INNOTEST^® sTREM2

This assay should be used in combination with the sTREM2 CAL-RVC pack, article no. 81057 (RUO), of the corresponding lot.
 

Test principle

The INNOTEST sTREM2 is a solid-phase enzyme immunoassay in which the sTREM2 protein is captured by a first monoclonal antibody, ADx601 (B02; rabbit; IgG). CSF samples are added and incubated with a biotinylated antibody, ADx602 (C10; rabbit; IgG). Both ADx601 and ADx602 are directed against the ectodomain of human TREM2 and the epitope of ADx601 is further specified in Figure 1. This antigen-antibody complex is then detected by a peroxidase-labeled streptavidin. After addition of substrate working solution, samples will develop a color. The color intensity is a measure for the amount of human sTREM2 protein in the sample.

Figure 1: Test principle INNOTEST sTREM2 (SV = streptavidin; HRP = horseradish peroxidase).

 
Background

TREM2 is a transmembrane receptor that is predominantly expressed by microglia in the central nervous system. sTREM2 results from the processing of the TREM2 ectodomain and can be detected in CSF. Studies demonstrated that CSF sTREM2 is a bioactive molecule capable of binding ligands (like Aβ), activating microglia and regulating immune responses during the Alzheimer’s disease (AD) continuum¹. CSF sTREM2 seems to be especially increased in early symptomatic stages of late-onset AD, whereas decreased CSF sTREM2 concentrations have been observed at the earliest asymptomatic phase when only abnormal Aβ pathology, but no tau pathology or neurodegeneration, is present. Rare variants in the TREM2 gene increase the risk for late-onset AD, and CSF sTREM2 concentrations have been found to differ between variants². Altogether, CSF sTREM2 can be seen as a surrogate measure of TREM2-mediated microglia function.

  
References

1. Yang J, et al. TREM2 ectodomain and its soluble form in Alzheimer’s disease. J Neuroinflammation, 2020;17:204.
2. Suárez-Calvet M, et al. Early increase of CSF sTREM2 in Alzheimer’s disease is associated with tau related-neurodegeneration but not with amyloid-β pathology. Mol Neurodegener, 2019;14:1.