Furthermore, lack of the membrane-anchored CX3CL1 in AD mice expressing only the soluble chemokine domain of the peptide (CX3CL1105Δ) resulted in increased expression of proinflammatory markers, including cytokines, reduction of CX3CR1 expression in microglia, and hyperphosphorylation of tau; these changes were accompanied by deficits in spatial learning (Bemiller et al. 2018; Lee et al. 2014). Here, CX3CR1 is linked to Alzheimer disease.