Bone marrow myelopoiesis dysfunction in Alzheimer's disease limits monocyte homing to the brain and drives disease progression.

Impaired bone marrow myelopoiesis driven by IFN-I response limits monocyte brain homing and accelerates Alzheimer's disease progression in mouse models and patients.

• Why it matters: Understanding systemic immune dysfunction in AD is crucial because it hampers the recruitment of protective monocytes to the brain, worsening disease outcomes.
• What they did: The study analyzed monocyte development in mouse models and patients, revealing that IFN-I signaling disrupts monocyte differentiation, and tested interventions like IFN-I blockade and bone marrow reconstitution.
• The result: Restoring normal myelopoiesis increased monocyte-derived macrophage homing to the brain, reduced pathology, and slowed disease progression, highlighting potential systemic therapeutic targets for AD.