Literature DB >> 24269021

Amyloid burden and neural function in people at risk for Alzheimer's Disease.

Sterling C Johnson1, Bradley T Christian, Ozioma C Okonkwo, Jennifer M Oh, Sandra Harding, Guofan Xu, Ansel T Hillmer, Dustin W Wooten, Dhanabalan Murali, Todd E Barnhart, Lance T Hall, Annie M Racine, William E Klunk, Chester A Mathis, Barbara B Bendlin, Catherine L Gallagher, Cynthia M Carlsson, Howard A Rowley, Bruce P Hermann, N Maritza Dowling, Sanjay Asthana, Mark A Sager.   

Abstract

To determine the relationship between amyloid burden and neural function in healthy adults at risk for n class="Disease">Alzheimer's Disease (AD), we used multimodal imaging with [C-11]Pittsburgh compound B positron emission tomography, [F-18]fluorodeoxyglucose, positron emission tomography , and magnetic resonance imaging, together with cognitive measurement in 201 subjects (mean age, 60.1 years; range, 46-73 years) from the Wisconsin Registry for Alzheimer's Prevention. Using a qualitative rating, 18% of the samples were strongly positive Beta-amyloid (Aβ+), 41% indeterminate (Aβi), and 41% negative (Aβ-). Aβ+ was associated with older age, female sex, and showed trends for maternal family history of AD and APOE4. Relative to the Aβ- group, Aβ+ and Aβi participants had increased glucose metabolism in the bilateral thalamus; Aβ+ participants also had increased metabolism in the bilateral superior temporal gyrus. Aβ+ participants exhibited increased gray matter in the lateral parietal lobe bilaterally relative to the Aβ- group, and no areas of significant atrophy. Cognitive performance and self report cognitive and affective symptoms did not differ between groups. Amyloid burden can be identified in adults at a mean age of 60 years and is accompanied by glucometabolic increases in specific areas, but not atrophy or cognitive loss. This asymptomatic stage may be an opportune window for intervention to prevent progression to symptomatic AD. Published by Elsevier Inc.

Entities:  

Keywords:  AD risk; Alzheimer's disease; Amyloid imaging; Cognitive function; Glucose metabolism

Mesh:

Substances:

Year:  2013        PMID: 24269021      PMCID: PMC4018215          DOI: 10.1016/j.neurobiolaging.2013.09.028

Source DB:  PubMed          Journal:  Neurobiol Aging        ISSN: 0197-4580            Impact factor:   4.673


  57 in total

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Review 3.  Alzheimer's disease: the amyloid cascade hypothesis.

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Review 4.  Brain aging, Alzheimer's disease, and mitochondria.

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10.  Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. A meta-analysis. APOE and Alzheimer Disease Meta Analysis Consortium.

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2.  Interaction of Cigarette Smoking History With APOE Genotype and Age on Amyloid Level, Glucose Metabolism, and Neurocognition in Cognitively Normal Elders.

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3.  Temporal Order of Alzheimer's Disease-Related Cognitive Marker Changes in BLSA and WRAP Longitudinal Studies.

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4.  Moderate Physical Activity is Associated with Cerebral Glucose Metabolism in Adults at Risk for Alzheimer's Disease.

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5.  Pathway-Specific Polygenic Risk Scores as Predictors of Amyloid-β Deposition and Cognitive Function in a Sample at Increased Risk for Alzheimer's Disease.

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6.  Proper names from story recall are associated with beta-amyloid in cognitively unimpaired adults at risk for Alzheimer's disease.

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9.  Cortical β-amyloid burden, gray matter, and memory in adults at varying APOE ε4 risk for Alzheimer's disease.

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Review 10.  What is normal in normal aging? Effects of aging, amyloid and Alzheimer's disease on the cerebral cortex and the hippocampus.

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