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Identification of a central regulator

C1q (green) and ApoE (red) deposits in the choroid plexus, super-resolution microscopy. Bar 1 µm.

A new study by IPEK researchers shows that the protein ApoE plays a key role in the pathogenesis of diseases associated with chronic inflammation, and identifies a new target for therapeutic strategies against atherosclerosis and Alzheimer’s disease.

Apolipoprotein E (ApoE for short) is a protein with multiple functions: Although originally identified as a transport molecule involved in fat metabolism, various additional properties have meanwhile been described: It has been implicated in the development of atherosclerosis, Alzheimer’s disease, AIDS and multiple other pathological conditions in which persistent inflammation is a common feature. However, despite major international research efforts for decades, a shared mechanism of action for its functional role has not been identified. Now researchers led by Dr. Changjung Yin, Professor Andreas Habenicht and Professor Christian Weber, in cooperation with the Leibniz Institute for Natural Products and Infection Biology in Jena and other partners, have demonstrated that ApoE is a key checkpoint regulator of a central signaling cascade that directly interferes in inflammation. Moreover, they showed that a drug which interferes with this cascade is capable of dampening diseases as diverse as atherosclerosis and Alzheimer-associated inflammation. These findings, which appear in the journal Nature Medicine, pinpoint a novel and promising target for the development of therapies to combat diseases associated with chronic inflammation.


These studies were supported by the DFG CRC 1123 and the Excellence Cluster SyNergy.


Nature Medicine 2019

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