ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Neuropeptide Y fragments derived from neprilysin processing are neuroprotective in a transgenic model of Alzheimer's disease.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.
- Meta-analysis of synaptic pathology in Alzheimer's disease reveals selective molecular vesicular machinery vulnerability.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2016Pooled it
- Multi-omic derived cell-type specific Alzheimer disease polygenic risk scores.Neurobiology of aging · 2025Article
- Brain-Bone Axis in Physiological and Pathological Conditions.International journal of molecular sciences · 2025Review
- Restoring neuropetide Y levels in the hypothalamus ameliorates premature aging phenotype in mice.GeroScience · 2025Article
- Association of Alzheimer's Disease with Promoter Variations in NPY2R Gene.Reports of biochemistry & molecular biology · 2025Article
- Multi-omics landscape of childhood simple obesity: novel insights into pathogenesis and biomarkers discovery.Cell & bioscience · 2024Article
- The Role of Neuropeptide Y in the Pathogenesis of Alzheimer's Disease: Diagnostic Significance and Neuroprotective Functions.Neurology international · 2024Review
- ABCA7-dependent induction of neuropeptide Y is required for synaptic resilience in Alzheimer's disease through BDNF/NGFR signaling.Cell genomics · 2024Article
- Proteomic changes in the hippocampus of large mammals after total-body low dose radiation.PloS one · 2024Article
- Neprilysin Inhibitors in Heart Failure: The Science, Mechanism of Action, Clinical Studies, and Unanswered Questions.JACC. Basic to translational science · 2023Review
- Neuroprotective Effects of Neuropeptide Y against Neurodegenerative Disease.Current neuropharmacology · 2022Review
- Genome-wide transcriptomic changes reveal the genetic pathways involved in insect migration.Molecular ecology · 2022Article
- Sleep Disturbance and Alzheimer's Disease: The Glial Connection.Neurochemical research · 2022Review
- A nonsense mutation in MME gene associates with autosomal recessive late-onset Charcot-Marie-Tooth disease.Molecular genetics & genomic medicine · 2022Article
- Contribution of proteases to the hallmarks of aging and to age-related neurodegeneration.Aging cell · 2022Review
- Design and Experimental Evaluation of a Peptide Antagonist against Amyloid β(1-42) Interactions with Calmodulin and Calbindin-D28k.International journal of molecular sciences · 2022Article
- Regulation of neuropeptide Y in body microenvironments and its potential application in therapies: a review.Cell & bioscience · 2021Review
- Redox-Active Metal Ions and Amyloid-Degrading Enzymes in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Neuropathology of the Brainstem to Mechanistically Understand and to Treat Alzheimer's Disease.Journal of clinical medicine · 2021Review
- Neuropeptide Y Expression Defines a Novel Class of GABAergic Projection Neuron in the Inferior Colliculus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
The endopeptidase neprilysin (NEP) is a major amyloid-beta (Abeta) degrading enzyme and has been implicated in the pathogenesis of Alzheimer's disease. Because NEP cleaves substrates other than Abeta, we investigated the potential role of NEP-mediated processing of neuropeptides in the mechanisms of neuroprotection in vivo. Overexpression of NEP at low levels in transgenic (tg) mice affected primarily the levels of neuropeptide Y (NPY) compared with other neuropeptides. Ex vivo and in vivo studies in tg mice and in mice that received lentiviral vector injections showed that NEP cleaved NPY into C-terminal fragments (CTFs), whereas silencing NEP reduced NPY processing. Immunoblot and mass spectrometry analysis showed that NPY 21-36 and 31-36 were the most abundant fragments generated by NEP activity in vivo. Infusion of these NPY CTFs into the brains of APP (amyloid precursor protein) tg mice ameliorated the neurodegenerative pathology in this model. Moreover, the amidated NPY CTFs protected human neuronal cultures from the neurotoxic effects of Abeta. This study supports the possibility that the NPY CTFs generated during NEP-mediated proteolysis might exert neuroprotective effects in vivo. This function of NEP represents a unique example of a proteolytic enzyme with dual action, namely, degradation of Abeta as well as processing of NPY.
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