In addition, we reported that monocyte-derived DCs from AD patients have a reduced ability to produce brain-derived neurotrophic factor following stimulation with Aβ1–42 peptide [23], providing evidence in support of the concept that myeloid DCs might participate in AD brain damage by promoting both inflammatory response and Aβ-dependent neurotoxic pathways. Here, BDNF is linked to Alzheimer disease.