HIV-1 infection facilitates Alzheimer's disease pathology in humanized APP knock-in immunodeficient mice.

ABSTRACT:

Objectives

Amyloid-β (Aβ) plaque deposition in the brain is a principal pathological feature of both Alzheimer's disease (AD) and progressive human immunodeficiency virus type one (HIV-1) infection. Both enable Aβ assembly and Aβ protein aggregation. The potential link between HIV-1 and AD remains uncertain, supporting the need for a reliable animal model. HIV-1 is tropic and pathogenic for humans. It does not replicate in mice. The restricted species tropism has slowed progress in basic research activities. The current study seeks to correct animal model limitations.

Methods

We created an AD mouse to address the need to develop an small animal model that allows studies of viral infection by making a knock-in (KI) with the human amyloid precursor protein (APP)^KM670,671N

SUBMITTER: Bhattarai S 

PROVIDER: S-EPMC12041850 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature