ArticleThe American journal of pathology2009
Endothelin-converting enzyme-2 is increased in Alzheimer's disease and up-regulated by Abeta.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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64 citing papers in PubMed, 100 citations in OpenAlex.
- Article
- Ciliary p75 neurotrophin receptor (p75NTR) facilitates the enrichment of exogenous amyloid beta (Aβ 1-42) peptide and promotes oxidative stress in human hippocampal astrocytes.BMC molecular and cell biology · 2026Article
- Oleic acid improves pathological changes in Aβ1-42-induced astrocytes and Alzheimer's disease mouse models through PKA/ACACB/CPT1A.Frontiers in neuroscience · 2026Article
- Single-Cell Multi-Modal Differential Analysis of the Human Neo-Cortex in HIV Infection Reveals Similarities with Hallmarks of Alzheimer's Disease.Research square · 2025Article
- The vascular contribution to cognitive decline in ageing and dementia.Nature reviews. Neuroscience · 2025Review
- Mechanistic Role of Astrocytic Rac1 Protein in Alzheimer's Disease.Aging and disease · 2025Review
- Clearing Amyloid-Beta by Astrocytes: The Role of Rho GTPases Signaling Pathways as Potential Therapeutic Targets.Brain sciences · 2024Review
- Plasma VEGFA and PGF impact longitudinal tau and cognition in preclinical Alzheimer's disease.Brain : a journal of neurology · 2024Article
- Article
- Advances in Amyloid-β Clearance in the Brain and Periphery: Implications for Neurodegenerative Diseases.Experimental neurobiology · 2023Review
- Astrocyte adaptation in Alzheimer's disease: a focus on astrocytic P2X7R.Essays in biochemistry · 2023Review
- Sovateltide Mediated Endothelin B Receptors Agonism and Curbing Neurological Disorders.International journal of molecular sciences · 2022Review
- Relationship between adult subventricular neurogenesis and Alzheimer's disease: Pathologic roles and therapeutic implications.Frontiers in aging neuroscience · 2022Review
- Microglia and Astrocytes in Alzheimer's Disease in the Context of the Aberrant Copper Homeostasis Hypothesis.Biomolecules · 2021Review
- Endothelin-1 axes in the framework of predictive, preventive and personalised (3P) medicine.The EPMA journal · 2021Review
- Endothelin ETInternational journal of molecular sciences · 2021Review
- Pericyte Contractile Responses to Endothelin-1 and Aβ Peptides: Assessment by Electrical Impedance Assay.Frontiers in cellular neuroscience · 2021Article
- Mind Over Matter: Confronting Challenges in Post-Mortem Brain Biobanking for Glioblastoma Multiforme.Biomarker insights · 2021Article
- Targeting Endothelin in Alzheimer's Disease: A Promising Therapeutic Approach.BioMed research international · 2021Review
- Engineering of fluorescent or photoactive Trojan probes for detection and eradication of β-Amyloids.Drug delivery · 2020Article
4 more citing papers are in PubMed but not listed here.
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4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is thought to be caused by the accumulation of amyloid beta (Abeta) peptide within the brain. Endothelin-converting enzyme-2 (ECE-2), which is expressed in neural tissues, cleaves 'big endothelin' to produce the vasoconstrictor endothelin-1. ECE-2 also degrades Abeta. We have examined ECE-2 expression in the temporal cortex of brain tissue from patients with AD, vascular dementia, and controls. Immunohistochemistry with specific antibodies showed ECE-2 to be abundant within pyramidal neurons in both the hippocampus and neocortex, but also to be present in certain astrocytes and microglia, particularly in AD brains. Quantitative real-time PCR showed ECE-2 mRNA to be markedly elevated in AD but not in vascular dementia. ECE-2 protein concentration, measured by sandwich enzyme-linked immunosorbent assay, was also significantly elevated in AD but not in vascular dementia. Exposure of SH-SY5Y human neuroblastoma cells to monomeric or oligomeric Abeta(1-42) caused an initial decrease in ECE-2 mRNA at 4 hours, but a marked increase by 24 hours. Our findings indicate that Abeta accumulation in AD is unlikely to be caused by ECE-2 deficiency. However, ECE-2 expression is up-regulated, perhaps to minimize Abeta accumulation, but this may also be a mechanism through which endothelin-1 production is increased and cerebral blood flow is reduced in AD. Our findings suggest that endothelin-1 receptor antagonists, already licensed for treating other diseases, could be of benefit in AD therapies.
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