ArticleNeurobiology of aging2016
Major amyloid-β-degrading enzymes, endothelin-converting enzyme-2 and neprilysin, are expressed by distinct populations of GABAergic interneurons in hippocampus and neocortex.
Article in Neurobiology of aging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 39 citations in OpenAlex.
- Clearing Amyloid-Beta by Astrocytes: The Role of Rho GTPases Signaling Pathways as Potential Therapeutic Targets.Brain sciences · 2024Review
- Nascent Aβ42 Fibrillization in Synaptic Endosomes Precedes Plaque Formation in a Mouse Model of Alzheimer's-like β-Amyloidosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Pathogenesis of Chronic Kidney Disease Is Closely Bound up with Alzheimer's Disease, Especially via the Renin-Angiotensin System.Journal of clinical medicine · 2023Review
- Local and long-range GABAergic circuits in hippocampal area CA1 and their link to Alzheimer's disease.Frontiers in neural circuits · 2023Review
- Intraneuronal accumulation of amyloid-β peptides as the pathomechanism linking autism and its co-morbidities: epilepsy and self-injurious behavior - the hypothesis.Frontiers in molecular neuroscience · 2023Article
- Targeting Endothelin in Alzheimer's Disease: A Promising Therapeutic Approach.BioMed research international · 2021Review
- Article
- Neprilysin expression and functions in development, ageing and disease.Mechanisms of ageing and development · 2020Review
- Dysregulation of Endothelin-1: Implications for Health Disparities in Alzheimer's Disease.Journal of personalized medicine · 2020Review
- Differential DNA methylation following chemotherapy for breast cancer is associated with lack of memory improvement at one year.Epigenetics · 2020Article
- Enhanced accumulation of N-terminally truncated Aβ with and without pyroglutamate-11 modification in parvalbumin-expressing GABAergic neurons in idiopathic and dup15q11.2-q13 autism.Acta neuropathologica communications · 2020Article
- Identification of Alzheimer's disease-associated rare coding variants in the ECE2 gene.JCI insight · 2020Article
- Article
- Targeting amyloid clearance in Alzheimer's disease as a therapeutic strategy.British journal of pharmacology · 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
- Family C G-Protein-Coupled Receptors in Alzheimer's Disease and Therapeutic Implications.Frontiers in pharmacology · 2019Review
- Modulation of SPARC/Hevin Proteins in Alzheimer's Disease Brain Injury.Journal of Alzheimer's disease : JAD · 2019Article
- 5-HIAA induces neprilysin to ameliorate pathophysiology and symptoms in a mouse model for Alzheimer's disease.Acta neuropathologica communications · 2018Article
- Asiaticoside Attenuates Cell Growth Inhibition and Apoptosis Induced by AβFrontiers in pharmacology · 2018Article
- Mutation-induced loss of APP function causes GABAergic depletion in recessive familial Alzheimer's disease: analysis of Osaka mutation-knockin mice.Acta neuropathologica communications · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Impaired clearance of amyloid-β peptide (Aβ) has been postulated to significantly contribute to the amyloid accumulation typical of Alzheimer's disease. Among the enzymes known to degrade Aβ in vivo are endothelin-converting enzyme (ECE)-1, ECE-2, and neprilysin (NEP), and evidence suggests that they regulate independent pools of Aβ that may be functionally significant. To better understand the differential regulation of Aβ concentration by its physiological degrading enzymes, we characterized the cell and region-specific expression pattern of ECE-1, ECE-2, and NEP by in situ hybridization and immunohistochemistry in brain areas relevant to Alzheimer's disease. In contrast to the broader distribution of ECE-1, ECE-2 and NEP were found enriched in GABAergic neurons. ECE-2 was majorly expressed by somatostatin-expressing interneurons and was active in isolated synaptosomes. NEP messenger RNA was found mainly in parvalbumin-expressing interneurons, with NEP protein localized to perisomatic parvalbuminergic synapses. The identification of somatostatinergic and parvalbuminergic synapses as hubs for Aβ degradation is consistent with the possibility that Aβ may have a physiological function related to the regulation of inhibitory signaling.
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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.