The evidence that overexpression of dementia-associated variants in vitro shows deficits in cell surface trafficking of TREM2, in the case of p.T66M and p.Y38C, or ligand (lipids and Aβ)-binding, in the case of p.R47H and p.R62H10, support the hypothesis that disease-associated mutant TREM2 proteins are functionally deficient. This evidence concerns the gene TREM2 and dementia.