Fingolimod mitigates synaptic deficits and psychosis-like behavior in APP/PSEN1 mice.

ABSTRACT:

Introduction

Current treatments for psychosis in Alzheimer's disease (AD), a syndrome characterized by more rapid deterioration and reduced synaptic protein abundance relative to non-psychotic AD, are inadequate. Fingolimod, a currently US Food and Drug Administration (FDA)-approved pharmacotherapy for multiple sclerosis, alters synaptic protein expression and warrants preclinical appraisal as a candidate pharmacotherapy for psychosis in AD.

Methods

Presenilin and amyloid precursor protein transgenic mice (APPswe/PSEN1dE9) and wild-type mice were randomized to fingolimod or saline for 7 days. Psychosis-associated behaviors were quantified by open field testing, pre-pulse inhibition of the acoustic startle response testing, and habituation of the acoustic startle response tes

SUBMITTER: Krivinko JM 

PROVIDER: S-EPMC9395154 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature