ArticlePloS one2009
Improved learning and memory in aged mice deficient in amyloid beta-degrading neutral endopeptidase.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Secretory form of viral protease NIa ameliorates amyloid-β pathology and cognitive deficits in a mouse model of Alzheimer's disease.Frontiers in aging neuroscience · 2026Article
- A novel variant of biallelic MME gene associated with autosomal recessive late-onset distal hereditary motor neuropathy in Chinese families.BMC medical genomics · 2024Article
- Neprilysin inhibitors and risk of Alzheimer's disease: A future perspective.Journal of cellular and molecular medicine · 2024Review
- The Drosophila melanogaster Neprilysin Nepl15 is involved in lipid and carbohydrate storage.Scientific reports · 2021Article
- Neprilysin expression and functions in development, ageing and disease.Mechanisms of ageing and development · 2020Review
- Spatially-Resolved Top-down Proteomics Bridged to MALDI MS Imaging Reveals the Molecular Physiome of Brain Regions.Molecular & cellular proteomics : MCP · 2018Article
- Neprilysin Inhibitors and Bradykinin.Frontiers in medicine · 2018Review
- Long-term neprilysin inhibition - implications for ARNIs.Nature reviews. Cardiology · 2017Review
- Green tea reduces body fat via upregulation of neprilysin.International journal of obesity (2005) · 2016Article
- MME mutation in dominant spinocerebellar ataxia with neuropathy (SCA43).Neurology. Genetics · 2016Article
- Drosophila Neprilysins Are Involved in Middle-Term and Long-Term Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Mutations in MME cause an autosomal-recessive Charcot-Marie-Tooth disease type 2.Annals of neurology · 2016Article
- Identification and characterization of Aβ peptide interactors in Alzheimer's disease by structural approaches.Frontiers in aging neuroscience · 2014Article
- The role of neprilysin in regulating the hair cycle.PloS one · 2013Article
- Genetic deficiency in neprilysin or its pharmacological inhibition initiate excessive stress-induced alcohol consumption in mice.PloS one · 2012Article
- Cognitive and cortical plasticity deficits correlate with altered amyloid-β CSF levels in multiple sclerosis.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2011Article
- Neprilysin-2 is an important β-amyloid degrading enzyme.The American journal of pathology · 2011Article
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Corrections and comments
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Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeutral endopeptidase, also known as neprilysin and abbreviated NEP, is considered to be one of the key enzymes in initial human amyloid-beta (Abeta) degradation. The aim of our study was to explore the impact of NEP deficiency on the initial development of dementia-like symptoms in mice. METHODOLOGY/PRINCIPAL
findingsWe found that while endogenous Abeta concentrations were elevated in the brains of NEP-knockout mice at all investigated age groups, immunohistochemical analysis using monoclonal antibodies did not detect any Abeta deposits even in old NEP knockout mice. Surprisingly, tests of learning and memory revealed that the ability to learn was not reduced in old NEP-deficient mice but instead had significantly improved, and sustained learning and memory in the aged mice was congruent with improved long-term potentiation (LTP) in brain slices of the hippocampus and lateral amygdala. Our data suggests a beneficial effect of pharmacological inhibition of cerebral NEP on learning and memory in mice due to the accumulation of peptides other than Abeta degradable by NEP. By conducting degradation studies and peptide measurements in the brain of both genotypes, we identified two neuropeptide candidates, glucagon-like peptide 1 and galanin, as first potential candidates to be involved in the improved learning in aged NEP-deficient mice. CONCLUSIONS/SIGNIFICANCE: Thus, the existence of peptides targeted by NEP that improve learning and memory in older individuals may represent a promising avenue for the treatment of neurodegenerative diseases.
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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.