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

Antonio Ciaramella, Francesca Salani, Federica Bizzoni, Maria Donata Orfei, Roberto Langella, Francesco Angelucci, Gianfranco Spalletta, Anna Rita Taddei, Carlo Caltagirone, Paola Bossù

Research output: Contribution to journalArticle


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 proinflammatory 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.

Original languageEnglish
Pages (from-to)29-32
Number of pages4
JournalBrain, Behavior, and Immunity
Publication statusPublished - Aug 2013



  • Amyloid β
  • Brain-derived neurotrophic factor
  • Dendritic cells

ASJC Scopus subject areas

  • Immunology
  • Behavioral Neuroscience
  • Endocrine and Autonomic Systems

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