ArticleActa neuropathologica communications2017
Expression of endogenous mouse APP modulates β-amyloid deposition in hAPP-transgenic mice.
Article in Acta neuropathologica communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 36 citations in OpenAlex.
- The Uppsala APP Mutation Promotes Wild-Type Amyloid-β Aggregation and Deposition In Vivo.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Polarimetric analysis of the Alzheimer's pathology in excised mouse brain tissue.Journal of biomedical optics · 2026Article
- The ABC transporter A7 modulates neuroinflammation via NLRP3 inflammasome in Alzheimer's disease mice.Alzheimer's research & therapy · 2025Article
- Ideal animal models according to multifaceted mechanisms and peculiarities in neurological disorders: present and challenges.Archives of pharmacal research · 2025Review
- Evaluating the inter-species transmission risk of amyloid beta peptide aggregates via ingestion.Alzheimer's research & therapy · 2024Article
- Physiological Roles of β-amyloid in Regulating Synaptic Function: Implications for AD Pathophysiology.Neuroscience bulletin · 2023Review
- Physiological expression of mutated TAU impaired astrocyte activity and exacerbates β-amyloid pathology in 5xFAD mice.Journal of neuroinflammation · 2023Article
- Therapeutic Candidates for Alzheimer's Disease: Saponins.International journal of molecular sciences · 2023Review
- Time- and Sex-Dependent Effects of Fingolimod Treatment in a Mouse Model of Alzheimer's Disease.Biomolecules · 2023Article
- A Novel Huntington's Disease Assessment Platform to Support Future Drug Discovery and Development.International journal of molecular sciences · 2022Article
- Isotope-labeled amyloid-β does not transmit to the brain in a prion-like manner after peripheral administration.EMBO reports · 2022Article
- Rodent Modeling of Alzheimer's Disease in Down Syndrome:Frontiers in neuroscience · 2022Review
- Machine Learning-Supported Analyses Improve Quantitative Histological Assessments of Amyloid-β Deposits and Activated Microglia.Journal of Alzheimer's disease : JAD · 2021Article
- Neural Derivates of Canine Induced Pluripotent Stem Cells-Like Cells From a Mild Cognitive Impairment Dog.Frontiers in veterinary science · 2021Article
- Evaluating β-amyloidosis progression in Alzheimer's disease with Mueller polarimetry.Biomedical optics express · 2020Article
- Aβ Plaques.Free neuropathology · 2020Article
- Article
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Authors and funding
10 authors at 8 institutions in 4 countries.
Funding
Abstract
Amyloid-β (Aβ) deposition is one of the hallmarks of the amyloid hypothesis in Alzheimer's disease (AD). Mouse models using APP-transgene overexpression to generate amyloid plaques have shown to model only certain parts of the disease. The extent to which the data from mice can be transferred to man remains controversial. Several studies have shown convincing treatment results in reducing Aβ and enhancing cognition in mice but failed totally in human. One model-dependent factor has so far been almost completely neglected: the endogenous expression of mouse APP and its effects on the transgenic models and the readout for therapeutic approaches.Here, we report that hAPP-transgenic models of amyloidosis devoid of endogenous mouse APP expression (mAPP-knockout / mAPPko) show increased amounts and higher speed of Aβ deposition than controls with mAPP. The number of senile plaques and the level of aggregated hAβ were elevated in mAPPko mice, while the deposition in cortical blood vessels was delayed, indicating an alteration in the general aggregation propensity of hAβ together with endogenous mAβ. Furthermore, the cellular response to Aβ deposition was modulated: mAPPko mice developed a pronounced and age-dependent astrogliosis, while microglial association to amyloid plaques was diminished. The expression of human and murine aggregation-prone proteins with differing amino acid sequences within the same mouse model might not only alter the extent of deposition but also modulate the route of pathogenesis, and thus, decisively influence the study outcome, especially in translational research.
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