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Triggering receptor expressed by myeloid cells 2 ( TREM 2), a member of the immunoglobulin superfamily, has anti‐inflammatory phagocytic function in myeloid cells. Several studies have shown that   TREM   2  gene variant rs75932628‐ T  increased the risks for  A lzheimer's disease ( AD ),  P arkinson's disease, frontotemporal dementia and amyotrophic lateral sclerosis. It has been suggested that the risks could be resulted from the loss of  TREM 2 function caused by the mutation. Indeed, new evidence showed that several mutations in the immunoglobulin‐like  V ‐region led to low cell surface expression of  TREM 2 and reduced phagocytic function. Because of the emerging importance in understanding  TREM 2 expression and functions in human neurodegenerative diseases, we conducted biochemical and morphological studies of  TREM 2 expression in human post‐mortem temporal cortical samples from  AD  and normal cases. Increased expression of  TREM 2 protein was found to significantly correlate with increases of phosphorylated‐tau and active caspase 3, a marker of apoptosis, and also loss of the presynaptic protein  SNAP 25. Strong intensities of  TREM 2 immunoreactivity were observed in the microglia associated with amyloid plaques and in neuritic pathology‐enriched areas. Based on the findings that  TREM 2 expression correlated with neurodegenerative markers, further investigation on whether there is abnormality of  TREM 2 functions in  AD  brains with nonmutated  TREM 2 is needed.

TREM 2 Protein Expression Changes Correlate with A lzheimer's Disease Neurodegenerative Pathologies in Post‐Mortem Temporal Cortices