ArticleFrontiers in neuroscience2026
Regional tau burden tracks with lower microglial HLA class II transcription in the human brain.
Article in Frontiers in 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: Human leukocyte antigen class II (HLA-II) genes mark several microglial states in Alzheimer's disease, but it remains unclear how their average transcription relates to tau measured in the same brain region. Methods: We used a locked 13-gene HLA-II panel selected by biological function, cross-cohort detection, and variance, without considering effect estimates. The primary analysis was conducted using the Seattle Alzheimer's Disease Brain Cell Atlas (SEA-AD): 361 donor-region observations from 79 donors across 6 cortical regions were modeled with within-donor pathology decomposition, region fixed effects, and a donor random intercept. A paired entorhinal-versus-somatosensory analysis in GSE160936 (11 donors) provided additional support for our findings. Sensitivity analyses addressed amyloid-β, RNA quality, neuronal-nuclei enrichment, microglial-state composition, published state annotations, alternative panels, region omission, and assay modality. Public human induced pluripotent stem cell (iPSC)-microglia data were used to provide a distinct tau-exposure context. Results: In the SEA-AD study, a higher local AT8-positive area within a donor was associated with a lower expanded HLA-II score ( Conclusion: In a larger multi-region cohort and a smaller paired cohort, we observed that regional tau burden was associated with lower levels of pooled microglial HLA-II transcription. The association was not explained solely by the measured proportion of the DAM-like state. However, the data do not establish tau specificity, direct suppression, protein-level antigen presentation, or a causal mechanism.
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