Open AccessTREM 2 Protein Expression Changes Correlate with A lzheimer's Disease Neurodegenerative Pathologies in Post‐Mortem Temporal Cortices
Author(s) -
Lue LihFen,
Schmitz Christopher T.,
Serrano Geidy,
Sue Lucia I.,
Beach Thomas G.,
Walker Douglas G.
Publication year - 2015
Publication title -
brain pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.986
H-Index - 132
eISSN - 1750-3639
pISSN - 1015-6305
DOI - 10.1111/bpa.12190
Subject(s) - trem2 , microglia , optineurin , biology , frontotemporal dementia , amyotrophic lateral sclerosis , neurodegeneration , immunoglobulin superfamily , alzheimer's disease , cancer research , antibody , immunology , pathology , dementia , disease , medicine , inflammation
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.