期刊
NEUROLOGY
卷 77, 期 21, 页码 1913-1920出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0b013e318238eec1
关键词
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资金
- University of Kansas Alzheimer Disease Center [P30AG035982]
- National Institute on Neurological Disorders and Stroke [K23NS058252]
- Eunice Kennedy Shriver National Institute of Child Health & Human Development [T32HD057850]
- Foundation for Physical Therapy
- Heartland Institute for Clinical & Translational Research, University of Kansas Medical Center's CTSA [KL2 RR033177, UL1 RR033179]
- National Institute on Aging [K01AG035042]
- Alzheimer's Disease Neuroimaging Initiative (ADNI) (NIH) [U01 AG024904]
- National Institute on Aging
- National Institute of Biomedical Imaging and Bioengineering
- Abbott
- AstraZeneca
- Bayer Schering Pharma
- Bristol-Myers Squibb
- Eisai Inc.
- Elan Corporation
- Genentech, Inc.
- GE Healthcare
- GlaxoSmithKline
- Innogenetics
- Johnson and Johnson
- Eli Lilly and Company
- Medpace, Inc.
- Merck and Co., Inc.
- Novartis
- Pfizer Inc
- Roche
- Schering-Plough Corp.
- Synarc, Inc.
- Alzheimer's Association
- Alzheimer's Drug Discovery Foundation
- NIH/NICHHD
- Janssen
- Wyeth
- Danone
- Dana Foundation
- [R01AG033673]
- [R01AG034614]
Objective: Both low and high body mass index (BMI) has been associated with cognitive impairment and dementia risk, including Alzheimer disease (AD). We examined the relationship of BMI with potential underlying biological substrates for cognitive impairment. Methods: We analyzed cross-sectional data from participants enrolled in the Alzheimer's Disease Neuroimaging Initiative (ADNI) with PET imaging using Pittsburgh Compound B (PiB, n = 101) or CSF analyses (n = 405) for beta-amyloid peptide (A beta) and total tau. We assessed the relationship of CSF biomarkers and global PiB uptake with BMI using linear regression controlling for age and sex. We also assessed BMI differences between those who were and were not considered biomarker positive. Finally, we assessed BMI change over 2 years in relationship to AD biomarkers. Results: No dementia, mild cognitive impairment (MCI), and AD groups were not different in age, education, or BMI. In the overall sample, CSF A beta (beta = 0.181, p < 0.001), tau (beta = -0.179, p < 0.001), tau/A beta ratio (beta = -0.180, p < 0.001), and global PiB uptake (beta = -0.272, p = 0.005) were associated with BMI, with markers of increased AD burden associated with lower BMI. Fewer overweight individuals had biomarker levels indicative of pathophysiology (p < 0.01). These relationships were strongest in the MCI and no dementia groups. Conclusions: The presence and burden of in vivo biomarkers of cerebral amyloid and tau are associated with lower BMI in cognitively normal and MCI individuals. This supports previous findings of systemic change in the earliest phases of the disease. Further, MCI in those who are overweight may be more likely to result from heterogeneous pathophysiology. Neurology (R) 2011; 77: 1913-1920
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