Alcohol and Alzheimer’s disease are often discussed separately, but they may intersect in important ways. In this study, researchers examined whether a history of alcohol use disorder was associated with worse cognitive function and different brain-volume patterns in people with Alzheimer’s disease.
Using data from the National Alzheimer’s Coordinating Center, the study compared four groups: people with Alzheimer’s disease and alcohol use disorder, people with Alzheimer’s disease alone, people with alcohol use disorder alone, and controls without either condition. The central finding was that alcohol use disorder was associated with greater dementia severity among participants with Alzheimer’s disease. In practical terms, people with both conditions showed worse overall clinical dementia severity than those with Alzheimer’s disease alone.
The study also found that Alzheimer’s disease was associated with broader and more severe brain-volume loss than alcohol use disorder alone. Participants with Alzheimer’s disease had lower total gray matter volume, lower white matter volume, and larger ventricular volumes than participants without Alzheimer’s disease. Regionally, Alzheimer’s disease was associated with smaller volumes in several areas involved in memory and higher-order cognition, including the hippocampal formation, inferior and superior parietal cortex, occipital cortex, inferior frontal gyrus, posterior cingulate cortex, and isthmus cingulate cortex.
Alcohol use disorder showed a different pattern. Rather than widespread volume loss, it was associated more specifically with lower gray matter volume in the somatomotor cortex, with a trend toward smaller hippocampal volume as well. That is notable because the hippocampal region is strongly involved in memory and was the strongest volumetric predictor of cognitive performance across the full sample. Smaller hippocampal volume tracked with worse cognitive functioning overall.
One of the most interesting messages from the study is that Alzheimer’s disease and alcohol use disorder may affect the brain in overlapping but not identical ways. The hippocampus appeared to be a shared point of vulnerability, whereas Alzheimer’s disease showed much more extensive atrophy across multiple cortical regions. Alcohol use disorder, by contrast, appeared to have a more selective association in this dataset.
At the same time, the paper does not show that alcohol directly causes Alzheimer’s disease. It was a cross-sectional study, meaning the data were analyzed at one point in time rather than tracked prospectively to establish cause and effect. The paper also could not measure alcohol-use severity or duration in detail, and many participants with alcohol use disorder had past rather than current alcohol misuse. That matters, because the authors note that abstinence may lessen or obscure some alcohol-related brain changes.
The most careful takeaway is this: in this sample, a history of alcohol use disorder was linked to worse dementia severity in people with Alzheimer’s disease, and both conditions were associated with brain changes relevant to cognition. Alzheimer’s disease showed the more extensive pattern of atrophy, while alcohol use disorder appeared to add to clinical burden and share at least some hippocampal involvement.
For readers, the message is not simply that “alcohol is bad for the brain,” but that heavy or disordered alcohol use may compound cognitive vulnerability in people with Alzheimer’s disease. The study supports the idea that alcohol-related pathology and Alzheimer’s pathology can coexist, and when they do, the combination may be associated with worse clinical presentation.