ArticleJournal of translational medicine2026
Targeting the astrocyte-microglia EFEMP1-GALNT10 axis: a spatially programmable therapeutic strategy for hippocampal vulnerability in Alzheimer's disease.
Article in Journal of translational medicine, 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
backgroundThe hippocampus is selectively vulnerable to Alzheimer’s disease (AD), but the spatially resolved, cell-type-specific drivers of this susceptibility remain unknown, hindering the development of targeted therapies.
methodsWe employed an integrated causal-spatial approach, combining single-nucleus RNA sequencing (snRNA-seq) from 53 post-mortem AD brains, multi-omics triangulation (Mendelian randomization and Bayesian colocalization), and cross-species spatial mapping in human cohorts and 5xFAD mice to identify drivers of hippocampal vulnerability.
resultsWe identified a novel astrocyte-microglia co-pathology axis centered on EFEMP1 and GALNT10. Causal inference prioritized this axis, supported by an EFEMP1 plasma protein quantitative trait locus (pQTL) with an exceptional effect size (OR = 7.96) and dual epigenetic-transcriptional regulation of microglial GALNT10. The axis demonstrated hippocampus-specific co-expression in humans (R = 0.81, p < 0.001), pathological amplification in 5xFAD mice (tM1 = 0.77 ± 0.04 vs. WT 0.69 ± 0.04, p < 0.001), and focal enrichment near Aβ plaques (EFEMP1: r = -0.79; GALNT10: r = -0.67, p < 0.001). Mechanistically, it forms a core interactome with EGFR and TIMP3, coupling extracellular matrix (ECM) dysregulation with neuroinflammation.
conclusionsOur study defines the EFEMP1-GALNT10 axis as a spatially coordinated driver of hippocampal vulnerability in AD. The integrated causal-spatial pipeline provides a generalizable framework for translating genetic associations into spatially resolved therapeutic targets.
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