Abstract
No in vivo human studies have examined the prevalence of Alzheimer’s disease (AD) neuropathology in individuals with alcohol-use disorder (AUD), although recent research suggests that a relationship between the two exists. Therefore, this study used Pittsburgh Compound-B ([11C]PiB) PET imaging to test the hypothesis that AUD is associated with greater brain amyloid (Aβ) burden in middle-aged adults compared to healthy controls. Twenty healthy participants (14M and 6F) and 19 individuals with AUD (15M and 4F), all aged 40–65 years, underwent clinical assessment, MRI, neurocognitive testing, and positron emission tomography (PET) imaging. Global [11C]PiB standard uptake value ratios (SUVRs), cortical thickness, gray matter volumes (GMVs), and neurocognitive function in subjects with AUD were compared to healthy controls. These measures were selected because they are considered markers of risk for future AD and other types of neurocognitive dysfunction. The results of this study showed no significant differences in % global Aβ positivity or subthreshold Aβ loads between AUD and controls. However, relative to controls, we observed a significant 6.1% lower cortical thickness in both AD-signature regions and in regions not typically associated with AD, lower GMV in the hippocampus, and lower performance on tests of attention as well as immediate and delayed memory in individuals with AUD. This suggest that Aβ accumulation is not greater in middle-aged individuals with AUD. However, other markers of neurodegeneration, such as impaired memory, cortical thinning, and reduced hippocampal GMV, are present. Further studies are needed to elucidate the patterns and temporal staging of AUD-related pathophysiology and cognitive impairment. Imaging β-amyloid in middle age alcoholics as a mechanism that increases their risk for Alzheimer’s disease; Registration Number: NCT03746366.
Highlights
A long-established relationship exists between alcohol use disorder (AUD) and cognitive impairment[1,2]
There were no significant differences in [11C]PiB standard uptake value ratios (SUVRs) between groups to indicate that subthreshold Aβ burden may be higher in the AUD group compared to the healthy controls (HCs) group
gray matter volumes (GMVs) in the hippocampus was significantly lower in the AUD group than in the HC group
Summary
A long-established relationship exists between alcohol use disorder (AUD) and cognitive impairment[1,2]. Given the retrospective nature of this study, a number of potential confounding variables may have been present (e.g., survivor bias, psychiatric and medical comorbidities, periods of abstinence from alcohol, and comorbid use of other substances), which complicates the interpretation of these data[7] Another recent study, in which 414 community members (age 70.9 ± 7.8 years), all without dementia or alcohol-related disorders, underwent carbon-11-labeled Pittsburgh Compound-B ([11C]PiB) positron emission tomography (PET) imaging, found no elevation in Aβ accumulation in heavy drinkers (>14 drinks per week) compared to their abstinent counterparts[8]. Given that the presence of any alcohol-related disorder was an exclusion criterion for this study, it is difficult to extend the interpretation of these findings to individuals with AUD These studies highlight that, despite considerable interest in characterizing the putative relationship between AUD and AD, the existing data are unable to support a consensus
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