β-amyloid protein induces mitophagy-dependent ferroptosis through the CD36/PINK/PARKIN pathway leading to blood-brain barrier destruction in Alzheimer's disease.

ABSTRACT:

Introduction

Blood-brain barrier (BBB) dysfunction may occur at the onset of Alzheimer's disease (AD). Pericytes are a vital part of the neurovascular unit and the BBB, acting as gatekeepers of the BBB. Amyloid β (Aβ) deposition and neurofibrillary tangles in the brain are the central pathological features of AD. CD36 promotes vascular amyloid deposition and leads to vascular brain damage, neurovascular dysfunction, and cognitive deficits. However, the molecular mechanism by which pericytes of the BBB are disrupted remains unclear.

Objectives

To investigate the effect of low-dose Aβ1-40 administration on pericyte outcome and the molecular mechanism of BBB injury.

Methods

We selected 6-month-old and 9-month-old APP/PS1 mice and wild-type (WT) mice of the same strain, a

SUBMITTER: Li J 

PROVIDER: S-EPMC9134700 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature