ArticleNature communications2025
Human and mouse proteomics reveals the shared pathways in Alzheimer's disease and delayed protein turnover in the amyloidome.
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 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mapping the effects of exercise on cognition and physical function: a scoping review of rodent studies.Frontiers in physiology · 2026Pooled it
- Alpha-synuclein structural variants driving tau pathology and disease interaction.Neural regeneration research · 2026Article
- 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
- Integrated multi-omics analysis identifies potential therapeutic targets for Alzheimer's disease.Neural regeneration research · 2026Article
- Targeting Mitochondrial Dysfunction in Microglia: A New Frontier for Treating Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- An AI-enabled structural atlas decodes kinase specificity across the human proteome.Nature biotechnology · 2026Article
- Astrocyte-driven small vessel disease is an early, amyloid-independent feature of PSEN1 E280A familial Alzheimer's disease.bioRxiv : the preprint server for biology · 2026Article
- Peripheral and Central miRNA Signatures in Alzheimer's Disease: Tissue-Specific Variability, Sex-Associated Differences, and Implications for Blood-Based Biomarkers.International journal of molecular sciences · 2026Review
- Deficient autophagy in retinal ganglion cells impairs the degradation of intracellular organelles, leading to neurodegeneration.Cell death & disease · 2026Article
- Article
- Longitudinal Proteomics Analysis of Cerebrospinal Fluid in Survivors of Childhood Acute Lymphoblastic Leukemia.Scientific data · 2026Article
- High-Fat Diet and a High Amyloid Load Interact to Induce PKC-α Dependent Synaptic Insulin Resistance.Molecular & cellular proteomics : MCP · 2026Article
- A Deep Quantitative Proteome Turnover Platform for Human iPSC-derived Neurons.bioRxiv : the preprint server for biology · 2026Article
- Dexter Energy Transfer Photocatalytic Microdissection of Amyloid Plaques in Alzheimer's Disease.JACS Au · 2026Article
- Decoding Alzheimer's Disease One Cell Class at a Time.Cellular and molecular neurobiology · 2026Review
- Single Plaque Proteomics Reveals the Composition and Dynamics of the Amyloid Microenvironment in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2026Article
- Cell type-resolved proteomics reveals intra- and intercellular signaling in Alzheimer's disease.bioRxiv : the preprint server for biology · 2026Article
- Homogentisic Acid Disrupts the Blood-Brain Barrier and Promotes Aβ Aggregation in Alzheimer's Disease.Current medical science · 2026Article
- Amyloid-ID: photocatalytic profiling of amyloid deposits in Alzheimer's disease tissue.Nature communications · 2026Article
- Neuroinflammatory stress preferentially impacts synaptic MAPK signaling and mitochondria in excitatory neurons.Molecular neurodegeneration advances · 2026Article
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32 authors.
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Abstract
Murine models of Alzheimer's disease (AD) are crucial for elucidating disease mechanisms but have limitations in fully representing AD molecular complexities. Here we present the comprehensive, age-dependent brain proteome and phosphoproteome across multiple mouse models of amyloidosis. We identified shared pathways by integrating with human metadata and prioritized components by multi-omics analysis. Collectively, two commonly used models (5xFAD and APP-KI) replicate 30% of the human protein alterations; additional genetic incorporation of tau and splicing pathologies increases this similarity to 42%. We dissected the proteome-transcriptome inconsistency in AD and 5xFAD mouse brains, revealing that inconsistent proteins are enriched within amyloid plaque microenvironment (amyloidome). Our analysis of the 5xFAD proteome turnover demonstrates that amyloid formation delays the degradation of amyloidome components, including Aβ-binding proteins and autophagy/lysosomal proteins. Our proteomic strategy defines shared AD pathways, identifies potential targets, and underscores that protein turnover contributes to proteome-transcriptome discrepancies during AD progression.
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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 Socratic graph.