Neuronal transcriptome, tau and synapse loss in Alzheimer's knock-in mice require prion protein.

ABSTRACT:

Background

Progression of Alzheimer's disease leads to synapse loss, neural network dysfunction and cognitive failure. Accumulation of protein aggregates and brain immune activation have triggering roles in synaptic failure but the neuronal mechanisms underlying synapse loss are unclear. On the neuronal surface, cellular prion protein (PrP^C) is known to be a high-affinity binding site for Amyloid-β oligomers (Aβo). However, PrP^C's dependence in knock-in AD models for tau accumulation, transcriptomic alterations and imaging biomarkers is unknown.

Methods

The necessity of PrP^C was examined as a function of age in homozygous App^NL-G-F/hMapt double knock-in mice (DKI). Phenotypes of App^NL-G-F/hMapt mice with a deletion of Pr

SUBMITTER: Stoner A 

PROVIDER: S-EPMC10647125 | biostudies-literature | 2023 Nov

REPOSITORIES: biostudies-literature