期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 79, 期 4, 页码 1801-1811出版社
IOS PRESS
DOI: 10.3233/JAD-201242
关键词
Alzheimer's disease; neuroinflammation imaging; obesity
资金
- National Institutes of Health [P50AG005681, P01AG026276, P01AG003991]
- WUSTL NIH KL2 Grant [KL2 TR000450]
- Radiological Society of North America Research Scholar Grant
- Foundation of the American Society of Neuroradiology Boerger Research Fund for Alzheimer's Disease and Neurocognitive Disorders
Our study revealed significant relationships between neuroinflammation, elevated BMI, and hippocampal volume, highlighting implications for neuroinflammation mechanisms of obesity-related brain dysfunction in cognitively normal elderly individuals.
Background: Obesity is related to quantitative neuroimaging abnormalities including reduced gray matter volumes and impaired white matter microstructural integrity, although the underlying mechanisms are not well understood. Objective: We assessed influence of obesity on neuroinflammation imaging that may mediate brain morphometric changes. Establishing the role of neuroinflammation in obesity will enhance understanding of this modifiable disorder as a risk factor for Alzheimer's disease (AD) dementia. Methods: We analyzed brain MRIs from 104 cognitively normal participants (CDR = 0) and biomarker negativity for CSF amyloid or tau. We classified body mass index (BMI) as normal (BMI <25, N = 62) or overweight and obese (BMI = 25, N = 42). Blood pressure was measured. BMI and blood pressure classifications were related to neuroinflammation imaging (NII) derived edema fraction in 17 white matter tracts. This metric was also correlated to hippocampal volumes and CSF biomarkers of inflammation and neurodegeneration: YKL-40, SNAP25, VILIP, tau, and NFL. Results: Participants with BMI <25 had lower NII-derived edema fraction, with protective effects of normal blood pressure. Statistically significant white matter tracts included the internal capsule, external capsule, and corona radiata, FDR corrected for multiple comparisons to alpha = 0.05. Higher NII-derived edema fractions in the internal capsule, corpus callosum, gyrus, and superior fronto-occipital fasciculus were related with smaller hippocampal volumes only in individuals with BMI >= 25. There were no statistically significant correlations between NII-derived edema fraction and CSF biomarkers. Conclusion: We demonstrate statistically significant relationships between neuroinflammation, elevated BMI, and hippocampal volume, raising implications for neuroinflammation mechanisms of obesity-related brain dysfunction in cognitively normal elderly.
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