ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2024
Distinct transcriptomic responses to Aβ plaques, neurofibrillary tangles, and APOE in Alzheimer's disease.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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26 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
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- Design, synthesis and pharmacological evaluation of coumarin tethered 1,3,4-oxadiazole conjugates as dual binding site acetylcholinesterase ligands targeting Alzheimer's disease.Molecular diversity · 2026Article
- Human microglial transitions at the Aβ-tau inflection point associate with divergent pathways to dementia and resilience.Nature medicine · 2026Article
- A critical appraisal of the link between apolipoprotein E and Tau.Current opinion in neurology · 2026Review
- Immune involvement in neuropsychiatric disorders: Insights from single-cell transcriptomic studies.Psychiatry and clinical neurosciences · 2026Review
- Histone demethylase PHF2 regulates inflammatory genes in Alzheimer's disease.Molecular psychiatry · 2026Article
- The quantified immune-aging dysregulation index: a large-language model-powered method for annotating and quantifying systems-level dysregulation.Frontiers in artificial intelligence · 2026Article
- Brain multiomic profiling identifies tau-related transcriptomic dysregulation in Alzheimer's disease.Brain communications · 2026Article
- Increased levels of GFAP and purinergic P2X7 receptor in Alzheimer's disease brain are associated with Aβ, tau pathologies and synaptic loss.Alzheimer's research & therapy · 2025Article
- sc4D: spatio-temporal single-cell transcriptomics analysis through embedded optimal transport identifies joint glial response to Alzheimer's disease pathology.bioRxiv : the preprint server for biology · 2025Article
- Amyloid-β, Tau, and α-Synuclein Protein Interactomes as Therapeutic Targets in Neurodegenerative Diseases.Cellular and molecular neurobiology · 2025Article
- ZipAEr: A compressive convolutional autoencoder for high-dimensional spatial omics data at subcellular resolution.Research square · 2025Article
- Artificial intelligence-driven multi-omics approaches in Alzheimer's disease: Progress, challenges, and future directions.Acta pharmaceutica Sinica. B · 2025Review
- Distinct inflammatory profiles in young-onset versus late-onset Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Spatial transcriptomics reveals an unexpected impact of tau and tau pathology on the expression of transthyretin.Frontiers in aging neuroscience · 2025Article
- Synaptic and extrasynaptic distribution of NMDA receptors in the cortex of Alzheimer's disease patients.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Systematic review and meta-analysis of bulk RNAseq studies in human Alzheimer's disease brain tissue.bioRxiv : the preprint server for biology · 2024Article
- TGF-β Signaling in Microglia: A Key Regulator of Development, Homeostasis and Reactivity.Biomedicines · 2024Review
- NMDARs in Alzheimer's Disease: Between Synaptic and Extrasynaptic Membranes.International journal of molecular sciences · 2024Review
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13 authors at 5 institutions in 2 countries.
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Abstract
introductionOmics studies have revealed that various brain cell types undergo profound molecular changes in Alzheimer's disease (AD) but the spatial relationships with plaques and tangles and APOE-linked differences remain unclear.
methodsWe performed laser capture microdissection of amyloid beta (Aβ) plaques, the 50 μm halo around them, tangles with the 50 μm halo around them, and areas distant (> 50 μm) from plaques and tangles in the temporal cortex of AD and control donors, followed by RNA-sequencing.
resultsAβ plaques exhibited upregulated microglial (neuroinflammation/phagocytosis) and downregulated neuronal (neurotransmission/energy metabolism) genes, whereas tangles had mostly downregulated neuronal genes. Aβ plaques had more differentially expressed genes than tangles. We identified a gradient Aβ plaque > peri-plaque > tangle > distant for these changes. AD APOE ε4 homozygotes had greater changes than APOE ε3 across locations, especially within Aβ plaques. DISCUSSION: Transcriptomic changes in AD consist primarily of neuroinflammation and neuronal dysfunction, are spatially associated mainly with Aβ plaques, and are exacerbated by the APOE ε4 allele.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.