Modeling neurovascular dysfunction in Alzheimer's disease using an isogenic brain-chip model.

ABSTRACT:

Background

The pathology of Alzheimer's Disease (AD) is characterized by aggregates of amyloid beta (Aβ) peptides and neurofibrillary tau tangles. Increased blood-brain barrier (BBB) permeability and reduced Aβ clearance, which signal neurovascular dysfunction, have also been proposed as early markers of AD. Despite intense scrutiny, the mechanisms of AD remain elusive and novel treatments that address core symptoms of dementia are limited. New alternative methods (NAMs) aim to develop in-vitro translational models that recapitulate human pathology more accurately than previous models and could contribute to the development of new therapies.

Methods

Here, we developed a NAM model of the cortical neurovascular unit (NVU) using brain cells derived from human induced pluripoten

SUBMITTER: Shen AN 

PROVIDER: S-EPMC12777506 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature