland
Image: The image is credited to Neuroscience News
Original research: Closed access. Title: “Cortical thickness is inversely associated with transcranial magnetic stimulation-evoked N45 potential among young adults whose heavy drinking began in adolescence” by Virve Kekkonen et al., published in Alcoholism Clinical and Experimental Research.
Abstract
Cortical thickness is inversely associated with transcranial magnetic stimulation-evoked N45 potential among young adults whose heavy drinking began in adolescence
Background
Adolescence represents a vulnerable window for brain development during which alcohol can exert harmful effects. Prior work has linked repeated adolescent binge drinking to reduced gray matter volume and increased markers of inhibitory neurotransmission, but correlations between structural measures and direct electrophysiological indices have not been thoroughly examined.
Methods
This exploratory study compared 26 young adults with a 10-year history of heavy alcohol use to 21 peers with minimal alcohol exposure. Simultaneous TMS-EEG was used to measure N45 potentials, reflecting a balance between GABAergic inhibition and NMDA receptor–mediated glutamatergic excitation. Cortical thickness was measured from MRI scans, and associations between gray matter thickness and N45 amplitudes were evaluated.
Results
The heavy-drinking group showed significantly thinner cortex in several regions and larger frontal N45 amplitudes compared to controls. Within the heavy-drinking group, thinner gray matter correlated with larger frontal N45 amplitudes in multiple regions—especially the frontal and parietal lobes—patterns not observed in the light-drinking group.
Conclusions
The results indicate that adolescent-onset heavy drinking is associated with a thinner cerebral cortex and heightened markers of inhibitory neurotransmission in specific brain regions in young adulthood. Additional studies are necessary to determine causal pathways and the biological mechanisms that link structural cortical changes to altered neurotransmission after adolescent heavy alcohol exposure.