ArticleMolecular neurodegeneration2014
Temporal gene profiling of the 5XFAD transgenic mouse model highlights the importance of microglial activation in Alzheimer's disease.
Article in Molecular neurodegeneration, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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97 citing papers in PubMed, 181 citations in OpenAlex.
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- Bridging autophagy and endolysosomal dysfunction: Role of bridging integrator 1 in Alzheimer's disease.Neural regeneration research · 2026Article
- Facilitation of hippocampal long-term potentiation by astrocytic Gq signaling is compromised in an advanced Alzheimer's disease model.Scientific reports · 2026Article
- Illuminating proinflammatory myeloid cells with PET tracers targeting GPR84.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- FOXO transcription factors in Alzheimer's Disease: balancing neuroprotection and neuronal degeneration.Molecular biology reports · 2026Review
- Native PLGA nanoparticles attenuate disease pathology via multiple pathways in 5xFAD Alzheimer's model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- PLGA Nanoparticle-based Anti-TLR2 scFv Gene Delivery for the Treatment of Alzheimer's Disease.Experimental neurobiology · 2026Article
- Reference gene variability across age and sex in 5XFAD mice highlights normalization challenges in Alzheimer's models.Scientific reports · 2026Article
- Sex-dependent effects of ultra-low-dose-THC preventive treatment on neuroinflammation and cognitive decline in 5xFAD mice.Biology of sex differences · 2026Article
- Natural microbial enrichment modulates microglial states and transcriptional programs relevant to Alzheimer's disease.Frontiers in immunology · 2026Article
- Super-Resolved Spatial Transcriptomics Reveals Early Changes in RNA Localization in the 5xFAD Hippocampus.bioRxiv : the preprint server for biology · 2025Article
- Amyloid-β plaque-associated microglia drive TSPO upregulation in Alzheimer's disease.Acta neuropathologica · 2025Article
- Exploring the co-morbid relationship between Alzheimer's disease and lung cancer in the 5xFAD transgenic mouse model.Animal models and experimental medicine · 2025Article
- In-Depth Cell-Type-Specific Proteome Landscape of the Brain from Human Amyloid-β Overexpression Mouse Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Human and mouse proteomics reveals the shared pathways in Alzheimer's disease and delayed protein turnover in the amyloidome.Nature communications · 2025Article
- Co-regulation of microglial subgroups in Alzheimer's amyloid pathology: Implications for diagnosis and drug development.PloS one · 2025Article
- Maresin-like 1 Ameliorates Neuropathology of Alzheimer's Disease in Brains of a Transgenic Mouse Model.Biomedicines · 2024Article
- Human-mouse proteomics reveals the shared pathways in Alzheimer's disease and delayed protein turnover in the amyloidome.bioRxiv : the preprint server for biology · 2024Article
- Spatiotemporal Dysregulation of Neuron-Glia Related Genes and Pro-/Anti-Inflammatory miRNAs in theInternational journal of molecular sciences · 2024Article
37 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe 5XFAD early onset mouse model of Alzheimer's disease (AD) is gaining momentum. Behavioral, electrophysiological and anatomical studies have identified age-dependent alterations that can be reminiscent of human AD. However, transcriptional changes during disease progression have not yet been investigated. To this end, we carried out a transcriptomic analysis on RNAs from the neocortex and the hippocampus of 5XFAD female mice at the ages of one, four, six and nine months (M1, M4, M6, M9).
resultsOur results show a clear shift in gene expression patterns between M1 and M4. At M1, 5XFAD animals exhibit region-specific variations in gene expression patterns whereas M4 to M9 mice share a larger proportion of differentially expressed genes (DEGs) that are common to both regions. Analysis of DEGs from M4 to M9 underlines the predominance of inflammatory and immune processes in this AD mouse model. The rise in inflammation, sustained by the overexpression of genes from the complement and integrin families, is accompanied by an increased expression of transcripts involved in the NADPH oxidase complex, phagocytic processes and IFN-γ related pathways.
conclusionsOverall, our data suggest that, from M4 to M9, sustained microglial activation becomes the predominant feature and point out that both detrimental and neuroprotective mechanisms appear to be at play in this model. Furthermore, our study identifies a number of genes already known to be altered in human AD, thus confirming the use of the 5XFAD strain as a valid model for understanding AD pathogenesis and for screening potential therapeutic molecules.
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