Using a mouse model of Alzheimer disease (i.e., double transgenic mice that overexpress mutant forms of human amyloid precursor protein and presenilin-1 specifically in the CNS), the authors could show that TNF-α, MIP1-α, and KC that MK2, TNF-α, MIP1-α, and KC expression was significantly up-regulated in the cortex but not the cerebellum. The gene discussed is CCL3; the disease is Alzheimer disease.