Imaging beta-amyloid (Aβ) burden in the brains of middle-aged individuals with alcohol-use disorders: a [11C]PIB PET study

Margaret R Flanigan, Sarah K Royse, David P Cenkner, Katelyn M Kozinski, Clara J Stoughton, Michael L Himes, Davneet S Minhas, Brian Lopresti, Meryl A Butters, Rajesh Narendran, Margaret R Flanigan, Sarah K Royse, David P Cenkner, Katelyn M Kozinski, Clara J Stoughton, Michael L Himes, Davneet S Minhas, Brian Lopresti, Meryl A Butters, Rajesh Narendran

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 .

Conflict of interest statement

The authors declare no competing interest.

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