期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 65, 期 2, 页码 629-639出版社
IOS PRESS
DOI: 10.3233/JAD-180297
关键词
Alzheimer's disease; amyloid PET; brain; cholesterol; dementia; diabetes; hypertension; metabolic syndrome; vascular
资金
- Intramural Research Program of the NIH, National Institute on Aging
Background: Recent studies showlinks between metabolic syndrome and Alzheimer's disease (AD) neuropathology. Understanding the link between vascular-related health conditions and dementia will help target at risk populations and inform clinical strategies for early detection and prevention of AD. Objective: To determine whether metabolic syndrome is associated with global cerebral amyloid-beta (A beta) positivity and longitudinal A beta accumulation. Methods: Prospective study of 165 participants who underwent (11) C-Pittsburgh compound B (PiB) PET neuroimaging to measure A beta, from June 2005 to May 2016. Metabolic syndrome was defined using the revised Third Adults Treatment Panel of the National Cholesterol Education Program criteria. Participants were classified as PiB+/-. Linear mixed effects models assessed the relationships between baseline metabolic syndrome and PiB status and regional A beta change over time. Results: A total of 165 cognitively normal participants of the Baltimore Longitudinal Study of Aging (BLSA) Neuroimaging substudy, aged 55-92 years (mean baseline age = 76.4 years, 85 participants were male), received an average of 2.5 PET-PiB scans over an average interval of 2.6 (3.08 SD) years between first and last visits. Metabolic syndrome was not associated with baseline PiB positivity or concurrent regional A beta. Metabolic syndrome was associated with increased rates of A beta accumulation in superior parietal and precuneus regions over time in the PiB+ group. Elevated fasting glucose and blood pressure showed individual associations with accelerated A beta accumulation. Conclusion: Metabolic syndrome was associated with accelerated A beta accumulation in PiB+ individuals and may be an important factor in the progression of AD pathology.
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