ArticleAge (Dordrecht, Netherlands)2009
Reduced neuronal co-localisation of nardilysin and the putative alpha-secretases ADAM10 and ADAM17 in Alzheimer's disease and Down syndrome brains.
Article in Age (Dordrecht, Netherlands), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 24 citations in OpenAlex.
- GGAs: Regulation of Multiple Sorting Pathways and Potential Association With Human Diseases.Journal of cellular and molecular medicine · 2026Review
- Selective reduction of ADAM10 in brain and cerebrospinal fluid of Alzheimer's disease patients.Alzheimer's research & therapy · 2026Article
- Review
- Regulation of Alpha-Secretase ADAM10Frontiers in molecular neuroscience · 2017Review
- Increased density of DISC1-immunoreactive oligodendroglial cells in fronto-parietal white matter of patients with paranoid schizophrenia.European archives of psychiatry and clinical neuroscience · 2016Article
- NGF controls APP cleavage by downregulating APP phosphorylation at Thr668: relevance for Alzheimer's disease.Aging cell · 2016Article
- Promoter Variants of the ADAM10 Gene and Their Roles in Temporal Lobe Epilepsy.Frontiers in neurology · 2016Article
- ADAM10 expression and promoter haplotype in Alzheimer's disease.Neurobiology of aging · 2012Article
- Chemokines, macrophage inflammatory protein-2 and stromal cell-derived factor-1α, suppress amyloid β-induced neurotoxicity.Toxicology and applied pharmacology · 2011Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The peptidase nardilysin is involved in degradation of neuropeptides and limited intracellular proteolysis. Recent reports point to an involvement of nardilysin in the pathophysiology of Alzheimer's disease. Nardilysin enhances the alpha-secretase activity of the disintegrin and metalloproteases (ADAMs) 10 and 17, thereby possibly contributing to reduced generation of amyloidogenic fragments from the amyloid precursor protein. A prerequisite for the alpha-secretase-stimulating effect of nardilysin on the activity of ADAMs in vivo is cellular co-expression of nardilysin with ADAM10 and/or ADAM17. We immunolocalised nardilysin, ADAM10, and ADAM17 in cortical regions of normal aged brain, in Alzheimer's disease, and in Down syndrome brains and counted the number of protease-expressing neurons. A considerable portion of neurons co-express nardilysin together with either ADAM10 or ADAM17. Compared to controls, in Alzheimer's disease and in Down syndrome brains there is a decreased cellular expression of all three antigens, and a reduction in the number of those neurons that co-express nardilysin with ADAM10 or with ADAM17. Our data are consistent with the notion that the proposed alpha-secretase-enhancing activity of nardilysin might play a role in human brain pathology.
Identifiers
What OpenQuestion holds
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.