ArticleInternational journal of clinical and experimental pathology2019
The expression of the nicotinic acetylcholine receptor α3 subunit in the brains of patients with Alzheimer's disease and its effects on α- and γ-secretases and Notch signal transduction in SH-SY5Y cells.
Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 2 citations in OpenAlex.
- α5-nAChR/ADAM10 signaling mediates nicotine-related cutaneous melanoma progression via STAT3 activation.Archives of dermatological research · 2024Article
- A novel Alzheimer's disease prognostic signature: identification and analysis of glutamine metabolism genes in immunogenicity and immunotherapy efficacy.Scientific reports · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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Abstract
objectiveThe aim of this study was to evaluate the correlation between the nicotinic acetylcholine receptor α3 subunit (α3nAChR) and β-amyloid (Aβ) in Alzheimer's disease (AD) patients' brains, α3nAChR on α and γ-secretases in amyloid precursor protein (APP) metabolism, and determine the possible correlation between α3nAChR and the Notch pathway.
methodsIn this study, the expression of α3nAChR and Aβ in Alzheimer's disease patients' and normal brains was determined by immunofluorescence, and human neuroblastoma SH-SY5Y cells were treated with α3nAChR siRNA or nicotine to investigate the effects of α3nAChR on the expression of ADAM10 (a component of α-secretase), presenilin 1 (PS1) and nicastrin (NCT) (γ-secretase components), and Notch1 and Hes1 (effectors in the Notch pathway) using quantitative real time PCR and immunoblot.
resultsThe expression of Aβ in AD patients' brains was high, but the distribution of α3nAChR in AD patients' brains was significantly lower than it was in the normal control group. The results revealed that α3nAChR silencing suppressed ADAM10, PS1, NCT, Notch1, and Hes1 expression in SH-SY5Y cells. Meanwhile, stimulation with nicotine resulted in increased expression levels of α3nAChR, ADAM10, PS1, NCT, Notch1 and Hes1.
conclusionThese results indicated that α3nAChR might work against the production of Aβ in the brains of Alzheimer's patients, and in the amyloidogenic cascade controlling APP metabolism, α3nAChR might enhance the secretion of α- and γ-secretases as well as Notch pathway activation, suggesting that α3nAChR potentially has a critical function in the non-amyloidogenic pathway of APP metabolism in Alzheimer's disease.
Indexed as
Identifiers
31934215PMC6949849W3011176344What OpenQuestion holds
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