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Recently, two independent studies indicated a strong association between a rare rs75932628-T variant encoding non-functional R47H in the TREM2 gene and an increased risk for Alzheimer's disease (AD). TREM2 expressed on monocytes/macrophages, dendritic cells, osteoclasts, and microglia serves as a phagocytotic receptor. At present, the precise pathological role of TREM2-expressing microglia in AD brains remains unknown. By immunohistochemistry, we studied the expression of TREM2 in AD and control brains. We found that none of Iba1-immunoreactive microglia expressed TREM2 in any cases examined. Although recent studies suggested that impaired clearance of amyloid-beta by microglia caused by loss of TREM2 function plays a key role in the pathogenesis of AD, we could not provide definite immunohistochemical evidence for supporting this view.

A survey of TREM2 antibodies reveals neuronal but not microglial staining in formalin-fixed paraffin-embedded postmortem Alzheimer's brain tissues