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ASSOCIATION OF PAST AND CURRENT BODY MASS INDEX WITH BRAIN AMYLOID DEPOSITION AND NEURODEGENERATION IN COGNITIVELY NORMAL ELDERLY

      Background

      Both low and high body mass index(BMI) has been associated with cognitive impairment and Alzheimer disease(AD) dementia. Nevertheless, very little information is available for the association between BMI over life course and brain amyloid beta(Aβ) burden and AD-specific neurodegeneration. In this study, we examined the relationship of past and current BMI with in vivo cerebral Aβ deposition and AD-signature region cortical thickness in cognitively normal elderly population.

      Methods

      Two-hundred twelve cognitively normal elderly subjects aged 60-90, who participated in the Korean Brain Aging Study for Early Diagnosis and Prediction of Alzheimer’s Disease (KBASE), were included in this study. All the subjects underwent comprehensive clinical and neuropsychological assessment, 11C-labelled Pittsburgh Compound B (PiB) positron emission tomography (PET), and Brain Magnetic resonance imaging(MRI). Mean cortical thickness values were obtained from AD-signature regions including the entorhinal, inferior temporal, middle temporal, and fusiform gyrus. BMI values for past lifetime periods((i.e., young adulthood: 20-30s and midlife: 40-50s) were calculated from self-recalled body weight and height, and current BMI was calculated from measured body weight and height. Multiple regression analyses were performed controlling age, gender, APOE e4 carrier status, and vascular risk scores.

      Results

      For the overall subjects, past BMI, BMI at young adulthood in particular, was negatively associated with global cerebral Aβ deposition, while current BMI was not. In contrast, current BMI showed significant positive association with AD-signature region cortical thickness, while past BMI did not. When subgroup analyses were performed for each gender, very similar relationships between lifetime BMIs and Aβ deposition and cortical thickness were still found for males, whereas no significant association was observed between the variables for females.

      Conclusions

      Our results suggest that relatively low past BMI, especially in male, may contribute to increase of cerebral Aβ burden and the risk of AD in late-life, while lower current BMI appears related with emerging neurodegeneration. The findings should be cautiously interpreted considering most of the subjects were in normal range for past and current BMI, and only small proportion of them were in overweight or obese state.
      Table 1Analyses of association between AD biomarker with BMI measure at each age
      Global Aβ depositionAD signature cortical thickness
      BSEβPBSEβP
      Current BMI-0.0080.006-0.0910.1840.0080.0040.1390.018
      Early adult BMI-0.0110.006-0.1180.0820.0070.0040.1080.063
      Mid life BMI-0.0160.007-0.1520.0250.0030.0040.0390.504
      Past BMI(20 to 50)-0.0150.007-0.1410.0370.0060.0040.0830.158
      Abbreviations: BMI=body mass index. All analyses were Adjusted by age, gender, APOE4 carrier status, Vascular risk factors.
      Table 2Analyses of association between PiB retention and BMI at each age and sex group in participant
      WomenMen
      βP valueβP value
      Early adult BMI-0.0020.786-0.0380.003
      Midlife BMI0.0030.673-0.0280.009
      Past BMI(20 to 50)0.0010.944-0.0360.003
      Current BMI0.0030.690-0.0210.042
      BMI=body mass index. All analysis were Adjusted for age, APOE4 carrier status, vascular risk factors.
      Table 3Analyses of association between AD sig cortical thickness and BMI at each age and sex group in participant
      WomenMen
      βP valueBP value
      Early adult BMI0.0020.7340.0050.532
      Midlife BMI0.0030.6000.0140.022
      Past BMI(20 to 50)0.0030.6210.0120.098
      Current BMI0.0060.2110.0130.023
      BMI=body mass index. All analysis were Adjusted for age, APOE4 carrier status, vascular risk factors.