ArticleNature communications2025
Single-nucleus and spatial transcriptomic profiling of human temporal cortex and white matter reveals key associations with AD pathology.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- A meta-refined human Alzheimer's disease-associated gene subset shows partial mouse-model pathway correspondence and limited cross-cohort machine-learning transportability.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Dual platform spatial transcriptomics reveals parvalbumin interneuron subtype vulnerability in mouse models of Alzheimer's disease.Nature communications · 2026Article
- Exploring human GABA transporter 3 binders for epilepsy through quantum reactivity analysis, molecular dynamics, machine learning prediction, and network pharmacology.Journal of molecular modeling · 2026Article
- Spatially resolved transcriptomic profiling identifies distinct signatures in parenchymal and vascular microenvironments in Alzheimer's Disease with Cerebral Amyloid Angiopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Spatial transcriptomics in Alzheimer's disease: technologies, challenges and discoveries.Molecular neurodegeneration advances · 2026Review
- Nutritional substrates and microglial metabolic fitness in brain aging and Alzheimer's disease: from lipid handling to TREM2-linked translation.Frontiers in nutrition · 2026Review
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Abstract
Alzheimer's disease, the leading cause of dementia in the elderly, is a neurodegenerative disorder that has been studied to uncover therapeutic pathways through its molecular and cellular hallmarks. Here, we present a comprehensive investigation of cellular heterogeneity from the temporal cortex region of 40 individuals, comprising healthy donors and individuals with differing AD pathology. Using single-nucleus transcriptomic analysis of 430,271 nuclei from both gray and white matter of these individuals, we identified cell type-specific subclusters in both neuronal and glial cell types with varying degrees of association with AD pathology. We extended this analysis by performing multiplexed in situ hybridization using the CARTANA platform, capturing 155 genes in 13 individuals with differing tau pathology. We not only replicated snRNA data key findings from our spatial data analysis but also identified a set of cell type-specific genes that show selective enrichment or depletion near pathological inclusions.
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