ArticleMolecular neurobiology2017
Endogenous Apolipoprotein E (ApoE) Fragmentation Is Linked to Amyloid Pathology in Transgenic Mouse Models of Alzheimer's Disease.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Should ApoE4 gene editing therapy be approached with caution when AD is accompanied by retinal neurodegenerative diseases?Frontiers in neurology · 2026Review
- Retinoic acid-related orphan receptor alpha (RORα) as a candidate multi-pathway target in Alzheimer's disease: mechanisms and therapeutic prospects.Frontiers in neuroscience · 2026Review
- Proteome-Based Biomarkers for Alzheimer's Disease: Old Acquisitions and Innovative Proposals.International journal of molecular sciences · 2025Review
- Recent Insights on the Role of Nuclear Receptors in Alzheimer's Disease: Mechanisms and Therapeutic Application.International journal of molecular sciences · 2025Review
- Multiple Roles of Apolipoprotein E4 in Oxidative Lipid Metabolism and Ferroptosis During the Pathogenesis of Alzheimer's Disease.Journal of molecular neuroscience : MN · 2024Review
- Nociceptor activity induces nonionotropic NMDA receptor signaling to enable spinal reconsolidation and reverse pathological pain.Science advances · 2023Article
- Apoe4 and Alzheimer's Disease Pathogenesis-Mitochondrial Deregulation and Targeted Therapeutic Strategies.International journal of molecular sciences · 2023Review
- Temporal Pattern of Neuroinflammation Associated with a Low Glycemic Index Diet in the 5xFAD Mouse Model of Alzheimer's Disease.Molecular neurobiology · 2022Article
- Stress-inducible phosphoprotein 1 (HOP/STI1/STIP1) regulates the accumulation and toxicity of α-synuclein in vivo.Acta neuropathologica · 2022Article
- Are apolipoprotein E fragments a promising new therapeutic target for Alzheimer's disease?Therapeutic advances in chronic disease · 2022Review
- Phagocytosis of Apoptotic Cells Is Specifically Upregulated in ApoE4 Expressing MicrogliaFrontiers in cellular neuroscience · 2019Article
- Apolipoprotein E Deficiency Exacerbates Spinal Cord Injury in Mice: Inflammatory Response and Oxidative Stress Mediated by NF-κB Signaling Pathway.Frontiers in cellular neuroscience · 2018Article
- EFAD transgenic mice as a humanJournal of lipid research · 2017Review
- Article
- Extraction of Soluble and Insoluble Protein Fractions from Mouse Brains and Spinal Cords.Bio-protocol · 2017Article
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Authors and funding
2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The epsilon 4 allele of the apolipoprotein E (ApoE4) gene is the most important risk factor implicated in Alzheimer's disease (AD) etiology. ApoE4 is more susceptible to proteolysis, and ApoE fragments have been shown to promote tau hyperphosphorylation and exert neurotoxic properties. While a plethora of studies deals with the effect of ApoE and its fragments on amyloid-β peptide (Aβ) deposition and clearance, it is largely unknown whether Aβ in turn influences human or murine ApoE expression and its proteolysis. The present study is the first to show that endogenous murine ApoE becomes proteolytically processed in a way reminiscent of human ApoE fragmentation in different AD mouse models, including APP/PS1KI or 5XFAD. Murine ApoE fragments were demonstrated to accumulate mainly in synaptic fractions in AD mouse models. In vitro experiments, as well as analysis of mouse models at different time points, suggest that the amount of total ApoE is associated with extracellular Aβ while the amount of its fragments is linked to intracellular Aβ levels. Murine ApoE fragmentation is a common feature in different AD transgenic mouse models and could be directly associated with intraneuronal Aβ accumulation. Extracellular amyloid induces an elevation in full-length ApoE expression, which might present a protective mechanism toward Aβ clearance. The demonstrated fragments of murine ApoE in vitro and in vivo might therefore play a crucial role in the progression of AD pathology in murine AD models.
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