Cell model containing human APP and PSEN1 genes and construction method thereof

Abstract

The invention provides a cell model containing human APP and PSEN1 genes and a construction method thereof. According to the cell model containing human APP and PSEN1 genes and the construction method thereof, lentivirus is selected to transfect cells, the human APP and PS1 are introduced into CHO cells, a stable passage cell line can be obtained, the lentivirus carries a green fluorescent protein gene, the cells can emit a green fluorescent signal under a fluorescence microscope, the identifiability of the cells is improved, so that the exogenous gene stability of the cells is judged. In addition, the cells carrying the human APP and PS1 genes can stably secrete A [beta] 1-42 and A [beta] 1-40. A cell screening model is formed by simulating pathogenesis characteristics of AD cells and is used for high-throughput screening of drugs capable of inhibiting secretion of the A beta 1-42 and the A beta 1-40.

Description

technical field [0001] The invention belongs to the technical field of drug screening models, and relates to a cell model containing human APP and PSEN1 genes and a construction method thereof. Background technique [0002] Alzheimer's disease (AD) is an age-related degenerative disease of the central nervous system and the most common cause of dementia. The pathogenesis of AD is very complex and has not yet been clarified. At present, there are mainly the following hypotheses: gene mutation hypothesis, β-amyloid deposition hypothesis, synaptic dysfunction hypothesis, hyperphosphorylation hypothesis of Tau protein, excitotoxic amino acid and immune inflammation hypothesis, etc., and the cascade of β-amyloid protein Hypothesis dominates. The increase of soluble β-amylase (Aβ) and the excessive deposition of Aβ are the main pathogenic factors of AD. The hypothesis holds that β-amyloid precursor protein (APP) is cleaved by β-secretase and γ-secretase into Aβ and released out...

AI Technical Summary

Problems solved by technology

The hypothesis holds that β-amyloid precursor protein (APP) is cleaved by β-secretase and γ-secretase into Aβ and released outside the cell, and accumulates outside the cell, ages to form senile plaques, and can cause a series of pathological symptoms of AD. These pathological processes in turn exacerbate the generation and deposition of β-amyloid, resulting in a cascade effect that leads to neurofibrillary tangles and loss of neurons

[0003] In the development of AD drugs, APP / PSEN1 transgenic mice are usually selected for drug efficacy analysis and mechanism research, but the cost of transgenic mice is relatively expensive, and it is not suitable for large-scale screening work

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