Deletion of MyD88 in astrocytes prevents β-amyloid-induced neuropathology in mice.

ABSTRACT: As the understanding of immune responses in Alzheimer's disease (AD) is in its early phases, there remains an urgency to identify the cellular and molecular processes driving chronic inflammation. In AD, a subpopulation of astrocytes acquires a neurotoxic phenotype which prompts them to lose typical physiological features. While the underlying molecular mechanisms are still unknown, evidence suggests that myeloid differentiation primary response 88 (MyD88) adaptor protein may play a role in coordinating these cells' immune responses in AD. Herein, we combined studies in human postmortem samples with a conditional genetic knockout mouse model to investigate the link between MyD88 and astrocytes in AD. In silico analyses of bulk and cell-specific transcriptomic data from human postmortem bra

SUBMITTER: Jong Huat T 

PROVIDER: S-EPMC9970273 | biostudies-literature | 2023 Feb

REPOSITORIES: biostudies-literature