Neuroplastin 65 deficiency reduces amyloid plaque formation and cognitive deficits in an Alzheimer's disease mouse model.

ABSTRACT:

Introduction

Alzheimer's disease (AD) is characterized by increasing cognitive dysfunction, progressive cerebral amyloid beta (Aβ) deposition, and neurofibrillary tangle aggregation. However, the molecular mechanisms of AD pathologies have not been completely understood. As synaptic glycoprotein neuroplastin 65 (NP65) is related with synaptic plasticity and complex molecular events underlying learning and memory, we hypothesized that NP65 would be involved in cognitive dysfunction and Aβ plaque formation of AD. For this purpose, we examined the role of NP65 in the transgenic amyloid precursor protein (APP)/presenilin 1 (PS1) mouse model of AD.

Methods

Neuroplastin 65-knockout (NP65^-/-) mice crossed with APP/PS1 mice to get the NP65-deficient APP/PS1 mice. In the p

SUBMITTER: Wu DD 

PROVIDER: S-EPMC10196121 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature