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Neurobiol Aging. 2019 Jul 22;82:110-119. doi: 10.1016/j.neurobiolaging.2019.07.005. [Epub ahead of print]

Associations among amyloid status, age, and longitudinal regional brain atrophy in cognitively unimpaired older adults.

Author information

1
Department of Veterans Affairs Medical Center, Center for Imaging of Neurodegenerative Diseases, San Francisco, CA, USA; Department of Psychiatry, University of California, CA, USA. Electronic address: rachel.nosheny@ucsf.edu.
2
Department of Clinical Sciences Malmö, Clinical Memory Research Unit, Lund University, Lund, Sweden.
3
Department of Veterans Affairs Medical Center, Center for Imaging of Neurodegenerative Diseases, San Francisco, CA, USA; Department of Radiology and Biomedical Imaging, University of California, CA, USA.
4
Department of Veterans Affairs Medical Center, Center for Imaging of Neurodegenerative Diseases, San Francisco, CA, USA.
5
Alzheimer's Therapeutic Research Institute, Keck School of Medicine of USC, San Diego, CA, USA.
6
Department of Veterans Affairs Medical Center, Center for Imaging of Neurodegenerative Diseases, San Francisco, CA, USA; Department of Psychiatry, University of California, CA, USA; Department of Radiology and Biomedical Imaging, University of California, CA, USA.

Abstract

The goal of this study was to compare regional brain atrophy patterns in cognitively unimpaired (CU) older adults with and without brain accumulation of amyloid-β (Aβ) to elucidate contributions of Aβ, age, and other variables to atrophy rates. In 80 CU participants from the Alzheimer's Disease Neuroimaging Initiative, we determined effects of Aβ and age on longitudinal, regional atrophy rates, while accounting for confounding variables including sex, APOE ε4 genotype, white matter lesions, and cerebrospinal fluid total and phosphorylated tau levels. We not only found overlapping patterns of atrophy in Aβ+ versus Aβ- participants but also identified regions where atrophy pattern differed between the 2 groups. Higher Aβ load was associated with increased longitudinal atrophy in the entorhinal cortex, amygdala, and hippocampus, even when accounting for age and other variables. Age was associated with atrophy in insula, fusiform gyrus, and isthmus cingulate, even when accounting for Aβ. We found age by Aβ interactions in the postcentral gyrus and lateral orbitofrontal cortex. These results elucidate the separate and related effects of age, Aβ, and other important variables on longitudinal brain atrophy rates in CU older adults.

KEYWORDS:

Aging; Alzheimer's disease; Amyloid-β; Brain atrophy

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