The stimulation of dendritic cells by amyloid beta 1-42 reduces BDNF production in Alzheimer's disease patients.

Dendritic cells (DCs), the main actors of immune responses and inflammation, may play a role in Alzheimer's disease (AD). Recent studies demonstrate that monocyte-derived DCs (MDDCs), generated in vitro in the presence of amyloid β1-42 peptide (Aβ1-42), show a functional alteration and an increased production of inflammatory molecules. Accordingly, MDDCs from AD patients show a more pronounced pro-inflammatory profile than DCs obtained from control subjects. In this study, we aimed at further investigating DC role in AD. Thus, we analyzed the in vitro effect of Aβ1-42 treatment on already differentiated DCs from AD patients, as compared to control subjects. We found that Aβ1-42 significantly decreases the expression of brain-derived neurotrophic factor (BDNF) in DCs derived from AD patients but not from control subjects. Thus, possibly due to their Aβ-induced reduction of neurotrophic support to neurons, DCs from AD patients might contribute to brain damage by playing a part in Aβ-dependent neuronal toxicity.