Mononuclear cells of patients with AD fail to upregulate TLRs with Aβ stimulation, in contrast to those from normal subjects that upregulate TLR expression.36 Delivering of TLR2-lentiviral genes into bone marrow–derived cells can rescue cognitive decline in TLR2-deficient AD mice.37 Normal human monocyte TLR4 levels may be higher than that in patients with AD. Here, TLR2 is linked to Alzheimer disease.