ArticleBrain communications2026
Tau burden across Braak stages is associated with regionally specific amyloid accumulation.
Article in Brain communications, 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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10 authors.
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Abstract
Alzheimer's disease is defined by the abnormal accumulation of amyloid-β (Aβ) plaques and tau neurofibrillary tangles, the two hallmark proteinopathies detectable via molecular imaging. Aβ deposition typically begins in neocortical regions and is hypothesized to constitute a permissive condition for the subsequent spread of tau. Tau pathology is known to spread systematically through select brain regions, typically described as Braak stages (I-VI), reflecting the spatiotemporal trajectory of tau distribution with disease progression. Evaluating the associations between regional Aβ accumulation and the spatial distribution of tau remains an important question in understanding disease progression. This study examined the associations between regional Aβ and tau burden, measured by positron emission tomography (PET), in 192 participants without dementia (178 cognitively unimpaired, 14 with mild cognitive impairment [MCI],) in the Biomarkers of Cognitive Decline Among Normal Individuals (BIOCARD) cohort (age range: 32-88 years; mean age: 68 years; 58% female), of whom 52 were Aβ positive. Aβ burden was assessed using standardized uptake value ratios (SUVR) obtained from several cortical areas [the medial orbitofrontal cortex (OFC), lateral OFC, precuneus, posterior cingulate, anterior cingulate, parietal, temporal, and superior frontal regions], using 11C-PIB PET. Tau burden was quantified using 18F-MK6240 PET, within regions of interest defined as Braak stages I-VI. Elastic net regression was employed to delineate the association of regional Aβ burden and tau PET accumulation across Braak stages, covarying for age, sex, education, and apolipoprotein E (
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