ArticleThe American journal of pathology2011
Neprilysin-2 is an important β-amyloid degrading enzyme.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 73 citations in OpenAlex.
- Allele specific expression in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- The neuroprotective potential of diosgenin: an integrated in silico, in vitro, and in vivo approach in colchicine-induced Alzheimer's model.Journal of computer-aided molecular design · 2026Article
- Article
- Neprilysin 2 catalyses the degradation of natriuretic peptides despite sacubitrilat Inhibition.Scientific reports · 2025Article
- Impact of Atrazine on Sucrose Sensitivity in Honey Bees.Insects · 2025Article
- Divergent actions of physiological and pathological amyloid-β on synapses in live human brain slice cultures.Nature communications · 2025Article
- Multiple Roles of Apolipoprotein E4 in Oxidative Lipid Metabolism and Ferroptosis During the Pathogenesis of Alzheimer's Disease.Journal of molecular neuroscience : MN · 2024Review
- Neprilysin Inhibitors in Heart Failure: The Science, Mechanism of Action, Clinical Studies, and Unanswered Questions.JACC. Basic to translational science · 2023Review
- Blood-brain barrier penetrating neprilysin degrades monomeric amyloid-beta in a mouse model of Alzheimer's disease.Alzheimer's research & therapy · 2022Article
- Contribution of proteases to the hallmarks of aging and to age-related neurodegeneration.Aging cell · 2022Review
- Amyloid β (Aβ) ELISA of Human iPSC-Derived Neuronal Cultures.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Transcriptional Profiles of Diploid MutantInsects · 2021Article
- Enhanced neprilysin-mediated degradation of hippocampal Aβ42 with a somatostatin peptide that enters the brain.Theranostics · 2021Article
- Neprilysin expression and functions in development, ageing and disease.Mechanisms of ageing and development · 2020Review
- MCF7 Spheroid Development: New Insight about Spatio/Temporal Arrangements of TNTs, Amyloid Fibrils, Cell Connections, and Cellular Bridges.International journal of molecular sciences · 2020Article
- Powering Amyloid Beta Degrading Enzymes: A Possible Therapy for Alzheimer's Disease.Neurochemical research · 2019Review
- Intracellular metalloprotease activity controls intraneuronal Aβ aggregation and limits secretion of Aβ via exosomes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Functional Amyloids and their Possible Influence on Alzheimer Disease.Discoveries (Craiova, Romania) · 2017Review
- Amyloid beta: structure, biology and structure-based therapeutic development.Acta pharmacologica Sinica · 2017Review
- Long-term neprilysin inhibition - implications for ARNIs.Nature reviews. Cardiology · 2017Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proteases that degrade the amyloid-β peptide (Aβ) are important in protecting against Alzheimer's disease (AD), and understanding these proteases is critical to understanding AD pathology. Endopeptidases sensitive to inhibition by thiorphan and phosphoramidon are especially important, because these inhibitors induce dramatic Aβ accumulation (∼30- to 50-fold) and pathological deposition in rodents. The Aβ-degrading enzyme neprilysin (NEP) is the best known target of these inhibitors. However, genetic ablation of NEP results in only modest increases (∼1.5- to 2-fold) in Aβ, indicating that other thiorphan/phosphoramidon-sensitive endopeptidases are at work. Of particular interest is the NEP homolog neprilysin 2 (NEP2), which is thiorphan/phosphoramidon-sensitive and degrades Aβ. We investigated the role of NEP2 in Aβ degradation in vivo through the use of gene knockout and transgenic mice. Mice deficient for the NEP2 gene showed significant elevations in total Aβ species in the hippocampus and brainstem/diencephalon (∼1.5-fold). Increases in Aβ accumulation were more dramatic in NEP2 knockout mice crossbred with APP transgenic mice. In NEP/NEP2 double-knockout mice, Aβ levels were marginally increased (∼1.5- to 2-fold), compared with NEP(-/-)/NEP2(+/+) controls. Treatment of these double-knockout mice with phosphoramidon resulted in elevations of Aβ, suggesting that yet other NEP-like Aβ-degrading endopeptidases are contributing to Aβ catabolism.
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Registered trials
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 OpenQuestion graph.