Journal
NEUROBIOLOGY OF AGING
Volume 58, Issue -, Pages 68-76Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2017.05.019
Keywords
Alzheimer's disease; Dementia; Down syndrome; Amyloid-beta; PiB; Mild cognitive impairment
Categories
Funding
- National Institute on Aging [R01AG031110, U01AG051406]
- Eunice Kennedy Schriver National Institute of Child Health and Human Development [P30 HD03352]
Ask authors/readers for more resources
Adults with Down syndrome (DS) have a high incidence of Alzheimer's disease (AD), providing a unique opportunity to explore the early, preclinical stages of AD neuropathology. We examined change in brain amyloid-beta accumulation via the positron emission tomography tracer [11C] Pittsburgh compound B (PiB) across 2 data collection cycles, spaced 3 years apart, and decline in cognitive functioning in 58 adults with DS without clinical AD. PiB retention increased in the anterior cingulate gyrus, precuneus cortex, parietal cortex, and anterior ventral striatum. Across the 2 cycles, 14 (27.5%) participants were consistently PiB+, 31 (60.8%) were consistently PiB, and 6 (11.7%) converted from PiB at cycle 1 to PiB+ at cycle 2. Increased global amyloid-beta was related to decline in verbal episodic memory, visual episodic memory, executive functioning, and fine motor processing speed. Participants who were consistently PiB+ demonstrated worsening of episodic memory, whereas participants who were consistently PiB evidenced stable or improved performance. Amyloid-beta accumulation may be a contributor to or biomarker of declining cognitive functioning in preclinical AD in DS. (C) 2017 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available