Affiliations: Department of Psychiatry, Section Clinical Neurobiology, Campus Benjamin Franklin, Charité, University Medicine Berlin, Germany
Correspondence:
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Correspondence to: Dr. Vera Clemens, Charité - University Medicine Berlin, Department of Psychiatry and Psychotherapy, Section Clinical Neurobiology, Campus Benjamin Franklin, Hindenburgdamm 30, 12203 Berlin, Germany. Tel.: +49 30 450 517708; Fax: +49 30 450 517647; E-mail: [email protected].
Abstract: Apolipoprotein E (ApoE) represents a pivotal target in Alzheimer’s disease (AD) and is modulated through retinoic acid (RA), an endogenous neuroprotective and anti-inflammatory compound. A major source of ApoE are microglia, which are pathologically activated in AD. Activated microglia are known to block RA signaling. This suggests a vicious cycle between inflammation, RA signaling, and ApoE homeostasis in AD pathogenesis. To test this hypothesis, we investigated effects of RA and proinflammatory activation on ApoE synthesis in primary human macrophage-derived microglial-like cells. Our results indicate that proinflammatory activation attenuates ApoE synthesis, an effect blocked by RA.
Keywords: Alzheimer’s disease, Apolipoprotein E, macrophages, retinoic acid, vitamin A
