9 research outputs found

    Table_1_High Glycemic Diet Is Related to Brain Amyloid Accumulation Over One Year in Preclinical Alzheimer's Disease.PDF

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    Objective: To test the hypothesis that high glycemic diet is related to 1-year change in brain amyloid based on our prior cross-sectional evidence that high glycemic diet is associated with brain amyloid.Methods: This longitudinal, observational study assessed the relationship between reported habitual consumption of a high glycemic diet (HGDiet) pattern and 1-year brain amyloid change measured by Florbetapir F18 PET scans in 102 cognitively normal older adults with elevated or sub-threshold amyloid status that participated in a 1-year randomized, controlled exercise trial at the University of Kansas Medical Center in Kansas City.Results: Among all participants (n = 102), higher daily intake of the HGDiet pattern (β = 0.06, p = 0.04), sugar (β = 0.07, p = 0.01), and total carbohydrate (β = 0.06, p = 0.04) were related to more precuneal amyloid accumulation. These relationships in the precuneus were accentuated in participants with elevated amyloid at enrollment (n = 70) where higher intake of the HGDiet pattern, sugar, and carbohydrate were related to more precuneal amyloid accumulation (β = 0.11, p = 0.01 for all measures). In individuals with elevated amyloid, higher intake of the HGDiet pattern was also related to more amyloid accumulation in the lateral temporal lobe (β = 0.09, p Conclusion: This longitudinal observational analysis suggests that a high glycemic diet relates to higher brain amyloid accumulation over 1 year in regions of the temporoparietal cortex in cognitively normal adults, particularly in those with elevated amyloid status. Further studies are required to assess whether there is causal link between a high glycemic diet and brain amyloid.Clinical Trial Registration:ClinicalTrials.gov, Identifier (NCT02000583).</p

    Table_2_High Glycemic Diet Is Related to Brain Amyloid Accumulation Over One Year in Preclinical Alzheimer's Disease.PDF

    No full text
    Objective: To test the hypothesis that high glycemic diet is related to 1-year change in brain amyloid based on our prior cross-sectional evidence that high glycemic diet is associated with brain amyloid.Methods: This longitudinal, observational study assessed the relationship between reported habitual consumption of a high glycemic diet (HGDiet) pattern and 1-year brain amyloid change measured by Florbetapir F18 PET scans in 102 cognitively normal older adults with elevated or sub-threshold amyloid status that participated in a 1-year randomized, controlled exercise trial at the University of Kansas Medical Center in Kansas City.Results: Among all participants (n = 102), higher daily intake of the HGDiet pattern (β = 0.06, p = 0.04), sugar (β = 0.07, p = 0.01), and total carbohydrate (β = 0.06, p = 0.04) were related to more precuneal amyloid accumulation. These relationships in the precuneus were accentuated in participants with elevated amyloid at enrollment (n = 70) where higher intake of the HGDiet pattern, sugar, and carbohydrate were related to more precuneal amyloid accumulation (β = 0.11, p = 0.01 for all measures). In individuals with elevated amyloid, higher intake of the HGDiet pattern was also related to more amyloid accumulation in the lateral temporal lobe (β = 0.09, p Conclusion: This longitudinal observational analysis suggests that a high glycemic diet relates to higher brain amyloid accumulation over 1 year in regions of the temporoparietal cortex in cognitively normal adults, particularly in those with elevated amyloid status. Further studies are required to assess whether there is causal link between a high glycemic diet and brain amyloid.Clinical Trial Registration:ClinicalTrials.gov, Identifier (NCT02000583).</p

    Regional blood flow pre- and post-exercise.

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    The figure shows relative cerebral blood flow in three regions of interest. Pre- and post-exercise time frames are equivalent, ~12 minutes of arterial spin labeling data collection. The hippocampus demonstrated an increase in post-exercise cerebral blood flow over pre-exercise in APOE4 carriers only (p = 0.05). The white bar is pre-exercise for APOE4 non-carriers. The light gray bar is post-exercise for APOE4 non-carriers. The dark graybar is pre-exercise for APOE4 carriers. The black bar is post-exercise for APOE4 carriers. Error bars are standard deviation. Cerebral blood flow is shown in percentage of the second PCASL acquisition before exercise. (TIF)</p

    Cerebral blood flow area under the curve does not differ after exercise based on APOE4 carriage.

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    Total cerebral blood flow following exercise is plotted for both the primary region of interest, cortical gray matter, and the cerebellar gray matter reference region. Black bars denote APOE4 carriers. Gray bars denote APOE4 non-carriers. Error bars are standard deviation.</p
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