Table 4.

Selected studies on fracktalkine-dependent synaptic pruning during development and neurodegeneration

Material used	Molecules investigated	Inhibitors used	Summary	References
Cx3cr1 KO mice	CX3CR1	Genetic deletion of Cx3cr1	Cx3cr1 KO mice had decrease in the microglial number, increase in the excitatory postsynaptic density and dendritic spine density on CA1 pyramidal neurons, accompanied by significantly increased LTD.	Paolicelli, 2011 [57]
Cx3cr1 KO mice	CX3CR1	Genetic deletion of Cx3cr1	Deficit in fractalkine signaling can cause decrease in the microglial number, defects in synaptic pruning and ultimately neurodevelopmental and neuropsychiatric disorders in mice.	Zhan, 2014 [58]
hAPP; Cx3cr1 KO mice	CX3CR1	Genetic deletion of Cx3cr1	Deficiency of fractalkine signaling worsened plaque-independent cognitive retention in hAPP-J20 mice.	Cho, 2011 [60]
5xTg; Cx3cr1 KO mice	CX3CR1	Genetic deletion of Cx3cr1	Fractalkine deletion can prevent neuronal loss in 5xTg mice.	Fuhrmann, 2010 [62]
hTau; Cx3cr1 KO mice	CX3CR1	Genetic deletion of Cx3cr1	Deficiency of fractalkine signaling aggravates microglia-mediated hyperphosphorylation of tau and inflammatory responses in a mouse model of systematic inflammation and hTau.	Bhaskar, 2010 [14]
APP/PS1; Cx3cr1 KO mice	CX3CR1	Genetic deletion of Cx3cr1	CX3CR1 deficiency is anti-amyloidogenic in APP/PS1 transgenic mouse model of AD.	Lee, 2010 [61]