Early immune cell response controlled by TREM2 reduces spread and harm of amyloid plaques

TREM2 deficiency leads to more diffuse and less dense Aβ plaques in a mouse model of Alzheimer's disease.

• TREM2 is a receptor on microglial cells that may influence responses to amyloid β accumulation in Alzheimer's disease.
• In murine models, TREM2 deficiency prevents microglial clustering around amyloid deposits.
• Amyloid-associated myeloid cells are derived from brain-resident microglia, not from peripheral blood monocytes.
• At the onset of Aβ-related pathology, Aβ accumulation was similar in TREM2-deficient and -sufficient 5XFAD mice.
• In the absence of TREM2, Aβ plaques were associated with significantly greater neuritic damage.

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