Research Paper Volume 12, Issue 2 pp 2005—2017
Late-life obesity is a protective factor for prodromal Alzheimer’s disease: a longitudinal study
- 1 Department of Neurology, Qingdao Municipal Hospital, Nanjing Medical University, Nanjing, China
- 2 College of Medicine and Pharmaceutics, Ocean University of China, Qingdao, China
- 3 Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China
- 4 Department of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China
- 5 Data used in preparation of this article were obtained from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database (adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in analysis or writing of this report. A complete listing of ADNI investigators can be found at: http://adni.loni.usc.edu/wp-content/uploads/how_to_apply/ADNI_Acknowledgement_List.pdf
received: November 24, 2019 ; accepted: December 31, 2019 ; published: January 25, 2020 ;https://doi.org/10.18632/aging.102738
How to Cite
Copyright © 2020 Sun et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Higher body mass index (BMI) in late-life has recently been considered as a possible protective factor for Alzheimer's disease (AD), which yet remains conflicting. To test this hypothesis, we have evaluated the cross-sectional and longitudinal associations of BMI categories with CSF biomarkers, brain β-amyloid (Aβ) load, brain structure, and cognition and have assessed the effect of late-life BMI on AD risk in a large sample (n = 1,212) of non-demented elderly from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database. At baseline, higher late-life BMI categories were associated with higher levels of CSF Aβ42 (p=0.037), lower levels of CSF total-tau (t-tau, p=0.026) and CSF t-tau/Aβ42 (p=0.008), lower load of Aβ in the right hippocampus (p=0.030), as well as larger volumes of hippocampus (p<0.0001), entorhinal cortex (p=0.009) and middle temporal lobe (p=0.040). But no association was found with CSF phosphorylated-tau (p-tau) or CSF p-tau/Aβ42. Longitudinal studies showed that higher BMI individuals experienced a slower decline in cognitive function. In addition, Kaplan–Meier survival analysis revealed that higher late-life BMI had a reduced risk of progression to AD over time (p = 0.009). Higher BMI in late-life decreased the risk of AD, and this process may be driven by AD-related biomarkers.
AD: Alzheimer’s disease; BMI: Body mass index; ADNI: Alzheimer’s Disease Neuroimaging Initiative; CSF: Cerebrospinal Fluid; Aβ42: β-amyloid42; NC: Normal cognition; MCI: Mild cognitive impairment; T-tau: Total-tau; P-tau: Phosphorylated-tau; DM2: Diabetes Mellitus Type 2; CVD: Cardiovascular diseases; MMSE: Mini-mental State Examination; ADAS-Cog: Alzheimer Disease Assessment Scale-cognitive subscale; ICV: intracranial volume; Region of interest (ROI): undefined.