ArticleAnnals of neurology2014
Modulation of amyloid precursor protein expression reduces β-amyloid deposition in a mouse model.
Article in Annals of neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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21 citing papers in PubMed, 28 citations in OpenAlex.
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- The amyloid precursor protein: a converging point in Alzheimer's disease.Molecular neurobiology · 2022Review
- Article
- Apolipoprotein E4 Effects a Distinct Transcriptomic Profile and Dendritic Arbor Characteristics in Hippocampal Neurons CulturedFrontiers in aging neuroscience · 2022Article
- Peroxiredoxin 6 mediates protective function of astrocytes in Aβ proteostasis.Molecular neurodegeneration · 2020Article
- Passive immunotherapy for N-truncated tau ameliorates the cognitive deficits in two mouse Alzheimer's disease models.Brain communications · 2020Article
- Anti-prion Protein Antibody 6D11 Restores Cellular Proteostasis of Prion Protein Through Disrupting Recycling Propagation of PrPMolecular neurobiology · 2019Article
- Angelica tenuissima Nakai Ameliorates Cognitive Impairment and Promotes Neurogenesis in Mouse Model of Alzheimer's Disease.Chinese journal of integrative medicine · 2018Article
- Translational inhibition of APP by Posiphen: Efficacy, pharmacodynamics, and pharmacokinetics in the APP/PS1 mouse.Alzheimer's & dementia (New York, N. Y.) · 2018Article
- Neuroinflammatory Cytokines Induce Amyloid Beta Neurotoxicity through Modulating Amyloid Precursor Protein Levels/Metabolism.BioMed research international · 2018Review
- APOE Genotype Differentially Modulates Effects of Anti-Aβ, Passive Immunization in APP Transgenic Mice.Molecular neurodegeneration · 2017Article
- Editorial: Translational Control of APP Expression for Alzheimer Disease Therapy.Annals of pharmacology and pharmaceutics · 2017Article
- Opposite Dysregulation of Fragile-X Mental Retardation Protein and Heteronuclear Ribonucleoprotein C Protein Associates with Enhanced APP Translation in Alzheimer Disease.Molecular neurobiology · 2016Article
- Effects of BACE1 haploinsufficiency on APP processing and Aβ concentrations in male and female 5XFAD Alzheimer mice at different disease stages.Neuroscience · 2015Article
- Beneficial effects of the β-secretase inhibitor GRL-8234 in 5XFAD Alzheimer's transgenic mice lessen during disease progression.Current Alzheimer research · 2015Article
- β-Amyloid peptides and amyloid plaques in Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015Review
- Reply: To PMID 24687915.Annals of neurology · 2014Article
- Amyloid-β precursor protein synthesis inhibitors for Alzheimer's disease treatment.Annals of neurology · 2014Article
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5 authors at 1 institution in 1 country.
Funding
Abstract
objectiveProteolytic cleavage of the amyloid precursor protein (APP) generates β-amyloid (Aβ) peptides. Prolonged accumulation of Aβ in the brain underlies the pathogenesis of Alzheimer disease (AD) and is regarded as a principal target for development of disease-modifying therapeutics.
methodsUsing Chinese hamster ovary (CHO) APP751SW cells, we identified and characterized effects of 2-([pyridine-2-ylmethyl]-amino)-phenol (2-PMAP) on APP steady-state level and Aβ production. Outcomes of 2-PMAP treatment on Aβ accumulation and associated memory deficit were studied in APPSW /PS1dE9 AD transgenic model mice.
resultsIn CHO APP751SW cells, 2-PMAP lowered the steady-state APP level and inhibited Aβx-40 and Aβx-42 production in a dose-response manner with a minimum effective concentration ≤ 0.5μM. The inhibitory effect of 2-PMAP on translational efficiency of APP mRNA into protein was directly confirmed using a 35S-methionine/cysteine metabolic labeling technique, whereas APP mRNA level remained unaltered. Administration of 2-PMAP to APPSW /PS1dE9 mice reduced brain levels of full-length APP and its C-terminal fragments and lowered levels of soluble Aβx-40 and Aβx-42 . Four-month chronic treatment of APPSW /PS1dE9 mice revealed no observable toxicity and improved animals' memory performance. 2-PMAP treatment also caused significant reduction in brain Aβ deposition determined by both unbiased quantification of Aβ plaque load and biochemical analysis of formic acid-extracted Aβx-40 and Aβx-42 levels and the level of oligomeric Aβ.
interpretationWe demonstrate the potential of modulating APP steady-state expression level as a safe and effective approach for reducing Aβ deposition in AD transgenic model mice.
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