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

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Margaret R. Flanigan ◽  
Sarah K. Royse ◽  
David P. Cenkner ◽  
Katelyn M. Kozinski ◽  
Clara J. Stoughton ◽  
...  

AbstractNo 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.

2015 ◽  
Vol 11 (7S_Part_3) ◽  
pp. P144-P145 ◽  
Author(s):  
Adam J. Schwarz ◽  
Sergey Shcherbinin ◽  
Bradley B. Miller ◽  
Peng Yu ◽  
Michael Navitsky ◽  
...  

2020 ◽  
Vol 16 (S2) ◽  
Author(s):  
Fedor Levin ◽  
Irina Jelistratova ◽  
Tobey J. Betthauser ◽  
Sterling C. Johnson ◽  
Stefan J. Teipel ◽  
...  

2017 ◽  
Vol 13 (7S_Part_2) ◽  
pp. P133-P133 ◽  
Author(s):  
Konstantinos Chiotis ◽  
Per Stenkrona ◽  
Ove Almkvist ◽  
Ryosuke Arakawa ◽  
Akihiro Takano ◽  
...  

2017 ◽  
Vol 13 (7S_Part_22) ◽  
pp. P1083-P1083
Author(s):  
Young Noh ◽  
Han Kyu Na ◽  
Seongho Seo ◽  
Sang-Yoon Lee ◽  
Hye Jin Jeong ◽  
...  

2017 ◽  
Vol 13 (7S_Part_15) ◽  
pp. P765-P765 ◽  
Author(s):  
Konstantinos Chiotis ◽  
Per Stenkrona ◽  
Ove Almkvist ◽  
Ryosuke Arakawa ◽  
Akihiro Takano ◽  
...  

2016 ◽  
Vol 310 (6) ◽  
pp. E388-E393 ◽  
Author(s):  
Jackob Moskovitz ◽  
Fang Du ◽  
Connor F. Bowman ◽  
Shirley S. Yan

Accumulation of oxidized proteins, and especially β-amyloid (Aβ), is thought to be one of the common causes of Alzheimer's disease (AD). The current studies determine the effect of an in vivo methionine sulfoxidation of Aβ through ablation of the methionine sulfoxide reductase A (MsrA) in a mouse model of AD, a mouse that overexpresses amyloid precursor protein (APP) and Aβ in neurons. Lack of MsrA fosters the formation of methionine sulfoxide in proteins, and thus its ablation in the AD-mouse model will increase the formation of methionine sulfoxide in Aβ. Indeed, the novel MsrA-deficient APP mice ( APP+/ MsrAKO) exhibited higher levels of soluble Aβ in brain compared with APP+ mice. Furthermore, mitochondrial respiration and the activity of cytochrome c oxidase were compromised in the APP+/ MsrAKO compared with control mice. These results suggest that lower MsrA activity modifies Aβ solubility properties and causes mitochondrial dysfunction, and augmenting its activity may be beneficial in delaying AD progression.


2020 ◽  
Vol 74 (4) ◽  
pp. 1243-1252
Author(s):  
José A. Luchsinger ◽  
Priya Palta ◽  
Brady Rippon ◽  
Luisa Soto ◽  
Fernando Ceballos ◽  
...  

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 141-141
Author(s):  
Tina Brinkley ◽  
Samuel Lockhart ◽  
Bonnie Sachs ◽  
Maryjo Cleveland ◽  
Benjamin Williams ◽  
...  

Abstract Mid-life obesity is associated with a higher risk for Alzheimer’s disease (AD). However, this association is attenuated or even reversed in late-life, when weight loss may be a preclinical sign of AD. While neuropathological changes likely occur alongside aging-related changes in body composition, this has not been largely investigated. We aimed to determine the association between adiposity and a specific pattern of reduced cortical thickness associated with AD risk and progression. Global and regional adiposity (via dual-energy x-ray absorptiometry) and AD-signature cortical thickness (via surface-based cortical analysis of 3T brain MRI scans) were measured in 35 middle-aged and older adults from the Wake Forest Alzheimer’s Disease Clinical Core (mean age: 69.4±7.8 years, 80% female, 91% White, 29% cognitively impaired). Partial correlations adjusted for age, sex, and cognitive status were examined overall and stratified by age (0.59, p≤0.05). No significant associations were observed in middle-aged adults. These findings suggest that AD-related cortical thinning may be accompanied by a global reduction in body fat among older adults.


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