CRISPR/Cas9-mediated CysLT1R deletion reverses synaptic failure, amyloidosis and cognitive impairment in APP/PS1 mice.

ABSTRACT: As a major pathological hallmark of Alzheimer's disease (AD), amyloid-β (Aβ) is regarded as a causative factor for cognitive impairment. Extensive studies have found Aβ induces a series of pathophysiological responses, finally leading to memory loss in AD. Our previous results demonstrated that cysteinyl leukotrienes receptor 1 (CysLT₁R) antagonists improved exogenous Aβ-induced memory impairment. But the role of CysLT₁R in AD and its underlying mechanisms still remain elusive. In this study, we investigated CysLT₁R levels in AD patients and APP/PS1 mice. We also generated APP/PS1-CysLT₁R^-/- mice by clustered regulatory interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9)-mediated CysLT₁R deletio

SUBMITTER: Chen F 

PROVIDER: S-EPMC7993729 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature