CRISPR/Cas9-mediated knock-in cells of the late-onset Alzheimer's disease-risk variant, SHARPIN G186R, reveal reduced NF-κB pathway and accelerated Aβ secretion.
Yuya AsanomiTetsuaki KimuraNobuyoshi ShimodaDaichi ShigemizuShumpei NiidaKouichi OzakiPublished in: Journal of human genetics (2024)
Keyphrases
- late onset
- crispr cas
- early onset
- induced apoptosis
- genome editing
- signaling pathway
- cell cycle arrest
- pi k akt
- oxidative stress
- cognitive decline
- lps induced
- genome wide
- cell death
- endoplasmic reticulum stress
- nuclear factor
- single cell
- gene expression
- immune response
- dna methylation
- toll like receptor
- mild cognitive impairment