BACKGROUND:
Chronic alcohol consumption, the resulting neurotoxic effects and the long-term neurological issues in particular due to altering brain functions can considerably enhance progressive decline in executive functions. While some believe that alcohol has benefits for the body, research findings have increasingly challenged this common belief. Brain studies have especially highlighted neuronal degeneration caused by alcohol intake; however, the impact of alcohol intoxication on the volumetric characteristics of subcortical regions remains underexplored.
METHODS:
Given the involvement of subcortical structures in cognitive decline, we examined the volumetric alterations in grey matter and utilized high-resolution T1-weighted structural brain data of 7,690 participants from the UK Biobank who drink alcohol regularly. We also included 3,019 individuals who never drink alcohol from the same cohort as the control group. We focused on the volumes of the Brain Stem, Thalamus, Caudate, Putamen, Amygdala, Hippocampus, and Pallidum, and we performed a multifactor Multivariate Analysis of Variance to examine differences in the combined mean of the grey matter volume of the above-mentioned regions between these two groups of participants. Post hoc tests were subsequently carried out and Holm’s Sequential Bonferroni procedure was used to correct for multiple comparisons.
RESULTS:
After adjusting for biological sex and age, our findings revealed significant shrinkage of the Brain Stem due to alcohol intoxication, while the Putamen demonstrated resilience. Importantly, we observed alcohol-induced inflammation in the Thalamus, Caudate, Amygdala, Hippocampus, and Pallidum.
CONCLUSION:
Given that neuroinflammatory conditions in subcortical regions can contribute to the development of Multiple Sclerosis, the inflammation observed in the Thalamus, Caudate, Amygdala, Hippocampus, and Pallidum highlights a heightened risk for neurodegenerative diseases linked to alcohol-induced neurotoxicity. Moreover, while age-related brain degeneration does not affect all individuals in later life, alcohol consumption introduces an additional risk factor that accelerates neurodegenerative processes. The association between brain stem shrinkage and frontotemporal dementia further suggests that alcohol may act as an early driver of neurodegeneration, shedding light on the long-term impact of sustained alcohol use on subcortical brain structures.