ArticleNature communications2024
Effects of SPI1-mediated transcriptome remodeling on Alzheimer's disease-related phenotypes in mouse models of Aβ amyloidosis.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A Multi-Ancestry GWAS Meta-Analysis Integrated with In-Depth Silico, Systems Biology, and Pharmacogenomics Approaches on Alzheimer's Disease Among 1,198,689 Subjects.Journal of molecular neuroscience : MN · 2025Pooled it
- Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Article
- Unique transcriptomic alterations in 5XFAD;PS19 mouse model identify glial lipid dysregulation and coordinated microglial-oligodendrocyte responses.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Development of a Novel AAV-Mediated microRNA Gene Therapy for Spatial Suppression of BACE1 to Improve Cognitive Function in Alzheimer's Disease Model Mice.Biomolecules · 2026Article
- Lymphoid-like Suppressive Microglia in Alzheimer's Disease: A New Neuroimmune Regulatory Axis?Cells · 2026Review
- Comprehensive analysis of interactions between brain aging and late-onset psychoses using heuristic mapping models.Communications medicine · 2026Article
- Single-nucleus analysis reveals human-specific oligodendrocyte polarization and conserved neuronal responses after severe traumatic brain injury.Nature communications · 2026Article
- Microfluidic low-input profiling reveals lncRNA roles in disease.bioRxiv : the preprint server for biology · 2026Article
- PU.1: the conductor of Alzheimer's symphony.Molecular neurodegeneration · 2026Article
- A common 19 bp APOE enhancer deletion is protective against Alzheimer's disease in African Americans.Nature communications · 2026Article
- Neurosenescence, inflammaging and neuroinflammation in neurodegenerative disorders.Frontiers in aging · 2026Review
- Single-nucleus multiomics reveals the disrupted regulatory programs in three brain regions of sporadic early-onset Alzheimer's disease.Science advances · 2025Article
- The complement cascade in Alzheimer's disease: modern implications of an ancient immune protagonist.Molecular neurodegeneration · 2025Review
- Deletion of neuronal Idol ameliorates Alzheimer's disease-related pathologies via APOE receptors.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Transcriptional Activation of theGenes · 2025Article
- Apolipoprotein ε4 exacerbates white matter impairment in a mouse model of Aβ amyloidosis by decreasing actively myelinating oligodendrocytes.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Integrative analysis reveals generalizable human neurodegenerative disease-associated glial states.bioRxiv : the preprint server for biology · 2025Article
- Article
- SPI1 activates mitochondrial unfolded response signaling to inhibit chondrocyte senescence and relieves osteoarthritis.Bone research · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
SPI1 was recently reported as a genetic risk factor for Alzheimer's disease (AD) in large-scale genome-wide association studies. However, it is unknown whether SPI1 should be downregulated or increased to have therapeutic benefits. To investigate the effect of modulating SPI1 levels on AD pathogenesis, we performed extensive biochemical, histological, and transcriptomic analyses using both Spi1-knockdown and Spi1-overexpression mouse models. Here, we show that the knockdown of Spi1 expression significantly exacerbates insoluble amyloid-β (Aβ) levels, amyloid plaque deposition, and gliosis. Conversely, overexpression of Spi1 significantly ameliorates these phenotypes and dystrophic neurites. Further mechanistic studies using targeted and single-cell transcriptomics approaches demonstrate that altered Spi1 expression modulates several pathways, such as immune response pathways and complement system. Our data suggest that transcriptional reprogramming by targeting transcription factors, like Spi1, might hold promise as a therapeutic strategy. This approach could potentially expand the current landscape of druggable targets for AD.
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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.