ArticleCurrent Alzheimer research2017
Apolipoprotein E-mediated Modulation of ADAM10 in Alzheimer's Disease.
Article in Current Alzheimer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Effects of Molecular Hydrogen Assessed by an Animal Model and a Randomized Clinical Study on Mild Cognitive Impairment.Current Alzheimer research · 2018Trial
- Selective reduction of ADAM10 in brain and cerebrospinal fluid of Alzheimer's disease patients.Alzheimer's research & therapy · 2026Article
- Serum Thioredoxin-80 is associated with age, ApoE4, and neuropathological biomarkers in Alzheimer's disease: a potential early sign of AD.Alzheimer's research & therapy · 2022Article
- Reduced TREM2 activation in microglia of patients with Alzheimer's disease.FEBS open bio · 2021Article
- Frontal cortex and striatal cellular and molecular pathobiology in individuals with Down syndrome with and without dementia.Acta neuropathologica · 2019Article
- Alpha-Secretase ADAM10 Regulation: Insights into Alzheimer's Disease Treatment.Pharmaceuticals (Basel, Switzerland) · 2018Review
- MicroRNA-455-3p as a Potential Biomarker for Alzheimer's Disease: An Update.Frontiers in aging neuroscience · 2018Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundThe APOE4 allele is the strongest genetic risk factor for Alzheimer's disease (AD). It has been associated with an accumulation of amyloid-β (Aβ) in the brain, which is produced through the sequential cleavage of the amyloid-β precursor protein (AβPP) by β - and γ-secretases. Alternatively, AβPP is also cleaved by α -secretases such as A Disintegrin and Metalloproteinase Domain-containing Protein 10 (ADAM10).
objectiveWhile several studies have investigated the impact of apoE on β- and γ-secretase, interactions between apoE and α-secretases have not been fully examined. We investigated the effect of each apoE isoform on ADAM10 in vitro and in human cortex samples.
methodADAM10 activity and kinetics was assessed in cell-free assays and the biological activity of ADAM10 further investigated in 7WCHO cells over-expressing wild type AβPP through ELISA. Finally, ADAM10 expression and activity was observed in the soluble fraction of both control and Alzheimer's Disease human cortex samples through ELISA.
resultsIn a cell free assay, ADAM10 activity was found to be significantly lower in apoE4 samples compared to apoE2. 7WCHO cells over expressing wild type AβPP exposed to apoE4 demonstrated reduced formation of sAβPPα compared to other apoE isoforms. We also identified APOE and AD dependent changes in ADAM10 activity and expression in the soluble brain fraction of human brain cortex.
conclusionOverall, our data demonstrates an apoE isoform-dependent effect on ADAM10 function and AβPP processing which may describe the elevated amyloid levels in the brains of AD subjects carrying the APOE4 allele.
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