Observational studyThe journal of prevention of Alzheimer's disease2026
Soluble and plaque amyloid associations with peripheral glucose dysregulation modulated by tau pathology in Alzheimer's disease.
Observational study in The journal of prevention of Alzheimer's disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Metabolic Dysfunction in Alzheimer's Disease: Brain Glucose Hypometabolism as an Early Precursor to Amyloid and Tau Pathology.Journal of clinical medicine · 2026Review
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlucose metabolic dysfunction in Alzheimer's disease (AD) has been reported to be associated with soluble amyloid-β oligomers (OAβ) and plaque amyloid. However, the potential modulatory role of tau pathology in these associations remains to be fully elucidated.
objectivesTo investigate whether tau pathology modifies the relationship between plasma OAβ burden, plaque amyloid, and systemic glucose metabolism in individuals across the AD spectrum.
designCross-sectional observational study.
settingMemory clinic-based cohort from a single tertiary academic medical center in Republic of Korea.
participantsA total of 113 older adults, including cognitively normal individuals, patients with mild cognitive impairment, and Aβ-PET-positive dementia patients. MEASUREMENTS: Plasma oligomeric Aβ (OAβ) levels were measured in blood samples using the Multimer Detection System, which quantifies oligomeric forms of Aβ in plasma. Aβ plaque deposition was assessed using [
resultsA significant interaction was identified between plasma OAβ levels and Braak stage III/IV, but not Braak I or V/VI, when referenced to Braak 0. Only at Braak 0, higher plasma OAβ levels were associated with higher HbA1c compared with Braak stage III/IV (β = -4.191, 95 % CI -7.714 to -0.669, p = 0.020). No significant interactions were observed for fasting glucose or for Aβ-PET SUVR. Sensitivity analyses adjusting for diabetes diagnosis and excluding dementia participants confirmed the robustness of these findings.
conclusionSoluble Aβ oligomers, rather than plaque amyloid, are selectively associated with systemic glucose dysregulation in the absence of overt tau pathology. Tau staging may be crucial for identifying AD subgroups vulnerable to metabolic dysfunction potentially associated with early Aβ toxicity.
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