| Experiment Id | GSE221712 | Name | Neuronal Transcriptome Disruption, Tau Accumulation and Synapse Loss in Alzheimer's Knock-in Mice Require Cellular Prion Protein |
| Experiment Type | RNA-Seq | Study Type | WT vs. Mutant |
| Source | GEO | Curation Date | 2023-08-28 |
| description | Cellular prion protein (PrPC) is a high-affinity cell-surface receptor for Amyloid-beta oligomers(ABetao). In certain overexpression models of Alzheimer's Disease (AD), pharmacology and genetics demonstrate its essential role for synaptic plasticity impairment, memory deficits and synapse loss. However, PrPC 's role in AD-related phenotypes with endogenous expression levels, its role in tau accumulation and its effect on imaging biomarkers are unknown. The necessity of PrPC for transcriptomic alterations driven by ABeta across cell types is unexplored. The role of PrPC was examined as a function of age in homozygous AppNL-G-F/hMapt double knock-in mice (DKI). Phenotypes of AppNL-G-F /hMapt mice with a deletion of Prnp expression (DKI; Prnp-/- ) were compared with DKI mice with intact Prnp, mice with a targeted deletion of Prnp (Prnp-/- ), and mice with intact Prnp (WT). Phenotypes examined included behavioral deficits, synapse loss by PET imaging, synapse loss by immunohistology, tau pathology, gliosis, inflammatory markers, and snRNA-seq transcriptomic profiling. |
