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• W2897637683 abstract "Loss of central cholinergic neurons and accumulation of amyloid plaques are pathogenic features of Alzheimer's disease (AD). Research has shown that α7-nicotinic acetylcholine receptors (α7-nAChR) mediate β-amyloid peptide (Aβ) internalization and contribute to neuronal death. The α7β2-nAChR, a recently-discovered nicotinic receptor subtype, is expressed in the septum and hippocampus of the brain regions of cell death early in AD. Studies have not yet focused on α7β2 nAChR mediated internalization of Aβ1-42. Based on previous research, α7β2 is suspected to have a higher affinity for Aβ. Our study focused on comparing α7β2- to α7-nAChR mediated internalization of Aβ. SH-EP1 human neuroepithelial cell lines stably expressing α7-nAChRs (Fig 1A) or α7β2-nAChRs (Fig 1B), and wild type cells were incubated with oligomeric Aβ1-42 or scrambled peptide (Fig 1C) followed by incubation with Amylo-Glo® dye (Biosensis). Fluorescence intensity was compared to determine relative amounts of Aβ internalization. Cell death assays were also performed. Receptor mediated internalization of Aβ1-42. SH-EP1 cells stably expressing a7-nAChRs or a7β2-nAChRs, and wild type cells were incubated with oligomeric Aβi-42, or scrambled peptide followed by incubation with Amylo-Glo® dye (Biosensis). Fluorescence intensity was used to compare relative amounts of Aβ1-42 internalization. (A) SH-EP1 cells expressing a7-nAChRs had markedly high levels of internalized Aβ1 -42 compared to the (B) same type of cells incubated with a scrambled peptide sequence Aβ1-42 (scrambled), which did not appear to have internalized the peptide. Cells expressing the a7-nAChRs (A) had a higher fluorescence intensity than cells expressing a7p2-nAChRs (C) when incubated with amyloid beta oligomers. These results suggest that a7-nAChRs have a higher internalization rate than a7β2-nAChRs. (Original grayscale images were pseudocolored to show details.) Cells expressing α7-nAChRs had more internalized Aβ versus cells with α7β2-nAChRs, but both were markedly higher than cells incubated with scrambled Aβ1-42 and wild type cells. Notably, cells expressing α7β2-nAChRs had a high rate of cell death. This suggests that internalization by α7β2-nAChRs could contribute to loss of function and cell death in AD. These results provide new insights into mechanisms of intracellular Aβ accumulation and cytotoxicity. The α7β2 receptor is expressed in the septum and hippocampus where cholinergic cell death is observed in AD pathology. Because Aβ aggregation is a hallmark of AD pathology that contributes to neurodegeneration, further understanding the role of nicotinic acetylcholine receptors, particularly α7β2-nAChR, on β-amyloid is crucial to working towards treatment options and preventative measures." @default.
• W2897637683 created "2018-10-26" @default.
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• W2897637683 date "2018-07-01" @default.
• W2897637683 modified "2023-10-16" @default.
• W2897637683 title "P4‐251: BETA AMYLOID OLIGOMER INTERNALIZATION VIA α7β2 NICOTINIC ACETYLCHOLINE RECEPTORS MAY CONTRIBUTE TO CHOLINERGIC CELL DEATH IN ALZHEIMER'S DISEASE" @default.
• W2897637683 doi "https://doi.org/10.1016/j.jalz.2018.07.073" @default.
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