ArticleFrontiers in aging neuroscience2026
Multimodal neuroimaging and electrophysiological signatures in amnestic mild cognitive impairment with different amyloid-β deposition status: correlations with cognitive function and diagnostic value.
Article in Frontiers in aging neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Amnestic mild cognitive impairment (aMCI) is a heterogeneous transitional cognitive state between normal aging and dementia. Aβ positivity elevates dementia conversion risk but does not equate to prodromal Alzheimer's disease (AD), and not all Aβ-positive aMCI individuals progress to clinical AD dementia. Distinguishing Aβ-positive from Aβ-negative aMCI facilitates pathological subtyping rather than definitive early AD diagnosis. This cross-sectional study aimed to characterize scalp-level resting-state EEG and structural MRI signatures specific to Aβ-positive aMCI, explore their covariate-adjusted correlations with cognitive performance and regional Aβ burden, and develop an internally validated multimodal auxiliary classification model for Aβ stratification. Methods: Fifty enrolled aMCI participants (30 Aβ-positive, 20 Aβ-negative) and 35 cognitively normal controls (NC) completed unified 20-min eyes-closed resting-state scalp EEG, 3.0 T structural MRI, Results: (1) Relative to Aβ-negative aMCI and NC groups, the Aβ-positive subgroup presented significantly elevated whole-scalp θ relative power and scalp θ/α ratio, decreased scalp α and β relative power (all Conclusion: The temporal scalp θ/α ratio and right precuneus gray matter volume are promising candidate non-invasive auxiliary biomarkers for Aβ pathological stratification in aMCI, rather than validated clinical diagnostic biomarkers. The multimodal model provides supplementary subtyping value within this single-center cohort, while external multicenter validation is mandatory before clinical application. This cross-sectional dataset cannot support prediction of longitudinal progression to AD dementia.
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