Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
Association of type 2 diabetes treatment status with in vivo biomarkers of Alzheimer's disease.
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Akinci Muge, Aziz Froogh, Guzman Diana, Cheung Lina, Kong Jian X, Silver Stephanie, Eimicke Joseph, Teresi Jeanne A, Brickman Adam M, Lao Patrick, Luchsinger José A
Аннотация
INTRODUCTION: The association of type 2 diabetes (T2D) treatment with Alzheimer's disease (AD) is unclear. We examined T2D treatment status in relation to amyloid beta (Aβ) burden and AD-related downstream processes.
METHODS: This cross-sectional study included 546 cognitively unimpaired adults (mean age = 64.2 ± 3.2 years, 65% women), classified into normal glucose tolerance (NGT; hemoglobin A1c [HbA1c] < 5.7%), prediabetes/untreated T2D (HbA1c ≥ 5.7%), and treated T2D groups. Multiple regression analyses assessed group differences in Aβ (18F-florbetaben) and tau (18F-MK-6240) positron emission tomography burden, magnetic resonance imaging-based AD signature cortical thickness, white matter hyperintensity (WMH) volume, and memory performance.
RESULTS: Compared to the NGT group, prediabetes/untreated T2D had greater anterior/posterior cingulate and superior parietal cortex Aβ burden, whereas treated T2D had lower cortical thickness and greater WMHs, independent of demographics and apolipoprotein E ε4 status. No group differences were found in tau or memory outcomes.
DISCUSSION: Prediabetes/untreated T2D, but not treated T2D, was associated with early Aβ deposition. Diabetes medications may mitigate brain Aβ burden.
METHODS: This cross-sectional study included 546 cognitively unimpaired adults (mean age = 64.2 ± 3.2 years, 65% women), classified into normal glucose tolerance (NGT; hemoglobin A1c [HbA1c] < 5.7%), prediabetes/untreated T2D (HbA1c ≥ 5.7%), and treated T2D groups. Multiple regression analyses assessed group differences in Aβ (18F-florbetaben) and tau (18F-MK-6240) positron emission tomography burden, magnetic resonance imaging-based AD signature cortical thickness, white matter hyperintensity (WMH) volume, and memory performance.
RESULTS: Compared to the NGT group, prediabetes/untreated T2D had greater anterior/posterior cingulate and superior parietal cortex Aβ burden, whereas treated T2D had lower cortical thickness and greater WMHs, independent of demographics and apolipoprotein E ε4 status. No group differences were found in tau or memory outcomes.
DISCUSSION: Prediabetes/untreated T2D, but not treated T2D, was associated with early Aβ deposition. Diabetes medications may mitigate brain Aβ burden.